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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]

Pythons exhibit a doubling of heart rate when metabolism increases several times during digestion. Pythons, therefore, represent a promising model organism to study autonomic cardiovascular regulation during the postprandial state, and previous studies show that the postprandial tachycardia is governed by a release of vagal tone as well as a pronounced stimulation from nonadrenergic, noncholinergic (NANC) factors. Here we show that infusion of plasma from digesting donor pythons elicit a marked tachycardia in fasting snakes, demonstrating that the NANC factor resides in the blood. Injections of the gastrin and cholecystokinin receptor antagonist proglumide had no effect on double-blocked heart rate or blood pressure. Histamine has been recognized as a NANC factor in the early postprandial period in pythons, but the mechanism of its release has not been identified. Mast cells represent the largest repository of histamine in vertebrates, and it has been speculated that mast cells release histamine during digestion. Treatment with the mast cell stabilizer cromolyn significantly reduced postprandial heart rate in pythons compared with an untreated group but did not affect double-blocked heart rate. While this study indicates that histamine induces postprandial tachycardia in pythons, its release during digestion is not stimulated by gastrin or cholecystokinin nor is its release from mast cells a stimulant of postprandial tachycardia. [ABSTRACT FROM AUTHOR]

The intrinsic heart rate of most vertebrates studied, including humans, is elevated during digestion, suggesting that a nonadrenergic-noncholinergic factor contributes to the postprandial tachycardia. The regulating factor, however, remains elusive and difficult to identify. Pythons can ingest very large meals, and digestion is associated with a marked rise in metabolism that is sustained for several days. The metabolic rise causes more than a doubling of heart rate and a fourfold rise in cardiac output. This makes the python an interesting model to investigate the postprandial tachycardia. We measured blood pressure and heart rate in fasting Python regius, and at 24 and 48 h after ingestion of a meal amounting to 25% of body wt. Digestion caused heart rate to increase from 25 to 56 mm, whereas blood pressure was unchanged. The postprandial rise in heart rate was partially due to a doubling of intrinsic heart rate. The H2-antagonist did not affect heart rate of fasting snakes but decreased heart rate by 15-20 mm at 24 h into digestion, whereas it had no effects at 48 h. Thus, the histaminergic tone on the heart rose from none to 30% at 24 h but vanished after 48 h. In anesthetized snakes, histamine caused a systemic vasodilatation and a marked increase in heart rate and cardiac output mediated through a direct effect on H2- receptors. Our study strongly indicates that histamine regulates heart rate during the initial phase of digestion in pythons. This study describes a novel regulation of the vertebrate heart. [ABSTRACT FROM AUTHOR]

Abstract: The present study investigates adrenergic regulation of the systemic and pulmonary circulations of the anaesthetised South American rattlesnake, Crotalus durissus. Haemodynamic measurements were made following bolus injections of adrenaline and adrenergic antagonists administered through a systemic arterial catheter. Adrenaline caused a marked systemic vasoconstriction that was abolished by phentolamine, indicating this response was mediated through α-adrenergic receptors. Injection of phentolamine gave rise to a pronounced vasodilatation (systemic conductance (G sys) more than doubled), while injection of propranolol caused a systemic vasoconstriction, pointing to a potent α-adrenergic, and a weaker β-adrenergic tone in the systemic vasculature of Crotalus. Overall, the pulmonary vasculature was far less responsive to adrenergic stimulation than the systemic circulation. Adrenaline caused a small but non-significant pulmonary vasodilatation and there was tendency of reducing this dilatation after either phentolamine or propranolol. Injection of phentolamine increased pulmonary conductance (G pul), while injection of propranolol produced a small pulmonary constriction, indicating that α-adrenergic and β-adrenergic receptors contribute to a basal regulation of the pulmonary vasculature. Our results suggest adrenergic regulation of the systemic vasculature, rather than the pulmonary, may be an important factor in the development of intracardiac shunts. [Copyright &y& Elsevier]

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]

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]

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]

Incubation of heat-denatured plasma from the rattlesnake Crotalus atrox with trypsin generated a bradykinin (BK) that contained two amino acid substitutions (Arg¹ → Val and Ser6 → Thr) compared with mammalian BK. Bolus intra-arterial injections of synthetic rattlesnake BK (0.01-10 nmol/kg) into the anesthetized rattlesnake, Crotalus durissus terrificus, produced a pronounced and concentration-dependent increase in systemic vascular conductance (Gsys). This caused a fall in systemic arterial blood pressure (Psys) and an increase in blood flow. Heart rate and stroke volume also increased. This primary response was followed by a significant rise in Psys and pronounced tachycardia (secondary response). Pretreatment with NG-nitro-L-arginine methyl ester reduced the NK-induced systemic vasodilatation, indicating that the effect is mediated through increased NO synthesis. The tachycardia associated with the late primary and secondary response to BK was abolished with propranolol and the systemic vasodilatation produced in the primary phase was also significantly attenuated by pretreatment, indicating that the responses are caused, at least in part, by release of cathecholamines and subsequent stimulation of β-adrenergic receptors. In contrast, the pulmonary circulation was relatively unresponsive to BK. [ABSTRACT FROM AUTHOR]

Endothelin-1 (ET-1) is a very potent vasoactive peptide released from endothelial cells, and ET-1 plays an important role in the maintenance and regulation of blood pressure in mammals. ET-1 signaling is mediated by two receptors: ET A and ET B. In mammals, ET A receptors are located on vascular smooth muscle where they mediate vasoconstriction. ET B receptors located on the endothelium mediate vasodilatation through the release of nitric oxide, whereas stimulation of ET B receptors placed on vascular smooth muscle leads to vasoconstriction. Less is known about ET-1 signaling in reptiles. In anaesthetized alligators, ET-1 elicits a biphasic blood pressure with a long-lasting initial decrease followed by a smaller increase in systemic blood pressure. In anaesthetized freshwater turtles, ET-1 causes a dose-dependent systemic vasodilatation mediated through ET B receptors. In the present study, we investigated the cardiovascular effects of ET-1 on the systemic and pulmonary vasculature of pythons. The presence of ET A and ET B receptors in the vasculature of pythons was verified by means of immunoblotting. Myography on isolated vessels revealed a dose-dependent vasoconstrictory response to ET-1 in both mesenteric and pulmonary arteries. Pressure measurements in recovered specimens revealed an ET-1-induced rise in systemic blood pressure supporting our in vitro findings. In conclusion, our study shows that ET-1 induces a strong pressor effect in the systemic circulation. [ABSTRACT FROM AUTHOR]