Changes in fibrinolytic activity in diving grey seals

In order to test the hypothesis that enhanced fibrinolytic activity is a factor which prevents the blood of diving seals from clotting, we instrumented two female grey seals (Halichoerus grypus) with subcutaneous electrodes for measurements of heart rate (HR) and an extradural intravertebral venous catheter for collection of blood samples before, during and after simulated dives of 10 min duration. Blood samples were used for in vitro determination of clot lysis time (CLT), which is a measure of the level of fibrinolytic activity, and for analyses of plasma levels of cortisol, noradrenaline and adrenaline (A). The seals displayed profound diving bradycardia indicative of a substantial reduction in blood flow rates (pre-dive HR: 78 (63–98) bpm; dive HR: 8 (7–10) bpm; (median (range); n=2)) and elevated catecholamine levels (pre-dive A: 121 (98–184) pg·ml⁻¹; peak dive/post-dive A: 3510 (447–6181) pg·ml⁻¹), both of which are factors which promote blood coagulation. Nevertheless, we found that CLT always increased in connection with diving (pre-dive CLT: 436 (356–568) min; peak CLT during diving: 1380 (640–1800) min), which implies a reduced, rather than enhanced, fibrinolytic activity in this situation. These results show that enhanced fibrinolytic activity is not part of the defence system which prevents fatal clotting from occurring in diving grey seals.     

The physiological responses of freshwater rainbow trout,Oncorhynchus mykiss,during acutely lethal copper exposure

Acutely lethal (24 h) exposure of adult rainbow trout (Oncorhynchus mykiss) to 4.9 mol copper·l^-1 in fresh water (pH 7.9, [Ca²⁺]0.8 mEq·l^-1) caused a rapid decline of plasma Na⁺ and Cl^- and arterial O₂ tension, and initially a pronounced tachycardia. The internal hypoxia probably resulted from histopathologies observed in the gills of fish exposed to copper, such as cell swelling, thickening and curling of the lamellae, and haematomas. Copper cannot therefore be considered purely as an ionoregulatory toxicant during acutely lethal conditions. Mortality during exposure to copper could not simply be explained by the plasma ionic dilution, nor by the internal hypoxia, since arterial O₂ content remained relatively unchanged. Secondary to the ionoregulatory and respiratory disturbances were a number of deleterious physiological responses which included a massive haemoconcentration (haematocrit values as high as 60%) and a doubling of the mean arterial blood pressure. The time-course of these changes suggest that cardiac failure was the final cause of death. In this respect copper exposure resembles low pH exposure in freshwater trout (Milligan and Wood 1982). Copper and H⁺ appear to be similar in both the primary site of their toxic action (the gills) and the secondary physiological consequences which result from acutely lethal exposures. Furthermore, the acute toxicity syndrome observed may be common to many metals which cause ionoregulatory and/or respiratory problems in freshwater fish.Abbreviations C _aO₂ arterial oxygen content - FR water flow rate - Hb haemoglobin - Hct haematocrit - H _m ⁺ net metabolic acid load - IU international unit - MABP mean arterial blood pressure - MCHC mean corpuscular haemoglobin content - MO₂ rate of oxygen consumption - P _aCO₂ arterial carbon dioxide tension - P _aO₂ arterial oxygen partial pressure - T _amm total ammonia (=NH₃+NH ₄ ⁺ ) - TCO₂ total carbon dioxide - TOC total organic carbon - %Hb–O₂ percentage of haemoglobin saturated with oxygen     

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     

Oxygen transport and cardiovascular responses in skipjack tuna (Katsuwonus pelamis) and yellowfin tuna (Thunnus albacares) exposed to acute hypoxia

Summary Responses to acute hypoxia were measured in skipjack tuna (Katsuwonus pelamis) and yellowfin tuna (Thunnus albacares) (1–3 kg body weight). Fish were prevented from making swimming movements by a spinal injection of lidocaine and were placed in front of a seawater delivery pipe to provide ram ventilation of the gills. Fish could set their own ventilation volumes by adjusting mouth gape. Heart rate, dorsal and ventral aortic blood pressures, and cardiac output were continuously monitored during normoxia (inhalant water (PO ₂>150 mmHg) and three levels of hypoxia (inhalant water PO ₂130, 90, and 50 mmHg). Water and blood samples were taken for oxygen measurements in fluids afferent and efferent to the gills. From these data, various measures of the effectiveness of oxygen transfer, and branchial and systemic vascular resistance were calculated. Despite high ventilation volumes (4–71·min^-1·kg^-1), tunas extract approximately 50% of the oxygen from the inhalant water, in part because high cardiac outputs (115–132 ml·min^-1·kg^-1) result in ventilation/perfusion conductance ratios (0.75–1.1) close to the theoretically ideal value of 1.0. Therefore, tunas have oxygen transfer factors (ml O₂·min^-1·mmHg^-1·kg^-1) that are 10–50 times greater than those of other fishes. The efficiency of oxygen transfer from water in tunas (65%) matches that measured in teleosts with ventilation volumes and order of magnitude lower. The high oxygen transfer factors of tunas are made possible, in part, by a large gill surface area; however, this appears to carry a considerable osmoregulatory cost as the metabolic rate of gills may account for up 70% of the total metabolism in spinally blocked (i.e., non-swimming) fish. During hypoxia, skipjack and yellowfin tunas show a decrease in heart rate and increase in ventilation volume, as do other teleosts. However, in tunas hypoxic bradycardia is not accompanied by equivalent increases, in stroke volume, and cardiac output falls as HR decreases. In both tuna species, oxygen consumption eventually must be maintained by drawing on substantial venous oxygen reserves. This occurs at a higher inhalant water PO₂ (between 130 and 90 mmHg) in skipjack tuna than in yellowfin tuna (between 90 and 50 mmHg). The need to draw on venous oxygen reserves would make it difficult to meet the oxygen demand of increasing swimming speed, which is a common response to hypoxia in both species. Because yellowfin tuna can maintain oxygen consumption at a seawater oxygen tension of 90 mmHg without drawing on venous oxygen reserves, they could probably survive for extended periods at this level of hypoxia.Abbreviations BP_da, BP_va dorsal, ventral aortic blood pressure - C _aO₂, C _vO₂ oxygen content of arterial, venous blood - DO₂ diffusion capacity - E_b, E_w effectiveness of O₂ uptake by blood, and from water, respectively - Hct hematocrit - HR heart rate - PCO₂ carbon dioxide tension - P _aCO₂, P _vCO₂ carbon dioxide tension of arterial and venous blood, respectively - PO₂ oxygen tension - P _aO₂, P _vO₂, P _iO₂, P _cO₂ oxygen tension of arterial blood, venous blood, and inspired and expired water, respectively - pHa, pHv pH of arterial and venous blood, respectively - P_w—b effective water to blood oxygen partial pressure difference - Pg partial pressure (tension) gradient - cardiac output - R vascular resistance - SV stroke volume - SEM standard error of mean - TO₂ transfer factor - U utilization - _g ventilation volume - O₂ oxygen consumption     

Seasonal changes in the oxygen storage capacity and aerobic dive limits of the muskrat (Ondatra zibethicus)

Summary The oxygen storage capacity and partitioning of body oxygen reserves were compared in summer-and winter-acclimatized muskrats (Ondatra zibethicus). Blood volume, blood oxygen capacity, and skeletal muscle myoglobin content were higher in December than in July (P<0.02). Total lung capacity increased only slightly in winter (P>0.05). The oxygen storage capacity of a diving muskrat was calculated at 25.2 ml O₂ STPD · kg^-1 in July, compared to 35.7 ml O₂ STPD · kg^-1 in December. Blood comprised the major storage compartment in both seasons, accounting for 57% and 65% of the total oxygen stores in summer and winter, respectively. Based on available oxygen stores and previous estimates of the cost of diving, the aerobic dive limit (ADL) increased from 40.9 s in July to 57.9 s in December. Concurrent behavioral studies suggested that most voluntary diving by muskrats is aerobic. However, the proportion of dives exceeding the calculated ADL of these animals was shown to vary with the context of the dive. Only 3.5% of all dives initiated by muskrats floating in the water exceeded their estimated ADL. Provision of a dry resting site and access to a submerged food source increased this proportion to 18–61%, depending on the underwater distance that foraging muskrats were required to swim. Serial dives exceeding the estimated ADL were not accompanied by extended postdive recovery periods.Abbreviations ADL acrobic dive limit - Hb hemoglobin - Hct hematocrit - Mb myoglobin - PaO₂ arterial O₂ tension - STPD standard temperature and pressure, dry     

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     

Gas exchange and blood gases of Puna teal (Anas versicolor puna) embryos in the Peruvian Andes

Oxygen consumption, air cell gases, hematology, blood gases and pH of Puna teal (Anas versicolor puna) embryos were measured at the altitude at which the eggs were laid (4150 m) in the Peruvian Andes. In contrast to the metabolic depression described by other studies on avian embryos incubated above 3700 m, O₂ consumption of Puna teal embryos was higher than even that of some lowland avian embryos at equivalent body masses. Air cell O₂ tensions dropped from about 80 toor in eggs with small embryos to about 45 toor in eggs containing a 14-g embryo; simultaneously air cell CO₂ tension rose from virtually negligible amounts to around 26 torr. Arterial and venous O₂ tensions (32–38 and 10–12 toor, respectively, in 12- to 14-g embryos) were lower than described previously in similarly-sized lowland wild avian embryos or chicken embryos incubated in shells with restricted gas exchange. The difference between air cell and arterial O₂ tensions dropped significantly during incubation to a minimum of 11 torr, the lowest value recorded in any avian egg. Blood pH (mean 7.49) did not vary significantly during incubation. Hemoglobin concentration and hematocrits rose steadily throughout incubation to 11.5 g · 100 ml^-1 and 39.9%, respectively, in 14-g embryos.Abbreviations PO₂ partial pressure gradient of O₂ - BM body mass - D diffusion coefficient - G gas conductance (cm³·s^-1·torr^-1) - conductance to water vapor - IP internal pipping of embryos - P _ACO₂ partial pressure of carbon dioxide in air cell - P _AO₂ partial pressure of oxygen in air cell - P _aCO₂ partial pressure of carbon dioxide in arterial blood - P _aCO₂ partial pressure of oxygen in arteries - P _H barometric pressure (torr) - PCO₂ partial pressure of carbon dioxide - P _IO₂ partial pressure in ambiant air - PO₂ partial pressure of oxygen - P _VCO₂ venous carbon dioxide partial pressure - P _VO₂ mixed venous oxygen partial pressure - SE standard error - VO ₂ oxygen consumption     

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     

Effect of ammonia on respiratory functions of blood of Tilapia zilli

The present paper attempts an examination of different changes of blood respiratory properties when Tilapia zilli is exposed to ammonia in three sublethal concentrations (1.1, 2.2 and 3.3 mg NH₃ l⁻¹) for 2 weeks. The results revealed that oxygen and carbon dioxide partial pressures (P_O2 and P_CO2) were changed differently and irregularly both in the caudal artery and in the heart. The acid–base status (pH, HCO⁻₃, TCO₂ and base excess) of arterial and venous blood changed towards alkalosis during the first week. These changes were exaggerated during the second week of ammonia exposure. O₂ saturation of arterial blood was decreased, while that of venous blood was increased due to the disturbances in blood gas transport and exchange mechanisms and in the acid–base status. The oxygen equilibrium curve was shifted to the left and P₅₀ was decreased during most of the experimental periods.     

Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers.

This study addressed the effects of apnea in air and apnea with face immersion in cold water (10 degrees C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial PO(2) and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.     

Response of heart rate and cloacal ventilation in the bimodally respiring freshwater turtle, Rheodytes leukops, to experimental changes in aquatic PO2

Changes in heart rate (f _H) and cloacal ventilation frequency (f _C) were investigated in the Fitzroy turtle, Rheodytes leukops, under normoxic (17.85 kPa) and hypoxic (3.79 kPa) conditions at 25°C. Given R. leukops’ high reliance on aquatic respiration via the cloacal bursae, the objective of this study was to examine the effect of varying aquatic PO₂ levels upon the expression of a bradycardia in a freely diving, bimodally respiring turtle. In normoxia, mean diving f _H and f _C for R. leukops remained constant with increasing submergence length, indicating that a bradycardia failed to develop during extended dives of up to 3 days. Alternatively, exposure to aquatic hypoxia resulted in the expression of a bradycardia as recorded by a decreasing mean diving f _H with increasing dive duration. The observed bradycardia is attributed to a hypoxic-induced metabolic depression, possibly facilitated by a concurrent decrease in f _C. Results suggest that R. leukops alters its strategy from aquatic O₂ extraction via cloacal respiration in normoxia to O₂ conservation when exposed to aquatic hypoxia for the purpose of extending dive duration. Upon surfacing, a significant tachycardia was observed for R. leukops regardless of aquatic PO₂, presumably functioning to rapidly equilibrate blood and tissue gas tensions with alveolar gas to reduce surfacing duration.     

Ventilatory accommodation of oxygen demand and respiratory water loss in a large bird,the emu (Dromaius novaehollandiae), and a re-examination of ventilatory allometry for birds

Ventilation was studied in the emu, a large flightless bird of mass 40kg, within the range of ambient temperatures from-5 to 45°C. Data for the emu and 21 other species were used to calculate allometric relationships for resting ventilatory parameters in birds (breath frequency=13.5 mass^-0.314; tidal volume=20.7 mass^1.0). At low ambient temperatures the ventilatory system must accommodate the increased metabolic demand for oxygen. In the emu this was achieved by a combination of increased tidal volume and increased oxygen extraction. Data from emus sitting and standing at-5°C, when metabolism is 1.5x and 2.6x basal metabolic rate, respectively, indicate that at least in the emu an increase in oxygen extraction can be stimulated by low temperature independent of oxygen demand. At higher ambient temperatures ventilation was increased to facilitate respiratory water loss. The emu achieved this by increased respiratory frequency. At moderate heat loads (30–35°C) tidal volume fell. This is usually interpreted as a mechanism whereby respiratory water loss can be increased without increasing parabronchial ventilation. At 45°C tidal volume increased; however, past studies have shown that CO₂ washout is minimal under these conditions. The mechanism whereby this is possible is discussed.Abbreviations BMR basal metabolic rate - BTPS body temperature, ambient pressure, saturated - EO ₂ oxygen extraction - EWL evaporative water loss - f _R ventilation frequency - RH relative humidity - RHL respiratory heat loss - SEM standard error of the mean - SNK student-Newman-Keuls multiple range test - STPD standard temperature and pressure, dry - T _a ambient temperatures(s) - T _b body temperature(s) - T _ex expired air temperature(s) - T _rh chamber excurrent air temperature - V _J ventilation - VO₂ oxygen consumption - V _T tidal volume - V/Q air ventilation to blood perfusion ratio     

Cardiovascular responses of semi-arboreal snakes to chronic,intermittent hypergravity

Cardiovascular functions were studied in semi-arboreal rat snakes (Elaphe obsoleta) following long-term, intermittent exposure to +1.5G _z (head-totail acceleration) on a centrifuge. Snakes were held in a nearly straight position within horizontal plastic tubes during periods of centrifugation. Centrifugal acceleration, therefore, subjected snakes to a linear force gradient with the maximal force being experienced at the tail. Compared to non-centrifuged controls,G _z-acceimated snakes showed greater increases of heart rate during head-up tilt or acceleration, greater sensitivity of arterial pressure to circulating catecholamines, higher blood levels of corticosterone, and higher blood ratios of prostaglandin F₂/prostaglandin E₂. Cardiovascular tolerance to increased gravity during gradedG _z acceleration was measured as the maximum (caudal) acceleration force at which carotid arterial blood flow became null. When such tolerances were adjusted for effects of body size and other continuous variables incorporated into an analysis of covariance, the difference between the adjusted mean values of control and acelimated snakes (2.37 and 2.84G _z, respectively) corresponded closely to the 0.5G difference between the acelimationG (1.5) and Earth gravity (1.0). As in other vertebrates, cardiovascular tolerance toG _z stress tended to be increased by acclimation, short body length, high arterial pressure, and comparatively large blood volume. Voluntary body movements were important for promoting carotid blood flow at the higher levels ofG _z stress.Abbreviations bpm heat beats per minute - FV fluid volume - G gravitational or acceleration force - G _z gravitational or acceleration force in the head-to-tail direction - Hct hematocrit - HIP hydrostatic indifferent point - PGE prostaglandin E₂ - PGF prostaglandin F_2a - PGFM stable metabolite of PGF - RCV red cell volume - RIA radioimmunoassay - SAS statistical analysis system - TBV total blood volume     

Circulation,metabolic rate,and body size in mammals

Summary This paper attempts to explain Kleiber's rule, which relates metabolic rate of mammals to their body mass, from the structure and function of the blood circulation system.Abbreviations a scaling factor - fractal dimension - hydrodynamic conductivity - l _n length of an arterial blood vessel at bifurcation level n - M body mass - N maximal number of bifurcation levels - p pressure - Q flow - r size of Bohr effect - r _n radius of an arterial blood vessel at bifurcation level n - V volume - VO ₂ rate of oxygen unloading - Z _n number of arterial blood vessels at bifurcation level n     

Differential responses to copper in rainbow trout (Oncorhynchus mykiss) acclimated to sea water and brackish water

Rainbow trout, Oncorhynchus mykiss, acclimated to 33% sea water (12 mg·ml^-1 salinity) experienced significant (10 meq·1^-1) increases in plasma [Na⁺] and [Cl^-] within 5 h of exposure to 6.3 mol copper·1^-1 indicating severe impairment of branchial ionoregulatory capacity. All plasma ion levels subsequently stabilised once the transbranchial [Na⁺] gradient was reduced to zero. The similar ionic strength of the external medium and their body fluids appeared to protect trout maintained in 33% sea water from further ionoregulatory stress and any secondary physiological disturbances during exposure to copper. Despite three- and fourfold greater transbranchial [Na⁺] and [Cl^-] gradients, trout acclimated to full-strength sea water (35 mg·ml^-1 salinity) suffered no major changes in plasma Na⁺, Cl^-, K⁺, or Ca²⁺, blood gases or haematology during 24 h exposure to 6.3 mol copper·1^-1. This reduction in toxicity in full strength sea water cannot be explained by differences in copper speciation. We suggest that during acute exposure to waterborne copper, active NaCl extrusion is unaffected due to the basolateral location of the gill Na⁺/K⁺-ATPase, but that ionoregulatory disturbances can occur due to gill permeability changes secondary to the displacement of surface-bound Ca²⁺. However, in full strength sea water the three-fold higher ambient [Ca²⁺] and [Mg²⁺] appear to be sufficient to prevent any detrimental permeability changes in the presence of 6.3 mol copper·1^-1. Plasma [NH ₊ ⁴ ] and [HCO _- ³ ] were both significantly elevated during exposure to copper, indicating that some aspects of gill ion transport (specifically the apical Na⁺/NH ₊ ⁴ and Cl^-/HCO _- ³ exchanges involved in acid/base regulation and nitrogenous waste excretion) are vulnerable to inhibition in the presence of waterborne copper.Abbreviations C _aO₂ arterial oxygen content - Hb haemoglobin - Hct haematocrit - MABP mean arterial blood pressure - MCHC mean cell haemoglobin content - MO₂ rate of oxygen consumption - P _a CO₂ arterial carbon dioxide tension - P _aO₂ arterial oxygen partial pressure - S salinity - SW sea water - T _Amm total ammonia (=NH₃+NH ₊ ⁴ ) - T _{CO 2} total carbon dioxide - TEP transepithelial potential - TOC total organic carbon - %Hb-O₂ percentage of haemoglobin saturated with oxygen     

Cardiovascular responses to electrical stimulation of the recurrent laryngeal nerve in conscious toads (Bufo marinus)

Summary Cardiovascular responses to electrical stimulation of the cut central end of the recurrent laryngeal nerve (rLN) were recorded in 19 conscious toads (Bufo marinus). Low intensity stimulation of the rLN (3.4±0.5 V, 1 ms, 10 Hz) elicited a slow 18–22% fall in heart rate and systolic and diastolic aortic arterial blood pressures (N=18), but had little or no effect upon ventilation (N=6). This low threshold depressor response (LTDR) was considered to represent the expression of the previously demonstrated pulmocutaneous baroreflex. Bilateral stimulation of the rLNs elicited greater LTDRs than did either left or right unilateral rLN stimulation. Blood pressure and heart rate responses to bilateral stimulation were 69–77% of the sum of responses to unilateral stimulation, and the mean summation was significant for the reduction in heart rate. Stimulus intensities of >4.7±0.7 V caused an immediate cessation of cardiac activity for up to 6.5±1.3 s (N=17) and a concomitant apnoea (N=6), which were followed by a lesser bradycardia and hypotension. This response was termed a high threshold depressor response (HTDR). During continued stimulation at intensities of >9.1±1.4 V, aortic blood pressure (Pa) and ventilation were rapidly restored, and aortic blood pressure continued to rise above control values (N=14). In some cases this high threshold pressor response (HTPR) was associated with an increase in heart rate. All responses to rLN stimulation were abolished by pithing (N=9) or by pentobarbital (40 mg/kg, i.p.,N=4), but LTDS and HTPRs could be elicited in urethanized (1.5–2.0 g/kg,N=4) toads.During depressor responses, aortic arterial resistance fell by 18% in 18 of 20 trials in 5 toads, whereas pulmocutaneous arterial resistance increased by 76% in 12 of 15 trials in 4 toads. During the HTPR, aortic arterial resistance increased 40%, while pulmocutaneous arterial resistance remained unchanged. We suggest that depressor responses may actively redistribute blood flow from the pulmocutaneous to the aortic circulation, whereas the reverse should occur during HTPRs.Abbreviations HTDR high threshold depressor response - HTPR high threshold pressor response - rLN recurrent laryngeal nerve - LTDR low threshold depressor response - Pa aortic blood pressure - PCA pulmocutaneous artery - Pd diastolic aortic pressure - Ppca pulmocutaneous blood pressure - PRU peripheral resistance unit - Ps systolic aortic pressure - Pv venous blood pressure - Ra aortic arterial resistance - Rpca pulmocutaneous arterial resistance     

Effects of serotonin on the cardio-circulatory system of the European eel (Anguilla anguilla) in vivo

The effects of serotonin on continuously recorded cardiac parameters (heart rate, cardiac output, cardiac stroke volume), ventral and dorsal aortic blood pressures, branchial and systemic vascular resistances were investigated in the European eel in vivo. Intravenous administration of serotonin (30 g · kg^–1) caused a marked bradycardia (45%) and a simultaneous decrease in cardiac output (50%), ventral (35%) and dorsal (50%) aortic blood pressures. Branchial resistance was markedly increased (60%) and systemic resistance decreased (30%). Cardiac stroke volume remained unchanged. The effects of serotonin on cardiac mained unchanged. The effects of serotonin on cardiac parameters were suppressed either by methysergide or a bilateral section of the cardiac vagus. Bradycardia could then be regarded as the consequence of a vagal mechanism triggered by serotonin action on central methysergide-sensitive serotonergic receptors. No inotropic effect of serotonin was observed. This lack of myocardiac contractility modification is discussed. The serotonin-mediated branchial vasoconstriction was attenuated by vagotomy, whereas the residual increase in branchial resistance (40%) was suppressed by methysergide. The serotonin-mediated branchial vasoconstriction could be the consequence of both a passive mechanism (compliance) caused by the decrease in cardiac output and an active mechanism involving methysergide-sensitive serotonergic receptors of the branchial vasculature. A possible involvement of this vasomotor effect in gill oxygen uptake is discussed. The serotonin-induced systemic vasodilation was insensitive either to cardiac vagotomy or to 5-HT_1/2, 5-HT₃ and 5-HT₄ receptor antagonists, suggesting the involvement of a local mechanism which remains to be assessed.Abbreviations CSV cardiac stroke volume - DAP dorsal aortic pressure - HR heart rate - QC cardiac output - VAP ventral aortic pressure - VR _b branchial vascular resistance - VR _s systemic vascular resistance - VR _t total vascular resistance - 5-HT 5-Hydroxytryptamine serotonin - RBI Research Biochemical Incorporated, metoclopramide HCl     

Evidence for multiple adrenoceptor sites in rainbow trout vasculature

The importance of neuronal and lumenal vascular adrenoceptors in the regulation of vascular reactivity was examined in rainbow trout (Oncorhynchus mykiss), in vivo and in vitro. In vivo, ganglionic blockade with hexamethonium or -adrenoceptor blockade, with either phentolamine or prazosin, produced similar (7 mmHg) decreases in dorsal aortic blood pressure. The drop in dorsal aortic pressure produced by phentolamine or prazosin was due to reduced systemic vascular resistance. Neither the -adrenoceptor antagonist, phenoxybenzamine nor chemical sympathectomy with 6-hydroxy-dopamine affected dorsal aortic pressure. However, after chemical sympathectomy, phenoxybenzamine lowered dorsal aortic pressure to levels similar to that produced by either phentolamine or prazosin. Plasma epinephrine and norepinephrine concentrations increased four- and twofold, respectively, in sympathectomized fish. Sympathectomy also produced a leftward shift in the epinephrine dose/response curve of the in vitro perfused splanchnic vasculature, placing the effective catecholamine concentration well within the in vivo plasma levels. These results indicate that following chemical sympathectomy arterial blood pressure is stabilized by circulating catecholamines through the combined effect of increased plasma catecholamine concentrations and increased sensitivity of vascular adrenoceptors. Phenoxybenzamine is incapable of blocking neuronal vascular adrenoceptors but is a potent antagonist of the up-regulated adrenoceptors, suggesting that the latter are localized on the lumenal side of the vessel.Abbreviations 6OH-DA 6-hydroxy dopamine - EC ₅₀ half-maximal response - EDTA ethylenediaminetetra-acetate - PE polyethylene - PBS phosphate-buffered saline - P _da dorsal aortic pressure - USP United States Pharmacopeia     

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial PaO2 = 38 mmHg), hypercapnia (PaCO2 = 72 mmHg), or hypoxic hypercapnia (PaO2 = 41; PaCO2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.     

Respiratory adaptations to diving in the nile monitor lizard,Varanus niloticus

Summary The objectives of this study included directin vivo measurements of circulating blood gases, pH, heart rate, and blood pressure during voluntary dives of unrestrained Nile monitor lizards. A Radiometer flow-through cuvette was employed for continuous recording of arterial PO₂, PCO₂ and pH. Hematological properties revealed no particular adaptations for diving. Mean values were: hematocrit = 24%; hemoglobin concentration = 7.1 g %; oxygen capacity = 9.3 vol %; red cell dimensions = 22×12 ; red cell count = 0.67 million/l. The respiratory properties of the blood, studiedin vitro andin vivo, show distinct adaptations to habitual diving. Oxygen affinity of blood is low (P₅₀ = 42.4 mm Hg at pH 7.45, 25 °) and the dissociation curve is markedly sigmoid (n = 3.1). These features, coupled with a Bohr factor ( logP ₅₀/pH) of –0.48, ensure increased utilization of oxygen while maintaining relatively high tissue PO₂. Arterial pH decreases during diving from about 7.5 to 7.1 due to combined respiratory and metabolic acidosis. High plasma bicarbonate (30 mM/l at PCO₂ = 25 mm Hg) and a buffering capacity of H C₃ ^–O/ pH = 18.9 mM/l increase the tolerance to this acidosis and prolong diving time. Thein vivo oxygen dissociation curve shows a 90 % depletion of arterial oxygen content during typical dives. Diving elicited a rapidly developing bradycardia with maximum of 85 % reduction in heart rate. The temperature sensitivity of HbO₂ binding was very low (H = –3kcal). This would minimize the HbO₂ affinity increase accompanying the decrease in body temperature likely to occur in lizards going from sun basking to submergence in water.Supported by a grant from the Danish Natural Science Research Council.