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To determine the costs of pulmonary ventilation without imposing severe oxygen limitations or acidosis that normally accompany exposures to hypoxia or hypercapnia, we opted to pharmacologically stimulate ventilation with doxapram (5 and 10 mg kg-1) in alligators. Doxapram is used clinically to alleviate ventilatory depression in response to anaesthesia and acts primarily on the peripheral oxygen-sensitive chemoreceptors. Using this approach, we investigated the hypothesis that pulmonary ventilation is relatively modest in comparison to resting metabolic rate in crocodilians and equipped seven juvenile alligators with masks for concurrent determination of ventilation and oxygen uptake. Doxapram elicited a dose-dependent and up to fourfold rise in ventilation, primarily by increasing ventilatory frequency. The accompanying rise in oxygen uptake was very small; ventilation in resting animals constitutes no more than 5% of resting metabolic rate. The conclusion that pulmonary ventilation is energetically cheap is consistent with earlier studies on alligators where ventilation was stimulated by hypoxia or hypercapnia. [ABSTRACT FROM AUTHOR]

Turtles of the genus Trachemys show a remarkable ability to survive prolonged anoxia. This is achieved by a strong metabolic depression, redistribution of blood flow and high levels of antioxidant defence. To understand whether nitric oxide (NO), a major regulator of vasodilatation and oxygen consumption, may be involved in the adaptive response of Trachemys to anoxia, we measured NO metabolites (nitrite, S-nitroso, Fe-nitrosyl and N-nitroso compounds) in the plasma and red blood cells of venous and arterial blood of Trachemys scripta turtles during normoxia and after anoxia (3 h) and reoxygenation (30 min) at 21 °C, while monitoring blood oxygen content and circulatory parameters. Anoxia caused complete blood oxygen depletion, decrease in heart rate and arterial pressure, and increase in venous pressure, which may enhance heart filling and improve cardiac contractility. Nitrite was present at high, micromolar levels in normoxic blood, as in some other anoxia-tolerant species, without significant arterial-venous differences. Normoxic levels of erythrocyte S-nitroso compounds were within the range found for other vertebrates, despite very high measured thiol content. Fe-nitrosyl and /V-nitroso compounds were present at high micromolar levels under normoxia and increased further after anoxia and reoxygenation, suggesting NO generation from nitrite catalysed by deoxygenated haemoglobin, which in turtle had a higher nitrite reductase activity than in hypoxia-intolerant species. Taken together, these data indicate constitutively high circulating levels of NO metabolites and significant increases in blood NO after anoxia and reoxygenation that may contribute to the complex physiological response in the extreme anoxia tolerance of Trachemys turtles. [ABSTRACT FROM AUTHOR]

Hypoxic pulmonary vasoconstriction (HPV) is an adaptive response that diverts pulmonary blood flow from poorly ventilated and hypoxic areas of the lung to better ventilated parts, matching blood perfusion to ventilation. HPV is an ancient and highly conserved response expressed in the respiratory organs of all vertebrates. However, the underlying mechanism and the role of the endothelium remain elusive. Isolated intrapulmonary arteries (internal diameter <346 µm) from the American alligator Alligator mississippiensis were mounted in microvascular myographs for isometric tension recording. Resting vessels and vessels contracted with either serotonin (5-HT) or endothelin-1 (ET-1) were exposed to sustained (45 mm) hypoxia (PO2<5 mmHg). In ET-1- contracted vessels, hypoxia induced a monophasic, sustained and fully reversible constriction, which was independent of the endothelium. In relaxed or in 5-HT-contracted vessels, hypoxia did not cause constriction. The effects of ET-1, ETA and ETB as well as the general ET-receptor antagonist were studied. ET-1 caused a contraction of the pulmonary arteries through stimulation of ETA-receptors. ETA and ETB immunoreactive staining revealed the location of both receptors in the smooth muscle layer and of ETB receptors in the endothelium. In conclusion, because precontraction with serotonin did not facilitate HPV, the required precontraction in alligators seems specific to ET-1, which implies that ET-1 plays an important permissive role for the HPV response In alligators. [ABSTRACT FROM AUTHOR]

Synbranchus marmoratus is a facultative air-breathing fish, which uses its buccal cavity as well as its gills for air-breathing. S. marmoratus shows a very pronounced tachycardia when it surfaces to air-breathe. An elevation of heart rate decreases cardiac filling time and therefore may cause a decline in stroke volume (Vs), but this can be compensated for by an increase in venous tone to maintain stroke volume. Thus, the study on S. marmoratus was undertaken to investigate how stroke volume and venous function are affected during air-breathing. To this end we measured cardiac output (a), heart rate (fH), central venous blood pressure (PCV), mean circulatory filling pressure (MCFP), and dorsal aortic blood pressures (PDA) in S. marmoratus. Measurements were performed in aerated water (PO2>130 mmHg), when the fish alternated between gill ventilation and prolonged periods of apnoeas, as well as during hypoxia (PO2⩽50 mmHg), when the fish changed from gill ventilation to air-breathing. Q increased significantly (luring gill ventilation compared to apnoea in aerated water through a significant increase in both fH and Vs. PCV and MCFP also increased significantly. During hypoxia, when the animals surface to ventilate air, we found a marked rise in fH, PCV, MCFP, Q and VS, whereas FDA decreased significantly. Simultaneous increases in PCV and MCFP in aerated, as well as in hypoxic water, suggests that the venous system plays an important regulatory role for cardiac filling and Vs in this species. In addition, we investigated adrenergic regulation of the venous system through bolus infusions of adrenergic agonists (adrenaline, phenylephrine and isoproterenol; 2 µg kg-1). Adrenaline and phenylephrine caused a marked rise in FCV and MCFP, whereas isoproterenol led to a marked decrease in FCV, and tended to decrease MCFP. Thus, it is evident that stimulation of both α- and β-adrenoreceptors affects venous tone in S. marmoratus. [ABSTRACT FROM AUTHOR]

The effects of endothelin-1 (ET-1) on systemic and pulmonary circulation were investigated in anaesthetised freshwater turtles (Trachemys scripta) instrumented with arterial catheters and blood flow probes. Bolus intra-arterial injections of ET-1 (0.4–400 pmol kg-1) caused a dose-dependent systemic vasodilatation that was associated with a decrease in systemic pressure (Psys) and a rise in systemic blood flow (Qsys), causing systemic conductance (Gsys) to increase. ET-1 had no significant effects on the pulmonary vasculature, heart rate (fH) or total stroke volume (VStot). This response differs markedly from mammals, where ET-1 causes an initial vasodilatation that is followed by a pronounced pressor response. In mammals, the initial dilatation is caused by stimulation of ETB-receptors, while the subsequent constriction is mediated by ETA-receptors. In the turtles, infusion of the ETB-receptor agonist BQ-3020 (150 pmol kg-1) elicited haemodynamic changes that were similar to those of ET-1, and the effects of ET-1 were not affected by the ETA-antagonist BQ-610 (0.15 μmol kg-1). Conversely, all effects of ET-1 were virtually abolished after specific ETB-receptor blockade with the ETB-antagonist BQ-788 (0.15 μmol kg-1). The subsequent treatment with the general ET-receptor antagonist tezosentan (15.4 μmol kg-1) did not produce effects that differed from the treatment with ETB-antagonist, and the blockade of ET-1 responses persisted. This present study indicates, therefore, that ETB-receptors are responsible for the majority of the cardiovascular responses to ET-1 in Trachemys. [ABSTRACT FROM AUTHOR]

The effects of adrenergic stimulation on mean circulatory filling pressure (MCFP), central venous pressure (PCV) and stroke volume (Vs), as well as the effects of altered MCFP through changes of blood volume were investigated in rattlesnakes (Crotalus durissus). MCFP is an estimate of the upstream pressure driving blood towards the heart and is determined by blood volume and the activity of the smooth muscle cells in the veins (venous tone). MCFP can be determined as the plateau in PCV during a total occlusion of blood flow from the heart. VS decreased significantly when MCFP was lowered by reducing blood volume in anaesthetised snakes, whereas increased MCFP through infusion of blood (up to 3 ml kg-1) only led to a small rise in Vs. Thus, it seems that end-diastolic volume is not affected by an elevated MCFP in rattlesnakes. To investigate adrenergic regulation on venous tone, adrenaline as well as phenylephrine and isoproterenol (α- and β-adrenergic agonists, respectively) were infused as bolus injections (2 and 10 μg kg-1). Adrenaline and phenylephrine caused large increases in MCFP and PCV, whereas isoproterenol decreased both parameters. This was also the case in fully recovered snakes. Therefore, adrenaline affects venous tone through both α- and β-adrenergic receptors, but the α-adrenergic receptor dominates at the dosages used in the present study. Injection of the nitric oxide donor SNP caused a significant decrease in PCV and MCFP. Thus, nitric oxide seems to affect venous tone. [ABSTRACT FROM AUTHOR]