Femoral to cerebral arterial blood flow redistribution and femoral vein distension during orthostatic tests after 4 days in the head-down tilt position or confinement

The first objective of this study was to confirm that 4 days of head-down tilt (HDT) were sufficient to induce orthostatic intolerance, and to check if 4 days of physical confinement may also induce orthostatic intolerance. Evidence of orthostatic intolerance during tilt-up tests was obtained from blood pressure and clinical criteria. The second objective was to quantify the arterial and venous changes associated with orthostatic intolerance and to check whether abnormal responses to the tilt test and lower body negative pressure (LBNP) may occur in the absence of blood pressure or clinical signs of orthostatic intolerance. The cerebral and lower limb arterial blood flow and vascular resistance, the flow redistribution between these two areas, and the femoral vein distension were assessed during tilt-up and LBNP by ultrasound. Eight subjects were given 4 days of HDT and, 1 month later, 4 days of physical confinement. Tilt and LBNP test were performed pre- and post-HDT and confinement. Orthostatic intolerance was significantly more frequent after HDT (63%) than after confinement (25%, P<0.001). Cerebral haemodynamic responses to tilt-up and LBNP tests were similar pre- and post-HDT or confinement. Conversely, during both tilt and LBNP tests the femoral vascular resistances increased less (P<0.002), and the femoral blood flow reduced less (P<0.001) after HDT than before HDT or after confinement. The cerebral to femoral blood flow ratio increased less after HDT than before (P<0.002) but remained unchanged before and after confinement. This ratio was significantly more disturbed in the subjects who did not complete the tilt test. The femoral superficial vein was more distended during post-HDT LBNP than pre-HDT or after confinement (P<0.01). In conclusion, 4 days of HDT were enough to alter the lower limb arterial vasoconstriction and venous distensibility during tilt-up and LBNP, which reduced the flow redistribution in favour of the brain in all HDT subjects. Confinement did not alter significantly the haemodynamic responses to orthostatic tests. The cerebral to femoral blood flow ratio measured during LBNP was the best predictor of orthostatic intolerance. Accepted: 12 December 1997     

Arterial blood pressure during voluntary diving in the tufted duck,Aythya fuligula

Arterial blood pressure was monitored in voluntarily diving tufted ducks. Mean arterial blood pressure while diving increased during the pre-dive tachycardia, fell to resting levels on submersion, then gradually increased before peaking on surfacing. Estimated total peripheral resistance fell during the pre-dive and post-dive tachycardia, presumably to allow the oxygen stores to be loaded and replenished respectively and/or for carbon dioxide levels to be reduced. Changes in mean arterial blood pressure and total peripheral resistance suggest that peripheral vasoconstriction occurs in some vascular beds during a dive. An increase in arterial blood pressure (and therefore perfusion pressure) may be employed to increase blood flow and oxygen delivery to the active leg muscles.Abbreviations ecg Electrocardiogram, f _H, heart rate - MABP mean arterial blood pressure - P _b blood pressure(s) - TPR total peripheral resistance - V _b cardiac output     

Cerebral cortical blood flow in rabbits during parabolic flights (hypergravity and microgravity)

We studied the effect of gravity on cerebral cortical blood flow (CBF), mean arterial blood pressure () and heart rate in six rabbits exposed to parabolic flights. The CBF was obtained using a laser-Doppler probe fixed on to a cranial window. Before weightlessness, the animals were exposed to chest-to-back directed acceleration (1.8–2.0 g). The CBF values were expressed as a percentage of CBF_o (mean CBF during 60 s before the 1st parabola). Propranolol (1 mg · kg⁻¹ IV) was given after the 11th parabola and pentobarbital (12–15 mg · kg⁻¹ IV) after the 16th parabola. Before the administration of the drugs, CBF increased (P < 0.01) during hypergravity [i.e. maximal CBF 151 (SD 64)% CBF_o. Simultaneously increased [maximal , 119 (SD 11) mmHg (P < 0.01)]. At the onset of weightlessness, CBF and reached maximal values [194 (SD 96)% CBF_o (P < 0.01) and 127 (SD 19) mmHg, (P < 0.01) respectively]. The microgravity-induced increase in CBF was transient since CBF returned to its baseline value after 8 (SD 2) s of microgravity. After propranolol administration, CBF was not statistically different during hypergravity but an elevation of CBF was still observed in weightlessness. The increases in CBF and also persisted during weightlessness after pentobarbital administration. These data would indicate that CBF of nonanesthetized rabbits increases during the first seconds of weightlessness and demonstrate the involvement of rapid active regulatory mechanisms since CBF returned to control values within 8 (SD 2) s. We concluded that this elevation in blood flow was not related to stress because it persisted after the administration of propranolol and pentobarbital. Accepted: 6 November 1997     

Pre-and post-branchial blood respiratory status during acute hypercapnia or hypoxia in rainbow trout,Oncorhynchus mykiss

Simultaneous venous (pre-branchial) and arterial (post-branchial) extracorporeal blood circulations were utilized to monitor continuously the rapid and progressive effects of acute environmental hypercapnia (water partial pressure of CO₂ 4.8±0.2 torr) or hypoxia (water partial pressure of O₂ 25±2 torr) on oxygen and carbon dioxide tensions and pH in the blood of rainbow trout (Oncorhynchus mykiss). During hypercapnia, the CO₂ tension in the arterial blood increased from 1.7±0.1 to 6.2±0.2 torr within 20 min and this was associated with a decrease of arterial extracellular pH from 7.95±0.03 to 7.38±0.03; the acid-base status of the mixed venous blood changed in a similar fashion. The decrease in blood pH in vivo was greater than in blood equilibrated in vitro with a similar CO₂ tension indicating a significant metabolic component to the acidosis in vivo. Under normocapnic conditions, venous blood CO₂ tension was slightly higher than arterial blood CO₂ tension difference was abolished or reversed during the initial 25 min of hypercapnia indicating that CO₂ was absorbed from the water during this period. Arterial O₂ tension remained constant during hypercapnia; however, venous blood O₂ tension decreased significantly (from 22.0±2.6 to 9.0±1.0 torr) during the initial 10 min. Hypercapnia elicited the release of catecholamines (adrenaline and noradrenaline) into the blood. The adrenaline concentration increased from 6±3 to 418±141 nmol · l^-1 within 25 min; noradrenaline concentration increased from 3±0.5 to 50±21 nmol · l^-1 within 15 min. During hypoxia arterial blood O₂ tension declined progressively from 108.4±9.9 to 12.8±1.7 torr within 30 min. Venous blood O₂ tension initially was stable but then decreased abruptly as catecholamines were released into the circulation. The release of catecholamines occurred concomitantly with a sudden metabolic acidosis in both blood compartments and a rise in CO₂ tension in the mixed venous blood only.Abbreviations CCO₂ plasmatotal carbondioxide - CtO₂ blood oxygen content - PO₂ partial pressure of oxygen - PCO₂ partial pressure of carbon dioxide - PaO₂ arterial bloodPO₂ - PaCO₂ arterial bloodPCO₂ - PvCO₂ venous bloodPCO₂ - PwO₂ waterPO₂ - PwCO₂ waterPCO₂ - Hb haemoglobin - SHbO₂ haemoglobin oxygen saturation - HPLC high-performance liquid chromatography - rbc red blood cell(s) - Hct haematocrit     

Genome and Hormones: Gender Differences in Physiology: Selected Contribution: Gender differences in the endothelin-B receptor contribution to basal cutaneous vascular tone in humans

To testwhether the contribution of endothelin-B (ET-B) receptors to restingvascular tone differs between genders, we administered the ET-Breceptor antagonist BQ-788 into the forearm skin of 11 male and 11 female subjects by intradermal microdialysis. Skin blood flow wasmeasured using laser-Doppler flowmetry at the microdialysis site. Theprobe was perfused with Ringer solution alone, followed by BQ-788 (150 nM) and finally sodium nitroprusside (28 mM) to effect maximalcutaneous vasodilation. Cutaneous vascular conductance (CVC) wascalculated (laser-Doppler flowmetry/mean arterial pressure) andnormalized to maximal levels (%max). In male subjects, baseline CVCwas (mean ± SE) 19 ± 3%max and increased to 26 ± 5%max with BQ-788 (P < 0.05 vs. baseline). In femalesubjects, baseline CVC was 13 ± 1%max and decreased to 10 ± 1%max in response to BQ-788. CVC responses to BQ-788 differed withgender (P < 0.05); thus the contribution of ET-Breceptors to resting cutaneous vascular tone differs between men andwomen. In men, ET-B receptors mediate tonic vasoconstriction, whereas,in women, ET-B receptors mediate tonic vasodilation.

     

Circulatory function at sub-zero temperature: venous responses to catecholamines and angiotensin II in the Antarctic fish <Emphasis Type="Italic">Pagothenia borchgrevinki</Emphasis>

Catecholamines increase arterial pressure by increasing cardiac output (Q) and stroke volume (V _s), while angiotensin II (ang II) also increases vascular resistance (R _sys) in the Antarctic fish Pagothenia borchgrevinki. Adrenaline, phenylephrine and ang II (Asn¹, Val⁵) were injected into P. borchgrevinki. Cardiovascular variables, including central venous pressure (P _cv) and mean circulatory filling pressure (P _mcf; an index of venous capacitance), were recorded to investigate if venous vasoconstriction can explain the increased V _s and Q and the arterial pressor response in this species. Routine P _cv and P _mcf were 0.11 ± 0.01 and 0.18 ± 0.02 kPa, respectively. All of the drugs caused moderate increases in P _cv and P _mcf and the responses were attenuated after α-adrenergic blockade with prazosin. Although dorsal aortic pressure (P _da) also increased in response to all agonists, the mechanisms differed. Adrenaline caused sustained increases in V _s and Q, while R _sys only rose transiently. Ang II had a slower effect than adrenaline and increased both R _sys and Q, while phenylephrine only increased R _sys. This study demonstrates that P _cv is positive and controlled by an α-adrenergic mechanism in P. borchgrevinki. However, given the relatively small venous response to adrenaline it seems more likely that the increases in V _s and Q from this agonist are due to direct effects on the heart.     

Sympathetic nerve regulation of cochlear blood flow during increases in blood pressure in humans

The purpose of this work was to show that regulation of the blood flow to the cochlea by the sympathetic nervous system occurs in humans at the level of the cochlear microcirculation during increases in blood pressure and that its involvement depends on the pressure level. Eight anaesthetized patients undergoing tympanoplasty for hearing disease took part in a pharmacological protocol of stimulation and inhibition of the autonomic nervous system (ANS) to provide variations in systolic blood pressure (BP_S) and cochlear blood flow (CBF). The CBF was measured by laser-Doppler flowmetry. Changes in autonomic nerve activity were brought about by changes in baroreceptor activity (BR) initiated by the injection of an α adrenergic agent before and after sympathetic and parasympathetic blockade. The CBF variations (δCBF) were plotted against BP_S increases at each stage of the ANS inhibition. The BR diminished significantly after α blockade, after α and β blockade, and after α and β blockade and atropine, by 50% (P < 0.01), 29% (P < 0.05), and 95% (P < 0.001) respectively. The BP_S increased significantly (P < 0.01) by 36 (SD 9)%, 47 (SD 1)%, and 67 (SD 16)% respectively. The CBF response to an increase in BP_S exhibited two opposing variations in the patients: CBF decreased significantly in one group, and increased significantly in the other group. In both groups, δCBF decrease and δCBF increase, respectively, were significant after ANS blockade; even so the decrease and increase, respectively, levelled off at BP_S around 160 mmHg before ANS blockade. For BP_S below 160 mmHg, correlations between δCBF and BP_S were significant before inhibition and after inhibition of ANS. For BP_S above 160 mmHg, BP_S and δCBF were not correlated before inhibition of ANS, and were significantly correlated after inhibition of ANS. For BP_S below 160 mmHg, CBF response to the BP_S increase was the same before and after ANS blockade, i.e. ANS control did not predominate; even so, for BP_S above 160 mmHg, the CBF response to BP_S increase was different before and after ANS blockade: CBF varied significantly after ANS blockade as it varied for BP_S below 160 mmHg, while it remained constant before ANS blockade that elicited ANS control of CBF. In conclusion, sympathetic nerve regulation via its vasomotor tone at the level of cochlear microcirculation occurred markedly when the blood pressure was above 160 mmHg; the autonomic nervous system would appear to control the cochlear blood flow against large variations in blood flow in response to hypertensive phenomena. Accepted: 7 October 1996     

Geomagnetic field modulates artificial static magnetic field effect on arterial baroreflex and on microcirculation

Spreading evidence suggests that geomagnetic field (GMF) modulates artificial magnetic fields biological effect and associated with increased cardiovascular morbidity. To explore the underlying physiological mechanism we studied 350 mT static magnetic field (SMF) effect on arterial baroreflex-mediated skin microcirculatory response in conjunction with actual geomagnetic activity, reflected by K and K _p indices. Fourteen experiments were performed in rabbits sedated by pentobarbital infusion (5 mg/kg/h). Mean femoral artery blood pressure, heart rate, and the ear lobe skin microcirculatory blood flow, measured by microphotoelectric plethysmogram (MPPG), were simultaneously recorded before and after 40 min of NdFeB magnets local exposure to sinocarotid baroreceptors. Arterial baroreflex sensitivity (BRS) was estimated from heart rate/blood pressure response to intravenous bolus injections of nitroprusside and phenylephrine. We found a significant positive correlation between SMF-induced increase in BRS and increment in microvascular blood flow (ΔBRS with ΔMPPG, r=0.7, p<0.009) indicated the participation of the arterial baroreflex in the regulation of the microcirculation and its enhancement after SMF exposure. Geomagnetic disturbance, as opposed to SMF, decreased both microcirculation and BRS, and counteracted SMF-induced increment in microcirculatory blood flow (K-index with ΔMPPG; r _s=−0.55, p<0.041). GMF probably affected central baroreflex pathways, diminishing SMF direct stimulatory effect on sinocarotid baroreceptors and on baroreflex-mediated vasodilatatory response. The results herein may thus point to arterial baroreflex as a possible physiological mechanism for magnetic-field cardiovascular effect. It seems that geomagnetic disturbance modifies artificial magnetic fields biological effect and should be taken into consideration in the assessment of the final effect. An erratum to this article can be found at     

Cardiovascular responses to thoracic skin cooling: comparison of incubating and non-incubating Bantam hens

Summary Body temperatures, metabolic rate, haemostatic parameters, and cardiovascular reactions to thoracic skin cooling were compared between incubating (broody) and non-broody Bantam hens. Under resting conditions, without thoracic skin cooling, cardiac output of broody hens was twice that of non-broody hens. However, their metabolic rate was increased by only one-third over that of non-broody hens, and the arteriovenous difference in oxygen concentration was smaller for broody birds. This indicates a higher rate of non-nutrient blood flow during incubation. A higher thoracic skin temperature (T _ths) for broody hens compared to non-broody hens suggests that brood patches are the probable site of this increased flow through arteriovenous anastomoses (AVAs). Thoracic skin cooling increased metabolic rate and significantly more in broody hens, but did not increase AVA blood flow. The relation between metabolic rate and total peripheral resistance indicated more intense vasodilation for broody hens at the relatively low metabolic rates during moderate cooling, and more intense vasoconstriction for the broody hens at the high metabolic rates during stronger cooling. This corresponds to T _ths measurements indicating dilation of brood patch AVAs with moderate cooling and AVA constriction with severe cooling. During moderate cooling, vasoconstriction in the feet and wattles of broody hens (but not of non-broody hens) freen non-nutrient blood flow for redistribution to the brood patches. Thus, the cardiovascular system of the hen seems to adjust to the special demands of incubation by a permanent increase of AVA flow in the brood patch, and by an additional capacity for brood patch vasodilation induced by cold stimuli in the range from 35 to 25°C. This corresponds well to the temperature range for development of galliform embryos.Abbreviations AVAs arteriovenous anastomoses - BP arterial blood pressure - CaO₂ and CvO₂ arterial and venous oxygen concentrations, respectively - HR heart rate - MAP mean arterial blood pressure - cardiac output - SV stroke volume - T _bs back skin temperature - T _c cofon temperature - T _f foot temperature - T _ths thoracic skin temperature - TPR total peripheral resistance - T _w wattle temperature - oxygen consumption     

The effects of endogenous or exogenous catecholamines on blood respiratory status during acute hypoxia in rainbow trout (Oncorhynchus mykiss)

Summary An extracorporeal circulation of rainbow trout (Oncorhynchus mykiss) was utilized to continuously monitor the rapid and progressive effects of endogenous or exogenous catecholamines on blood respiratory/acid-base status, and to provide in vivo evidence for adrenergic retention of carbon dioxide (CO₂) in fish blood (cf. Wood and Perry 1985). Exposure of fish to severe aquatic hypoxia (final P _wO₂=40–60 torr; reached within 10–20 min) elicited an initial respiratory alkalosis resulting from hypoxia-induced hyperventilation. However, at a critical arterial oxygen tension (P _aO₂) between 15 and 25 torr, fish became agitated for approximately 5 s and a marked (0.2–0.4 pH unit) but transient arterial blood acidosis ensued. This response is characteristic of abrupt catecholamine mobilization into the circulation and subsequent adrenergic activation of red blood cell (RBC) Na⁺/H⁺ exchange (Fievet et al. 1987). Within approximately 1–2 min after the activation of RBC Na⁺/H⁺ exchange by endogenous catecholamines, there was a significant rise in arterial PCO₂ (P _aCO₂) whereas arterial PO₂ was unaltered; the elevation of P _aCO₂ could not be explained by changes in gill ventilation. Pre-treatment of fish with the -adrenoceptor antagonist phentolamine did not prevent the apparent catecholamine-mediated increase of P _aCO₂. Conversely, pre-treatment with the -adrenoceptor antagonist sotalol abolished both the activation of the RBC Na⁺/H⁺ antiporter and the associated rise in P _aCO₂, suggesting a causal relationship between the stimulation of RBC Na⁺/H⁺ exchange and the elevation of P _aCO₂. To more clearly establish that elevation of plasma catecholamine levels during severe hypoxia was indeed responsible for causing the elevation of P _aCO₂, fish were exposed to moderate hypoxia (final P _wO₂=60–80 torr) and then injected intraarterially with a bolus of adrenaline to elicit an estimated circulating level of 400 nmol·l^-1 immediately after the injection. This protocol activated RBC Na⁺/H⁺ exchange as indicated by abrupt changes in arterial pH (pHa). In all fish examined, P _aCO₂ increased after injection of exogenous adrenaline. The effects on P _aO₂ were inconsistent, although a reduction in this variable was the most frequent response. Gill ventilation frequency and amplitude were unaffected by exogenous adrenaline. Therefore, it is unlikely that ventilatory changes contributed to the consistently observed rise in P _aCO₂. Pretreatment of fish with sotalol did not alter the ventilatory response to adrenaline injection but did prevent the stimulation of RBC Na⁺/H⁺ exchange and the accompanying increases and decreases in P _aCO₂ and P _aO₂, respectively. These results suggest that adrenergic elevation of P _aCO₂, in addition to the frequently observed reduction of P _aO₂ are linked to activation of RBC Na⁺/H⁺ exchange. The physiological significance and the potential mechanisms underlying the changes in blood respiratory status after addition of endogenous or exogenous catecholamines to the circulation of hypoxic rainbow trout are discussed.Abbreviations P _aCO₂ arterial carbon dioxide tension - P _aO₂ arterial oxygen tension - P _da dorsal aortic pressure - pHa arterial pH - P _wO₂ water oxygen tension - RBC red blood cell - V _f breathing frequency     

Effect of naloxone on renal cortical microcirculation in haemorrhagic shock

In order to assess the effect of opioid receptor antagonists, naloxone and noradrenaline, on renal cortical microcirculation, India ink infusion was made through the renal artery, one hour after treatment with each drug, in dogs subjected to haemorrhagic shock. Naloxone (1 mg/kg) treatment showed a dual beneficial effect of significant improvement (P < 0.001) in the mean arterial pressure without increasing the renal resistance as indicated by the presence of ink particles in about 75% of the cortical glomeruli. However, in the case of noradrenaline (2 Μ/kg/min)-treated animals, although mean arterial pressure increased significantly (P < 0.001) only very few glomeruli (25%) in the cortical region showed ink particles, demonstrating severe vasoconstriction. In the control group infused only with saline, although most of the glomeruli (92%) were filled with ink particles, there was a significant decline in the mean arterial pressure (P < 0.001).     

The effect of exogenous catecholamines on the ventilatory and cardiac responses of normoxic and hyperoxic rainbow trout,Oncorhynchus mykiss

Ventilation frequency, opercular pressure amplitude, heart rate, dorsal aortic pressure, arterial pH, arterial O₂ tension, and plasma catecholamine levels were recorded in rainbow trout, Oncorhynchus mykiss, during normoxia (19.7 kPa, 148 mmHg) or hyperoxia (51.2 kPa, 384 mmHg) after injection of various concentrations of catecholamines. In normoxic fish, adrenaline injection resulted in a depression of arterial O₂ tension, hypoventilation due to a drop in ventilation frequency, and a drop in heart rate, while dorsal aortic pressure increased. Noradrenaline depressed ventilation frequency, but opercular pressure amplitude increased to a far greater extent, and dorsal aortic pressure increased. During hyperoxia, adrenaline injection lowered ventilation frequency, opercular amplitude and heart rate, but dorsal aortic pressure increased. The stimulatory effects of noradrenaline on ventilation were abolished during hyperoxia, but the cardiac responses were similar to those seen during normoxia. These results indicate that catecholamines can modify the ventilatory output from the respiratory centre, and modification of ventilation frequency can occur independently of opercular pressure amplitude.Abbreviations f _g ventilation frequency - HPLC high performance liquid chromatography - P _op opercular pressure amplitude - f _h heart rate - P _DA dorsal aortic pressure - pH_a arterial pH - P _aO₂ arterial oxygen tension - PO₂ oxygen tension     

Effects of direct transfer from freshwater to seawater on respiratory and circulatory variables and acid-base status in rainbow trout

Summary The effects of increased ambient salinity (35 mg · ml^-1) were studied at 1, 6, and 24 h after direct transfer of rainbow trout from freshwater to seawater. Two series of experiments were carried out successively. The first series was designed to simultaneously study all the respiratory (except Hb affinity for O₂), circulatory, and acid-base variables in each fish. In this series, fish were fitted with catheters chronically inserted into the cardiac bulbus, the dorsal aorta, and the opercular and buccal cavities. In the second series, designed to study haemoglobin O₂ affinity, fish were fitted with only a dorsal aorta catheter. The ventilatory flow ( ) was markedly increased just after transfer (by 55% at 1 h), then more moderately (by 20% at 6 h and 32% at 24 h). The initial hyperventilation peak was associated with frequent couphing motions. These ventilatory changes resulted essentially from increase in ventilatory amplitude. Initially, standard oxygen consumption (MM}O₂) decreased slightly, the moderately increased (by 12% at 24 h), so that the oxygen convection requirement ( ) increased substantially. In spite of an increased ventilation, the partial pressure of oxygen in arterial blood (P _aO₂) decreased slightly at 1 h, prior to returning to control levels, while partial pressure of carbon dioxide in arterial blood (P _aCO₂) was not significantly decreased. Gill oxygen transfer factor decreased substantially at 1 h (by 35%) then more moderately (by 7% at 1 h and 12% at 24 h). These results suggest a decrease in gas diffusing capacity of the gills. As P _aCO₂ remained approximatively unchanged, the gradual decrease in arterial pH (pH_a) from 7.94 to 7.67 at 24 h must therefore be regarded as a metabolic acidosis. The strong ion difference decreased markedly because the concentration of plasma chloride increased more than that of sodium. Arterial O₂ content (C _aO₂) gradually decreased (by 38% at 24 h) simultaneously with the decrease in pH_a, while the ratio P _aO₂/C _aO₂ increased. In parallel, seawater exposure induced a marked decrease in affinity of haemoglobin for O₂, so that at 24 h, P₅₀ was increased by 26% above the value obtained in freshwater-adapted trout. The increase in could be ascribed initially (at 1 h) to the decrease of P _aO₂ and later to a stimulation of respiratory neurons resulting from the lowered medullary interstitial pH. The decrease in C _aO₂ could be interpreted mainly as a consequence of a decreased affinity of haemoglobin for O₂, likely to be due to the blood acidosis and a predictable increase in chloride concentration within erythrocytes. Cardiac output ( ) slightly decreased at 1 h, then progressively increased by 30% at 24 h. Branchial vascular resistance increased at 1 h by 28%, then decreased by 18% of the control value at 24 h. Systemic vascular resistance decreased markedly by 40% at 24 h. As heart rate (HR) remained significantly unchanged, the cardiac stroke volume initially decreased then increased in relation to the changes in . The increase of , allowing compensation for the effect of decreased C _aO₂ in tissue O₂ supply, was interpreted as a passive consequence of the decrease in total vascular resistance occurring during seawater exposure.Abbreviations a.u. arbitrary units - C _aO₂ arterial oxygen content - pH₅₀ arterial pH at P₅₀ - C _vO₂ venous oxygen content - Hb haemoglobin - HR heart rate - Hct hematocrit - n_Hill Hill coefficient - O₂ standard oxygen consumption - P _aCO₂ arterial partial pressure of carbon dioxide - P _aO₂ arterial partial pressure of oxygen - P _vO₂ oxygen partial pressure in mixed venous blood - P₅₀ oxygen tension at half saturation of haemoglobin - P _VA, P _DA blood pressure in ventral and dorsal aorta - pH_a arterial pH - PIO₂, PEO₂ oxygen partial pressure of inspired and expired water - PO₂ oxygen partial pressure - cardiac output - SEM standard error of mean - S.I.D. strong ion difference - SV cardiac stroke volume - TO₂ gill oxygen transfer factor - U oxygen extraction coefficient - VA ventilatory amplitude - VF ventilatory frequency - VR_G, VR_S branchial and systemic vascular resistances - ventilatory flow - ventilatory oxygen convection requirement     

The influence of chronic anaemia on catecholamine secretion in the rainbow trout (Oncorhynchus mykiss)

The effect of long-term (7 day) anaemia on catecholamine release was examined in rainbow trout (Oncorhynchus mykiss) in vivo during acute exposure to hypoxia and in situ using a perfused post-cardinal vein preparation. The first goal was to distinguish among reductions in blood O₂ partial pressure, O₂ concentration and haemoglobin percentage saturation as potential stimuli for, or correlates of, catecholamine secretion during hypoxia. The second goal was to elucidate the role of these factors in promoting enhanced chromaffin cell responsiveness in trout subjected to chronic hypoxia (Montpetit and Perry 1998). Anaemic fish (haematocrit lowered from 28.4±2.4% to 11.9±1.6%) displayed a marked reduction in haemoglobin-O₂ binding affinity [P ₅₀ (P _aO₂ at 50% Hb-O₂ saturation) was increased from 14.7 mm Hg to 24.3 mm Hg]. Upon exposure to hypoxia, the anaemic fish released catecholamines into their circulation at higher values of arterial O₂ partial pressure (∼52 mm Hg versus ∼18 mm Hg) and haemoglobin O₂ saturation (<70% versus <55%) than did control fish. In addition, anaemic fish achieved significantly greater circulating levels of total catecholamines (noradrenaline plus adrenaline) during acute hypoxia (294.8±67.3 versus 107.0±35.6 nmol l⁻¹). These results do not support the view that catecholamine release is triggered by a reduction in haemoglobin O₂ saturation or arterial PO₂, per se. Nor are they consistent with the idea that catecholamine release occurs at a threshold value of arterial PO₂ corresponding to a critical reduction in blood O₂ concentration. The effects of the non-selective cholinergic receptor carbachol on catecholamine secretion from chromaffin tissue were assessed using perfused posterior cardinal vein preparations derived from control or anaemic fish. For adrenaline secretion, there was no statistically significant change in the ED₅₀ (dose eliciting 50% response). For noradrenaline secretion however, preparations originating from anaemic fish displayed an enhanced responsiveness to carbachol as indicated by a significant 4.5-fold reduction in the carbachol ED₅₀ value from 2.53 × 10⁻⁶ mol kg⁻¹ to 5.67 × 10⁻⁷ mol kg⁻¹. These results demonstrate that anaemia-induced hypoxaemia, in the absence of any lowering of PO₂, is able to modulate the responsiveness of chromaffin cells to cholinergic stimulation. Accepted: 21 April 1999     

Intra- and extracranial artery blood velocity during a sudden blood pressure decrease in humans

The intra- and extracerebral Doppler artery blood velocity responses to a 10-mmHg abrupt blood pressure (BP) decrease in ten healthy men were studied. This decrease was obtained using two cuffs placed over both thighs. First, cuffs were inflated to pressures greater than the arterial BP for 5 min. Next, they were deflated to 60 mmHg in order to prevent venous return from the legs. We obtained a decrease in mean arterial BP of from 101 (10) to 90 (10) mmHg [mean (SD), P < 0.01] without modifications in the heart rate [HR, 88 (14) beats min⁻¹]. Middle cerebral artery mean blood velocity (MCAmv) decreased immediately from 50 (10) to 42 (12) cm s⁻¹ (P < 0.05). Simultaneously, temporal superficial artery mean blood velocity (TSAmv) decreased from 11 (3) to 7 (2) cm s⁻¹ (P < 0.05) and common carotid artery blood flow (CCAbf ) decreased from 305 (23) to 233 (33) ml min⁻¹ (P < 0.05). After 5 s, MCAmv and CCAbf returned to baseline values, whereas TSAmv [8 (2) cm s⁻¹], mean arterial BP [86 (10) mmHg] remained low and HR increased [92 (12) beats min⁻¹]. TSAmv, BP and HR returned to baseline values in 1 min. These data confirm that cerebral blood flow (CBF) is very rapidly regulated but that blood flow in extracranial territories is not and that it follows the arterial BP changes. Accepted: 8 April 1997     

Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

During dynamic exercise in the heat, increasesin skin blood flow are attenuated in hypertensive subjects whencompared with normotensive subjects. We studied responses to passiveheat stress (water-perfused suits) in eight hypertensive and eightnormotensive subjects. Forearm blood flow was measured byvenous-occlusion plethysmography, mean arterial pressure (MAP) wasmeasured by Finapres, and forearm vascular conductance (FVC) wascalculated. Bretylium tosylate (BT) iontophoresis was used to blockactive vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites,and cutaneous vascular conductance was calculated. In normothermia, FVCwas lower in hypertensive than in normotensive subjects(P < 0.01). During heat stress, FVCrose to similar levels in both groups(P > 0.80); concurrent cutaneousvascular conductance increases were unaffected by BT treatment(P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia (P < 0.05, hypertensive vs.normotensive subjects). During hyperthermia, MAP fell in hypertensivesubjects but showed no statistically significant change in normotensivesubjects (P < 0.05, hypertensive vs.normotensive subjects). The internal temperature at which vasodilationbegan did not differ between groups (P > 0.80). FVC is reduced during normothermia in unmedicatedhypertensive subjects; however, they respond to passive heat stress ina fashion no different from normotensive subjects.

     

Cold-induced vasodilation and vasoconstriction in the finger of tropical and temperate indigenes

While heat acclimatization reflects the development of heat tolerance, it may weaken an ability to tolerate cold. The purpose of this study was to explore cold-induced vasodilation (CIVD) responses in the finger of tropical indigenes during finger cold immersion, along with temperate indigenes. Thirteen tropical male indigenes (subjects born and raised in the tropics) and 11 temperate male indigenes (subjects born and raised in Japan and China) participated. Subjects immersed their middle finger at 4.3±0.8 °C water for 30 min. Rectal temperature, skin temperatures, finger skin blood flow, blood pressure and subjective sensations were recorded during the test. The results showed that: (1) the tropical group demonstrated a lower minimum (T_min), maximum (T_max) and mean finger temperature (T_mean) compared to those of the temperate group (P<0.05); (2) seven tropical indigenes demonstrated a late-plateau type of CIVD pattern, which is characterized by a pronounced 1st vasoconstriction and a single CIVD with a faint and weak 2nd vasoconstriction, whereas no temperate indigene demonstrated the late-plateau type; and (3) the hand temperature at the end of finger immersion was 3 °C lower in the tropical than the temperate group (P<0.05). These results indicate that tropical indigenes have less active responses of arterio-venous anastomoses in the finger and weaker vasoconstrictions after the first CIVD response during finger cold immersion, which can be considered as being more vulnerable to cold injury of the periphery in severe cold.     

Non-invasive quantification of peripheral arterial volume distensibility and its non-linear relationship with arterial pressure

Arterial wall function is associated with different physiological and clinical factors. Changes in arterial pressure cause major changes in the arterial wall. This study presents a simple non-invasive method to quantify arterial volume distensibility changes with different arterial pressures.The electrocardiogram, finger and ear photoplethysmogram were recorded from 15 subjects with the right arm at five different positions (90°, 45°, 0°, ?45° and ?90° referred to the horizontal level). Arm pulse propagation time was determined by subtracting ear pulse transit time from finger pulse transit time, and was used to obtain arterial volume distensibility. The mean arterial blood pressure with the arm at the horizontal level was acquired, and changes with position were calculated using the hydrostatic principle that blood pressure in the arm is linearly related to its vertical distance from the horizontal level.The mean arm pulse propagation times for the five different positions were 88, 72, 57, 54 and 52 ms, with the corresponding mean arterial volume distensibility of 0.234%, 0.158%, 0.099%, 0.088% and 0.083% per mmHg. For all consecutive changes in arm position, arm pulse propagation time and arterial volume distensibility, were significantly different (all probability P<0.05). The slopes of arm pulse propagation time and arterial volume distensibility against arterial pressure decreased significantly between each consecutive arm position from 90° to ?45° (all P<0.01), indicating significant non-linearity.The experimental results fitted the physiological exponential model and Langewouters’ arctangent model well, and were also comparable to published data with arterial volume distensibility approximately tripling for transmural pressure changes from 101 to 58 mmHg.In conclusion, the inverse and non-linear relationship between arterial volume distensibility and arterial pressure has been quantified using a simple arm positioning procedure, with the greatest effect at low pressures. This work is an important step in developing a simple non-invasive technique for assessing peripheral arterial volume distensibility.     

Local blood flow velocities in the carotid body of fetal sheep and newborn lambs

Summary Elastically-suspended microelectrodes were used in the vascularly isolated blood-perfused carotid body of fetal and newborn lambs as well as of 6–7-day-old lambs to measure local blood flow velocities by means of hydrogen clearance. Fetal sheep (n=9) carotid bodies elicited mean local blood velocity values between 0.008 and 0.11 cm·s^–1, whereas newborn lamb carotid bodies (n=7) showed values between 0.008 and 0.067 cm·s^–1 at a perfusion pressure range between 30 and 150 mmHg. The 6–7-day-old lamb carotid bodies (n=5) were characterized by values of 0.003 and 0.049 cm·s^–1 over the same perfusion pressure range. Fetal carotid body values were statistically significantly higher than the values of the 6–7-day-old lamb carotid bodies, whereas the newborn carotid body values showed no significant difference to both other groups. The flow velocity/perfusion pressure relationship peaked at perfusion pressure values between 100 and 150 mmHg in all groups with a reduced steepness in the lamb carotid body. It is concluded that local blood flow velocities in the carotid body are similar to that in other organs, and that after birth local blood flow velocities in the carotid body decrease during the first week of life, probably induced by vasoconstriction, changed blood gas values, and/or increasing shunt flow.Abbreviations significance level - D diffusion coefficient - i.v. intravenous - n number of experiments - PCO ₂ carbon dioxide partial pressure - pH negative logarithm of hydrogen ion concentration - PH ₂ hydrogen partial pressure - Po PH₂ with perfusion - P PH₂ without perfusion - PO ₂ oxygen partial pressure - PP perfusion pressure - r radius     

Static magnetic field effect on the arterial baroreflex-mediated control of microcirculation: implications for cardiovascular effects due to environmental magnetic fields

Increasing evidence suggests that time-varying and static magnetic fields in the environment might affect the cardiovascular system. To explore the underlying physiology, the effect of static magnetic fields (SMFs) on the carotid baroreflex control of microcirculation was studied. Twenty-four hemodynamic monitorings were performed in rabbits sedated by pentobarbital infusion (5 mg/kg/h) during experiments that lasted 120 min. Mean femoral artery blood pressure, heart rate, and ear lobe skin microcirculatory blood flow, measured by microphotoelectric plethysmogram (MPPG), were simultaneously recorded before and after a 40 min exposure of the sinocarotid baroreceptors to Nd₂–Fe₁₄–B alloy magnets (n = 14) or sham magnets (n = 10, control series). The local SMF field was 350 mT, at the baroreceptors’ site. Arterial baroreflex sensitivity (BRS) was estimated from heart rate/blood pressure response to intravenous bolus injections of nitroprusside and phenylephrine. A significant positive correlation was found between the SMF-induced increase in BRS (ΔBRS = BRS_afterSMF − BRS_priorSMF) and the increment in microvascular blood flow (ΔMPPG = MPPG_afterSMF − MPPG_priorSMF) (r = 0.66, p < 0.009). The SMF probably modulated the arterial baroreflex-mediated microcirculatory control. This could represent one possible mechanism how environmental magnetic fields act on the cardiovascular system, and a method how to complexly adjust macro- and microcirculation with potential clinical implementation.