Cerebral hemodynamics during microgravity.

As one of the causes of the space adaptation syndrome, an increased intracranial pressure due to the cephalad fluid shift is suggested. In the present study, we measured intracranial pressure (ICP), aortic pressure and cerebral flow velocity (CFV) in anesthetized rats (n=5) during 4.5 sec of microgravity induced by free drop. The rats were set at horizontal prone (Flat) and 30-degree head-up whole body tilting (HU) positions to examine the effect of gravitational pressure gradient. Then, arterial pressure at the eye level (APeye), cerebral perfusion pressure (CPP; CPP=APeye-ICP), and CPP-CFV relationship was calculated. In HU position, ICP, APeye, and CPP increased by 2.2 +/- 0.4, 12.3 +/- 2.0, and 10.1 +/- 1.7 mmHg respectively. However, CFV did not change significantly. In Flat position, none of these variables did not change significantly. In HU position the slope of CPP-CFV relationship decreased, suggesting the increased cerebral flow resistance. However, it did not change in Flat position. These results can be understood by the disappearance of gravitational pressure gradient by microgravity and the cerebral autoregulation.     

Acute and delayed vasoconstriction after subarachnoid hemorrhage: local cerebral blood flow, histopathology, and morphology in the rat basilar artery.

The decreased local cerebral blood flow (LCBF) and cerebral ischemia that occur after subarachnoid hemorrhage (SAH) may be caused by acute and/or delayed vasospasm. In 36 Sprague-Dawley (350-450 g) rats SAH was induced by transclival puncture of the basilar artery. Mean arterial blood pressure (MABP), LCBF, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were measured in all rats for 30 min before and 60 min after SAH was induced. One set of control (n : 7) and experimental animals (n : 7) was sacrificed after the 60 min of initial post-hemorrhage measurements were recorded. Four days after SAH induction, LCBF and MABP were measured again for 60 min in subgroups of surviving experimental rats (n : 7) and control rats (n : 7). Histopathologic and morphologic examinations of the basilar artery were performed in each subgroup. There was a sharp drop in LCBF just after SAH was induced (55.50 +/- 11.46 mlLD/min/100 g and 16.1 +/- 3.6 mlLD/min/100 g for baseline and post-SAH, respectively; p < 0.001). The flow then gradually increased but had not returned to pre-SAH values by 60 min (p < 0.05). At 4 days after SAH induction, although LCBF was lower than that observed in the control group and pre-SAH values, it was not significantly different from either of these flow rates (p > 0.05). ICP (baseline 7.05 +/- 0.4 mmHg) increased acutely to 75.2 +/- 7.1 mmHg, but returned to normal levels by 60 min after SAH. CPP (baseline 84.5 +/- 6.3 mmHg) dropped accordingly (to 18.6 +/- 3.1 mmHg), and then increased, reaching 72.2 +/- 4.9 mmHg at 60 min after SAH (p > 0.05). Examinations of the arteries revealed decreased inner luminal diameter and distortion of the elastica layer in the early stage. LCBF in nonsurviver rats (n : 8) was lower than that in the animals that survived (p < 0.01). At 4 days post-hemorrhage, the rats' basilar arteries showed marked vasculopathy. The findings showed that acute SAH alters LCBF, ICP, and CPP, and that decreased LCBF affects mortality rate. Subsequent vasculopathy occurs in delayed fashion, and this was observed at 4 days after the hemorrhage event.     

Mechanosensitive cardiac C-fiber response to changes in left ventricular filling, coronary perfusion pressure, hemorrhage, and volume expansion in rats

Left ventricular (LV) end-diastolic pressure (LVEDP) increase due to volume expansion (VExp) enhances mechanosensitive vagal cardiac afferent C-fiber activity (CNFA), thus decreasing renal sympathetic nerve activity (RSNA). Hypotensive hemorrhage (hHem) attenuates RSNA despite decreased LVEDP. We hypothesized that CNFA increases with any change in LVEDP. Coronary perfusion pressure (CPP), supposedly affected in both conditions, might also be a stimulus of CNFA. VExp and hHem were performed in anesthetized male Sprague-Dawley rats while blood pressure, heart rate, and RSNA were measured. Cervical vagotomy abolished RSNA response in both reflex responses. Single-unit CNFA was recorded while LVEDP was changed. Rapid changes (+/- 4, +/-6, +/-8 mmHg) were obtained by graded occlusion of the caval vein and descending aorta. Prolonged changes were obtained by VExp and hHem. Furthermore, CNFA was recorded in a modified Langendorff heart while CPP was changed (70, 100, 40 mmHg). Rapid LVEDP changes increased CNFA [caval vein occlusion: +16 +/- 3 Hz (approximately +602%); aortic occlusion: +15 +/- 3 Hz (approximately +553%); 70 units; P < 0.05]. VExp and hHem (n = 6) increased CNFA [VExp: +10 +/- 4 Hz (approximately +1,033%); hHem: +10 +/- 2 Hz (approximately +1,225%); P < 0.05]. An increase in CPP increased CNFA [+2 +/- 1 Hz (approximately +225%); P < 0.05], whereas a decrease in CPP decreased CNFA [-0.8 +/- 0.4 Hz (approximately -50%); P < 0.05]. All C fibers recorded originated from the LV. CNFA increased with any LVEDP change but changed equidirectionally with CPP. Thus neither LVEDP nor CPP fully accounts directly for afferent C-fiber and reflex sympathetic responses. The intrinsic afferent stimuli and receptive fields accounting for reflex sympathoinhibition still remain cryptic.     

Cerebral perfusion pressure in giraffe: modelling the effects of head-raising and -lowering

Loss of consciousness caused by positional changes of the head results from reduced cerebral blood flow (CBF). CBF is related to cerebral perfusion pressure (CPP). CPP is the difference between mean arterial pressure (MAP) at the head and intracranial pressure (ICP). The positional change of the giraffe head between ground level and standing upright is the largest of all animals yet loss of consciousness does not occur. We have investigated the possibility that an increase in CPP protects giraffe from fainting, using a mechanical model that functioned as an anatomical U-tube. It consisted of a rigid ascending “carotid” limb, a collapsible “brain” tube drained by a rigid, “vertebral venous plexus” (VVP) tube, and a collapsible “head” tube drained by a collapsible tube representing the “jugular vein”. The descending tubes could be rotated relative to the “carotid” tube to be horizontal, or at 30°, 45°, and 60° to the vertical to simulate changes in head position. Pressure at the top of the “carotid” tube was intracranial MAP, at the top of the “VVP” tube was ICP, and the difference CPP. In the simulated “head-up” position and a fluid flow rate of 4 L min⁻¹, CPP was ∼170 mmHg. With the VVP tube horizontal, CPP fell from ∼170 to 45 mmHg, but increased to ∼67 mmHg at 30° “down”, to ∼70 mmHg at 45° “down” and to ∼75 at 60° “down”. The fall in CPP in the head-down positions resulted from a decrease in viscous resistance in, and dissipation of pressure to, the “head” and “jugular” tubes. These data provide an estimate of cranial pressure changes in giraffe during positional changes of the head, and suggest that an increase in CPP plays a significant role in maintaining CBF during head-raising and that it may be an important mechanism for preventing fainting in giraffe.     

Butorphanol/xylazine/ketamine immobilization of free-ranging Baird's tapirs in Costa Rica

Cardiopulmonary effects and the utility of a butorphanol/xylazine/ketamine combination were evaluated during twenty immobilizations of sixteen Baird's tapirs (Tapirus bairdii) between March 1996 and January of 1998 in Corcovado National Park (Costa Rica). The animals were attracted to a bait site and darted from tree platforms. The tapirs were estimated to weigh between 200 to 300 kg. Actual weights of three tapirs taken at later dates fell within the estimated range. A butorphanol, 48+/-1.84 (x +/- SE) mg/animal IM, and xylazine, 101+/-2.72 mg/animal IM, combination was used to immobilize the animals. In some instances, ketamine was used either IM or IV at 187+/-40.86 mg/animal to prolong the immobilization period in addition to the butorphanol/xylazine combination. Naltrexone was used IM to reverse butorphanol at 257+/-16.19 mg/animal. Either yohimbine, 34+/-0.61 or tolazoline at 12+/-10.27 mg/animal, was used to reverse xylazine. The mean time from dart impact to first visible effect was 4.63+/-0.50 min (x +/- SE). Mean time to sternal recumbency was 12.21+/-1.08 min. Mean time the tapirs were immobilized was 45.63+/-3.6 min. Mean time to return to sternal recumbency and standing in animals that received yohimbine and naltrexone was 3.16+/-1.06 and 5.33+/-1.45 min, respectively. Mean time to return to sternal recumbency and standing in animals that received tolazoline and naltrexone was 1.57+/-0.39 and 3.14+/-0.51 min, respectively. Cardiopulmonary parameters including heart rate, respiratory rate, body temperature, electrocardiogram, percent oxygen satoration, and indirect blood pressure were recorded. Arterial blood gas analysis was performed on four animals. A mild degree of hypoxemia was evidenced by low arterial oxygen saturations. Five of 14 (36%) animals measured had oxygen saturations below 90%. Bradycardia (heart rates <45 BPM) was an expected finding in 11 (55%) immobilizations. Induction, recovery and muscle relaxation of each immobilization was graded. Premature arousal, which occurred in six (30%) animals, was the only problem associated with the immobilizations. Butorphanol/xylazine is a recommended protocol for immobilization of calm, free-ranging tapirs lasting less than 30 min. Supplemental intravenous administration of ketamine is recommended for longer procedures. Nasal insufflation of oxygen is recommended.     

Regional difference of blood flow in anesthetized rats during reduced gravity induced by parabolic flight.

To examine a hypothesis that change in regional blood flow due to decreased hydrostatic pressure gradient and redistribution of blood during reduced gravity (rG) is different between organs, changes in cerebrocortical blood flow (CBF) and blood flow in the temporal muscle (MBF) with exposure to rG were measured in anesthetized rats in head-up tilt and flat positions during parabolic flight. Carotid arterial pressure (CAP), jugular venous pressure (JVP), and abdominal aortic pressure were also measured simultaneously. In the head-up tilt group, CBF increased by 15 +/- 3% within 3 s of entry into rG and rapidly recovered during rG. MBF also increased, but the change was significantly greater than that of CBF. JVP increased by 1.8 +/- 0.5 mmHg, probably due to loss of hydrostatic pressure gradient, since the measuring point of JVP was 2-3 cm above the hydrostatic indifference point. CAP and abdominal aortic pressure increased by 16.7 +/- 2 and 7.7 +/- 2 mmHg, respectively, compared with the 1-G condition. Muscle vascular resistance [(CAP-JVP)/MBF] decreased on entry into rG, but no significant change was observed in cerebrocortical vascular resistance [(CAP-JVP)/CBF]. In the flat group, no significant change was observed in all the variables. The results indicate that arteriolar vasodilatation occurs in the temporal muscle but not in the cerebral cortex. Thus the blood flow control mechanism at the onset of rG is different between intra- and extracranial organs.     

Human urotensin II increases coronary perfusion pressure in the isolated rat heart: potentiation by nitric oxide synthase and cyclooxygenase inhibition.

Urotensin II (U-II) is a cyclic peptide, recently cloned in man and present in cardiac tissue and arteries. The effects of human U-II (hU-II) on coronary perfusion pressure (CPP) were investigated in isolated rat hearts perfused retrogradely via the aorta at constant flow. hU-II produced a concentration-dependent increase in CPP (pEC50 8.6 +/- 0.3, n = 8), the maximum increase in CPP (12 +/- 4 mmHg) was obtained at 10(-7) M hU-II. At higher concentrations of hU-II CPP fell back towards baseline. Endothelin-1 produced a maximum increase in CPP of 63 +/- 11 mmHg within the concentration-range studied. Addition of the NO synthase inhibitor L N(G)nitro-arginine methyl ester (10(-4) M) and the cyclooxygenase inhibitor, indomethacin (10(-5) M) to the perfusion solution had no effect on the pEC50 value for hU-II, but significantly increased the maximum constriction (to 34 +/- 7 mmHg, n = 8, p < 0.05) and inhibited the later dilator response to hU-II. These results suggest that receptors for hU-II are present in the coronary vasculature and that smooth muscle contraction is modulated by the release of dilator factors, including NO and prostacyclin. Endothelial function is therefore likely to be of primary importance in modulating the coronary vasoconstrictor effects of hU-II in vivo.     

Leg intravenous pressure during head-up tilt

Leg vascular resistance is calculated as the arterial-venous pressure gradient divided by blood flow. During orthostatic challenges it is assumed that the hydrostatic pressure contributes equally to leg arterial, as well as to leg venous pressure. Because of venous valves, one may question whether, during orthostatic challenges, a continuous hydrostatic column is formed and if leg venous pressure is equal to the hydrostatic pressure. The purpose of this study was, therefore, to measure intravenous pressure in the great saphenous vein of 12 healthy individuals during 30 degrees and 70 degrees head-up tilt and compare this with the calculated hydrostatic pressure. The height difference between the heart and the right medial malleolus level represented the hydrostatic column. The results demonstrate that there were no differences between the measured intravenous pressure and the calculated hydrostatic pressure during 30 degrees (47.2 +/- 1.0 and 46.9 +/- 1.5 mmHg, respectively) and 70 degrees head-up tilt (83.9 +/- 0.9 and 85.1 +/- 1.2 mmHg, respectively). Steady-state levels of intravenous pressure were reached after 95 +/- 12 s during 30 degrees and 161 +/- 15 s during 70 degrees head-up tilt. In conclusion, the measured leg venous pressure is similar to the calculated hydrostatic pressure during orthostatic challenges. Therefore, the assumption that hydrostatic pressure contributes equally to leg arterial as well as to leg venous pressure during orthostatic challenges can be made.     

ACTH does not mediate divergent stress responsiveness in rainbow trout.

Two lines of rainbow trout selected for high (HR) and low (LR) responsiveness to a standardised confinement stressor displayed a sustained divergence in plasma cortisol levels during a 3-h period of confinement (max.: HR: 167+/-13 ng ml(-1); LR: 103+/-8 ng ml(-1); P<0.001). However, no significant difference in plasma ACTH levels was evident (max: HR: 153+/-9 pg ml(-1); LR: 142+/-7 pg ml(-1)). Dexamethasone (DEX) was administered to HR and LR fish to block endogenous adrenocorticotropin (ACTH) release. Administration of a weight-adjusted dose of ACTH to the DEX-blocked fish elevated plasma cortisol levels to a significantly greater extent in HR (233+/-24 ng ml(-1)) than LR (122+/-14 ng ml(-1)) fish (P<0.001). Plasma cortisol levels in DEX-blocked HR and LR fish after sham injection were low but also significantly different (HR: 6.7+/-1 ng ml(-1); LR: 2.2+/-0.2 ng ml(-1); P<0.001). These results indicate that modulation of cortisol responsiveness to stressors in HR and LR fish resides, at least in part, downstream of the hypothalamic-pituitary axis.     

N omega-nitro-L-arginine influences cerebral metabolism in awake sheep.

Cerebral vasodilation in hypoxia may involve endothelium-derived relaxing factor-nitric oxide (NO). An inhibitor of NO formation, N omega-nitro-L-arginine (LNA, 100 micrograms/kg i.v.), was given to conscious sheep (n = 6) during normoxia and again in hypocapnic hypoxia (arterial PO2 approximately 38 Torr). Blood samples were obtained from the aorta and sagittal sinus, and cerebral blood flow (CBF) was measured with 15-microns radiolabeled microspheres. During normoxia, LNA elevated (P < 0.05) mean arterial pressure from 82 +/- 3 to 88 +/- 2 (SE) mmHg and cerebral perfusion pressure (CPP) from 72 +/- 3 to 79 +/- 3 mmHg, CBF was unchanged, and cerebral lactate release (CLR) rose temporarily from 0.0 +/- 1.9 to 13.3 +/- 8.7 mumol.min-1 x 100 g-1 (P < 0.05). The glucose-O2 index declined (P < 0.05) from 1.67 +/- 0.16 to 1.03 +/- 0.4 mumol.min-1 x 100 g-1. Hypoxia increased CBF from 59.9 +/- 5.4 to 122.5 +/- 17.5 ml.min-1 x 100 g-1 and the glucose-O2 index from 1.75 +/- 0.43 to 2.49 +/- 0.52 mumol.min-1 x 100 g-1 and decreased brain CO2 output, brain respiratory quotient, and CPP (all P < 0.05), while cerebral O2 uptake, CLR, and CPP were unchanged. LNA given during hypoxia decreased CBF to 77.7 +/- 11.8 ml.min-1 x 100 g-1 and cerebral O2 uptake from 154 +/- 22 to 105.2 +/- 12.4 mumol.min-1 x 100 g-1 and further elevated mean arterial pressure to 98 +/- 2 mmHg (all P < 0.05), CLR was unchanged, and, surprisingly, brain CO2 output and respiratory quotient were reduced dramatically to negative values (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of exercise training on resting blood pressures of Dahl rats

To determine whether female Dahl salt-sensitive (SS) hypertensive rats would adapt to chronic treadmill exercise by exhibiting lower resting systolic blood pressures (RSBP), a 12-wk training program was undertaken. Female Dahl salt-resistant (SR) rats were also trained for the same time period a a similar intensity [40-70% maximal O2 consumption (VO2max)] and duration (55 min). Postexperimental treadmill run times and VO2max values [SR: nontrained (NT) 87 +/- 1, trained (T) 97 +/- 2; SS: NT 82 +/- 2, T 92 +/- 3 ml.min-1 X min-1 X kg-1] indicated that the prescribed program had produced a trained state. However, the training program caused no group differences between the SR or the SS and their nontrained controls in measurements associated with sodium chloride intake, fluid consumption, urine production, 24-h sodium excretion, plasma volumes, plasma insulin, or blood volumes. Chronic exercise did significantly lower RSBP in the SR subgroup after 6 wk (NT 123 +/- 4, T 110 +/- 3 mmHg) and 8 wk (NT 120 +/- 4, T 106 +/- 2 mmHg) and remained lower throughout the remaining weeks of the experiment. On the other hand, the RSBP results of the trained SS rats were significantly higher than the nontrained SS rats after 6 wk (NT 155 +/- 8, T 191 +/- 7 mmHg) and were never significantly different than the controls for the remainder of the study.(ABSTRACT TRUNCATED AT 250 WORDS)     

High dose Erythropoietin increases brain tissue oxygen tension in Severe Vasospasm after Subarachnoid Hemorrhage

ABSTRACT: BACKGROUND: Vasospasm-related delayed cerebral ischemia (DCI) significantly impacts on outcome after aneurysmal subarachnoid hemorrhage (SAH). Erythropoietin (EPO) may reduce the severity of cerebral vasospasm and improve outcome, however, underlying mechanisms are incompletely understood. In this study, the authors aimed to investigate the effect of EPO on cerebral metabolism and brain tissue oxygen tension (PbtO2). METHODS: Seven consecutive poor grade SAH patients with multimodal neuromonitoring (MM) received systemic EPO therapy (30.000 IU per day for 3 consecutive days) for severe cerebral vasospasm. Cerebral perfusion pressure (CPP), mean arterial blood pressure (MAP), intracranial pressure (ICP), PbtO2 and brain metabolic changes were analyzed during the next 24 hours after each dose given. Statistical analysis was performed with a mixed effects model. RESULTS: A total of 22 interventions were analyzed. Median age was 47 years (32-68) and 86% were female. Three patients (38%) developed DCI. MAP slightly decreased 2 hours after intervention (P<0.04) without significantly affecting CPP and ICP. PbtO2 significantly increased over time (P<0.05) to a maximum of 7+/-4mmHg increase 16 hours after infusion. Brain metabolic parameters did not change over time. CONCLUSIONS: EPO increases PbtO2 in poor grade SAH patients with severe cerebral vasospasm. The effect on outcome needs further investigation.     

Dynamic cerebral autoregulation is preserved during acute head-down tilt.

Complete ganglion blockade alters dynamic cerebral autoregulation, suggesting links between systemic autonomic traffic and regulation of cerebral blood flow velocity. We tested the hypothesis that acute head-down tilt, a physiological maneuver that decreases systemic sympathetic activity, would similarly disrupt normal dynamic cerebral autoregulation. We studied 10 healthy young subjects (5 men and 5 women; age 21 +/- 0.88 yr, height 169 +/- 3.1 cm, and weight 76 +/- 6.1 kg). ECG, beat-by-beat arterial pressure, respiratory rate, end-tidal CO2 concentration, and middle cerebral blood flow velocity were recorded continuously while subjects breathed to a metronome. We recorded data during 5-min periods and averaged responses from three Valsalva maneuvers with subjects in both the supine and -10 degrees head-down tilt positions (randomized). Controlled-breathing data were analyzed in the frequency domain with power spectral analysis. The magnitude of input-output relations were determined with cross-spectral techniques. Head-down tilt significantly reduced Valsalva phase IV systolic pressure overshoot from 36 +/- 4.0 (supine position) to 25 +/- 4.0 mmHg (head down) (P = 0.03). Systolic arterial pressure spectral power at the low frequency decreased from 5.7 +/- 1.6 (supine) to 4.4 +/- 1.6 mmHg2 (head down) (P = 0.02), and mean arterial pressure spectral power at the low frequency decreased from 3.3 +/- 0.79 (supine) to 2.0 +/- 0.38 mmHg2 (head down) (P = 0.05). Head-down tilt did not affect cerebral blood flow velocity or the transfer function magnitude and phase angle between arterial pressure and cerebral blood flow velocity. Our results show that in healthy humans, mild physiological manipulation of autonomic activity with acute head-down tilt has no effect on the ability of the cerebral vasculature to regulate flow velocity.     

Night-time behavior of stabled and pastured peri-parturient ponies

Pregnant and lactating pony mares were observed in two environments, stable and pasture. Twenty-six pony mares were observed on pasture for 2 weeks before and after parturition. The behavior of each mare was recorded every 30 min from 18.00 to 06.00 h. The mutually exclusive behaviors were standing (either standing alert or standing at rest with a hindlimb flexed), grazing (prehending or masticating grass), walking, lying in sternal recumbency and lying in lateral recumbency. The total time-budget for prepartum mares on pasture was 55.3 ± 4.1% grazing, 32.9 ± 3.3% standing, 6.0 ± 1.5% lying in sternal recumbency, 2.7 ± 0.7% walking and 1.4 ± 0.6% lying in lateral recumbency. Grazing and standing occurred at all times, but grazing was most common from 18.00 to 21.00 h and after 05.00 h. Lying was most common between 01.00 and 04.00. Lying in lateral recumbency occurred only after dark, in pre-partum mares. The total time-budget for post-partum mares on pasture was 68.6 ± 4.0% grazing, 22.5 ± 3.0% standing, 4.7 ± 1.0% walking, 4.2 ± 1.2% lying in sternal recumbency and 0.2 ± 0.2% lying in lateral recumbency. Lying in lateral recumbency was seen only at 18.00 h. Lying in sternal recumbency occurred between 21.00 and 04.30 h. More time was spent grazing by the post-partum mares than by the pre-partum mares.The same behaviors were recorded for stabled pony mares except that eating hay rather than grazing constituted the ingestive behavior quantified. The total time-budget for pregnant stabled ponies was 71 ± 3% standing, 15 ± 3% eating, 0.5 ± 0% lying in lateral recumbency, 0.5 ± 0.2% walking and 12.1 ± 2.3% lying in sternal recumbency. Eating decreased and standing increased during the night. Most lying was seen between 01.30 and 05.00 h. Lying in lateral recumbency occurred between 19.30 and 03.30 h. The total nocturnal time-budget of post-partum stalled ponies was 67 ± 3% eating, 19 ± 3% standing and 13.0 ± 2.3% lying in sternal recumbency. Post-partum mares were not observed to walk or to lie in lateral recumbency.The change in behavior after parturition may reflect: (1) nutritional demands of lactation; (2) maternal protective behavior; (3) response to seasonal changes in the environment.     

Equine sweating responses to submaximal exercise during 21 days of heat acclimation.

This study examined sweating responses in six exercise-trained horses during 21 consecutive days (4 h/day) of exposure to, and daily exercise in, hot humid conditions (32-34 degrees C, 80-85% relative humidity). On days 0, 3, 7, 14, and 21, horses completed a standardized exercise test on a treadmill (6 degrees incline) at a speed eliciting 50% of maximal O(2) uptake until a pulmonary artery temperature of 41.5 degrees C was attained. Sweat was collected at rest, every 5 min during exercise, and during 1 h of standing recovery for measurement of ion composition (Na(+), K(+), and Cl(-)) and sweating rate (SR). There was no change in the mean time to reach a pulmonary artery temperature of 41.5 degrees C (range 19.09 +/- 1.41 min on day 0 to 20.92 +/- 1.98 min on day 3). Peak SR during exercise (ml. m(-2). min(-1)) increased on day 7 (57.5 +/- 5. 0) but was not different on day 21 (48.0 +/- 4.7) compared with day 0 (52.0 +/- 3.4). Heat acclimation resulted in a 17% decline in SR during recovery and decreases in body mass and sweat fluid losses during the standardized exercise test of 25 and 22%, respectively, by day 21. By day 21, there was also a 10% decrease in mean sweat Na(+) concentration for a given SR during exercise and recovery; this contributed to an approximately 26% decrease in calculated total sweat ion losses (3,112 +/- 114 mmol on day 0 vs. 2,295 +/- 107 mmol on day 21). By day 21, there was a decrease in sweating threshold ( approximately 1 degrees C) but no change in sweat sensitivity. It is concluded that horses responded to 21 days of acclimation to, and exercise in, hot humid conditions with a reduction in sweat ion losses attributed to decreases in sweat Na(+) concentration and SR during recovery.     

Carotid artery pulse wave time characteristics to quantify ventriculoarterial responses to orthostatic challenge.

Central blood pressure waveforms contain specific features related to cardiac and arterial function. We investigated posture-related changes in ventriculoarterial hemodynamics by means of carotid artery (CA) pulse wave analysis. ECG, brachial cuff pressure, and common CA diameter waveforms (by M-mode ultrasound) were obtained in 21 healthy volunteers (19-30 yr of age, 10 men and 11 women) in supine and sitting positions. Pulse wave analysis was based on a timing extraction algorithm that automatically detects acceleration maxima in the second derivative of the CA pulse waveform. The algorithm enabled determination of isovolumic contraction period (ICP) and ejection period (EP): ICP=43+/-8 (SD) ms (4-ms precision), and EP=302+/-16 (SD) ms (5-ms precision). Compared with the supine position, in the sitting position diastolic blood pressure (DBP) increased by 7+/-4 mmHg (P<0.001) and R-R interval decreased by 49+/-82 ms (P=0.013), reflecting normal baroreflex response, whereas EP decreased to 267+/-19 ms (P<0.001). Shortening of EP was significantly correlated to earlier arrival of the lower body peripheral reflection wave (r2=0.46, P<0.001). ICP increased by 7+/-7 ms (P<0.001), the ICP-to-EP ratio increased from 14+/-3% (supine) to 19+/-3% (P<0.001) and the DBP-to-ICP ratio decreased by 7% (P=0.023). These results suggest that orthostasis decreases left ventricular output as a result of arterial wave reflections and, presumably, reduced cardiac preload. We conclude that CA ultrasound and pulse wave analysis enable noninvasive quantification of ventriculoarterial responses to changes in posture.     

Pleural pressure as a function of body position in rabbits

Pleural pressure was measured at end expiration in spontaneously breathing anesthetized rabbits. A liquid-filled capsule was implanted into a rib to measure pleural liquid pressure with minimal distortion of the pleural space. Capsule position relative to lung height was measured from thoracic radiographs. Measurements were made when the rabbits were in the prone, supine, right lateral, and left lateral positions. Average lung heights in the prone and supine positions were 4.21 +/- 0.58 and 4.42 +/- 0.51 (SD) cm, respectively (n = 7). Pleural pressure was -2.60 +/- 1.87 (SD) cmH2O at 50.2 +/- 7.75% lung height in the prone position and -3.10 +/- 1.22 cmH2O at 51.4 +/- 6.75% lung height in the supine position. There was no difference between the values recorded in the prone and supine positions. Placement of the capsule into the right or left chest had no effect on the magnitude of the pleural pressure recorded in rabbits in right and left lateral recumbency (n = 12). Measurements over the nondependent lung were repeatable when rabbits were turned between the right and left lateral positions. Lung height in laterally recumbent rabbits averaged 4.55 +/- 0.52 (SD) cm.     

In vivo evidence for endothelin-1-mediated attenuation of alpha1-adrenergic stimulation

Experiments were designed to determine the influence of endothelin A (ET(A)) receptors on the pressor response to acute environmental stress in Dahl salt-resistant (DR) and Dahl-sensitive (DS) rats. Mean arterial pressure (MAP) was chronically monitored by telemetry before and after treatment with the selective ET(A) receptor antagonist ABT-627. Rats were restrained and subjected to pulsatile air jet stress (3 min). In untreated animals, the total pressor response (area under the curve) to acute stress was not different between DR vs. DS rats (8.1 +/- 1.7 vs. 15.6 +/- 2.6 mmHg x 3 min, P = 0.10). Conversely, treatment with ABT-627 potentiated the total pressor response only in DR rats (36.3 +/- 6.2 vs. 22.6 +/- 5.9 mmHg x 3 min, DR vs. DS, P < 0.05). Treatment with ABT-627 allowed greater responses in anesthetized DR rats to exogenous phenylephrine (1-4 microg/kg) during ganglionic blockade (P < 0.05) and produced a significant increase in plasma norepinephrine at baseline and during stress in conscious DR rats compared with untreated animals (P < 0.05). ET(A) receptor blockade had no effect on these responses in DS rats. Our results suggest that endothelin-1 can inhibit alpha-adrenergic-mediated effects in DR, but not DS rats, consistent with the hypothesis that ET(A) receptor activation functions to reduce sympathetic nerve activity and responses in vascular smooth muscle to sympathetic stimulation.     

Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans

We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 +/- 1 mmHg, P < 0.05) and less during WI + NS (4 +/- 1 mmHg) and NS (3 +/- 1 mmHg). The decrease in heart rate (HR) by 13 +/- 1 beats/min (P < 0.05) and the increase in arterial pulse pressure (PP) by 17 +/- 4 mmHg (P < 0.05) during supine was more pronounced (P < 0.05) than during WI + NS (10 +/- 2 beats/min and 7 +/- 2 mmHg, respectively) and WI (8 +/- 2 beats/min and 6 +/- 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS (P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change.     

Acute hemodynamic responses in the head during microgravity induced by free drop in anesthetized rats

To examine acute hemodynamic responses to microgravity (microG) in the head, we measured carotid artery pressure (CAP) and jugular vein pressure (JVP) to calculate cephalic perfusion pressure (CPP = CAP - JVP) and recorded images of microvessels in the iris to evaluate capillary blood flow velocity (CBFV) and capillary diameter (CD) in anesthetized rats during 4.5 s of microG induced by free drop. Rats were placed in 30 degrees head-up whole body-tilted (HU, n = 7) or horizontal (flat, n = 6) position. In the flat group, none of the measured variables was significantly affected by microG, whereas in the HU group, CAP, JVP, and CPP increased, respectively, by 23.4 +/- 2.6, 1.3 +/- 0.2, and 22.9 +/- 3.1 mmHg, and CBFV and CD increased, respectively, by 33 +/- 8 and 9 +/- 3%, showing an increase in capillary blood flow. To further examine the mechanisms underlying these CAP and JVP increases, another experiment was performed in which CAP and JVP were measured in anesthetized rats (n = 6) during a postural change from HU to flat. In these animals, the change in JVP was similar to that observed during actual microG, but no change in CAP was seen, indicating that the JVP increase during actual microG is caused by disappearance of the gravitational pressure gradient in the head-to-foot axis, whereas the CAP increase is not. In conclusion, actual microG elicits an increase in CPP due to a greater increase in CAP than JVP, resulting in increased capillary blood flow. Although the increase in JVP is explained by the disappearance of gravitational pressure gradient in the head-to-foot axis as a result of microG, the larger increase in CAP is not.