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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]

Systemic vascular resistance (Rsys) of freshwater turtles increases substantially during anoxia, but the underlying mechanisms are not fully understood. We investigated whether hydrogen sulfide (H2S), an endogenously produced metabolite believed to be an O2 sensor! transducer of vasomotor tone, contributes to the increased Rsys of anoxic red-eared slider turtles (Trachemys scripta). Vascular infusion of the H2S donor NaHS in anesthetized turtles at 21°C and fully recovered normoxic turtles at 5°C and 21°C revealed H2S to be a potent vasoconstrictor of the systemic circulation. Likewise, wire myography of isolated turtle mesenteric and pulmonary arteries demonstrated H2S to mediate an anoxia-induced constriction. Intriguingly, however, NaHS did not exert vasoconstrictory effects during anoxia (6 h at 21°C; 14 days at 5°C) when plasma H2S concentration, estimated from the colorimetric measurement of plasma acid-labile sulfide concentration, likely increased by ∼3- and 4-fold during anoxia at 2 1°C, and 5°C, respectively. Yet, blockade of endogenous H2S production by DL-propargylglycine or hydroxylamine (0.44 mmol/kg) partially reversed the decreased systemic conductance (Gsys) exhibited by 5°C anoxic turtles. These findings suggest that the signal transduction pathway of H2S-mediated vasoactivity is either maximally activated in the systemic circulation of anoxic turtles and/or that it is oxygen dependent. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) is rapidly emerging as a biologically significant signaling molecule. Studies published before 2000 report low or undetectable H2S (usually as total sulfide) levels in blood or plasma, whereas recent work has reported sulfide concentrations between 10 and 300 µM. suggesting it acts as a circulating signal. In the first series of experiments, we used a recently developed polarographic sensor to measure the baseline level of endogenous H2S gas and turnover of exogenous H2S gas in real time in blood from numerous animals, including lamprey, trout, mouse, rat, pig, and cow. We found that, contrary to recent reports, H2S gas was essentially undetectable (<100 nM total sulfide) in all animals. Furthermore, exogenous sulfide was rapidly removed from blood, plasma, or 5% bovine serum albumin in vitro and from intact trout in vivo. To determine if blood H2S could transiently increase, we measured oxygen-dependent H25 production by trout hearts in vitro and in vivo. H2S has been shown to mediate ischemic preconditioning (IPC) in mammals. IPC is present in trout and, unlike mammals, the trout myocardium obtains its oxygen from relatively hypoxic systemic venous blood. In vitro, myocardial H2S production was inversely related to Po2, whereas we failed to detect H2S in ventral aortic blood from either normoxic or hypoxic fish in vivo. These results provide an autocrine or paracrine mechanism for myocardial coupling of hypoxia to H2S in IPC, i.e., oxygen sensing, but they fail to provide any evidence that H2S signaling is mediated by the circulation. [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]

Abstract: Pulmonary ventilation requires energy, but the estimated costs of breathing in reptiles vary from 1 to 30% of resting metabolic rate. The low values have been estimated from changes in oxygen uptake during hypoxia or hypercapnia, but it remains possible that these treatments affected metabolism. We equipped alligators with masks for simultaneous measurements of ventilation and oxygen uptake during hypercapnia, hypoxia and bilateral vagotomy. Hypercapnia and hypoxia caused a marked increase in total ventilation, but oxygen uptake remained unchanged indicating a very low energetic cost of breathing. Upon vagotomy, breathing pattern changed to occasional and exceedingly deep breaths (76.1±11.1mlkg−1) followed by buccal oscillations and shallower breaths (22.2±2.3mlkg−1) interspersed between long non-ventilatory periods. This change in breathing pattern did not affect oxygen uptake. The duration of inspiration increased substantially upon vagotomy, so that inspiratory flow rate did not increase proportionally to tidal volume. These prolonged inspiratory times leads to less flow resistance and may explain that tidal volume could be increased substantially without a measurable energetic cost. [Copyright &y& Elsevier]

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]

We performed simultaneous measurements of ventilation, oxygen uptake and carbon dioxide production in the South American lizard, Tupinambis merianae, equipped with a mask and maintained at 25 °C. Ventilation of resting animals was stimulated by progressive exposure to hypercapnia (2, 4 and 6%) or hypoxia (15, 10, 8 and 6%) in inspired gas mixture. This was carried out in both fasting and digesting animals. The ventilatory response to hypercapnia and hypoxia were affected by digestive state, with a more vigorous ventilatory response in digesting animals compared to fasting animals. Hypoxia doubled total ventilation while hypercapnia led to a four-fold increase in total ventilation both accomplished through an increase in tidal volume. Oxygen uptake remained constant during all hypercapnic exposures while there was an increase during hypoxia. Cost of ventilation was estimated to be 17% during hypoxia but less than 1% during hypercapnia. Our data indicate that ventilation can be greatly elevated at a small energetic cost. [Copyright &y& Elsevier]

Abstract: Hydrogen sulfide (H2S), nitric oxide (NO) and nitrite (NO2 −) are formed in vivo and are of crucial importance in the tissue response to hypoxia, particularly in the cardiovascular system, where these signaling molecules are involved in a multitude of processes including the regulation of vascular tone, cellular metabolic function and cytoprotection. This report summarizes current advances on the mechanisms by which these signaling pathways act and may have evolved in animals with different tolerance to hypoxia, as presented and discussed during the scientific sessions of the annual meeting of the Society for Experimental Biology in 2011 in Glasgow. It also highlights the need and potential for a comparative approach of study and collaborative effort to identify potential link(s) between the signaling pathways involving NO, nitrite and H2S in the whole-body responses to hypoxia. [Copyright &y& Elsevier]