Change of cardiac function, but not form, in postprandial pythons

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The ventricles of non-crocodilian reptiles are incompletely divided and provide an opportunity for mixing of oxygen-poor blood and oxygen-rich blood (intracardiac shunting). However, both cardiac morphology and in vivo shunting patterns exhibit considerable interspecific variation within reptiles. In the present study, we develop an in situ double-perfused heart approach to characterise the propensity and capacity for shunting in five reptile species: the turtle Trachemys scripta, the rock python Python sebae, the yellow anaconda Eunectes notaeus, the varanid lizard Varanus exanthematicus and the bearded dragon Pogona vitticeps. To simulate changes in vascular bed resistance, pulmonary and systemic afterloads were independently manipulated and changes in blood flow distribution amongst the central outflow tracts were monitored. As previously demonstrated in Burmese pythons, rock pythons and varanid lizards exhibited pronounced intraventricular flow separation. As pulmonary or systemic afterload was raised, flow in the respective circulation decreased. However, flow in the other circulation, where afterload was constant, remained stable. This correlates with the convergent evolution of intraventricular pressure separation and the large intraventricular muscular ridge, which compartmentalises the ventricle, in these species. Conversely, in the three other species, the pulmonary and systemic flows were strongly mutually dependent, such that the decrease in pulmonary flow in response to elevated pulmonary afterload resulted in redistribution of perfusate to the systemic circuit (and vice versa). Thus, in these species, the muscular ridge appeared labile and blood could readily transverse the intraventricular cava. We conclude that relatively minor structural differences between non-crocodilian reptiles result in the fundamental changes in cardiac function. Further, our study emphasises that functionally similar intracardiac flow separation evolved independently in lizards (varanids) and snakes ( pythons) from an ancestor endowed with the capacity for large intracardiac shunts.

Section: Mechanistic Considerationsmentioning

confidence: 99%

In situcardiac perfusion reveals interspecific variation of intraventricular flow separation in reptiles

Joyce

Axelsson

Altimiras

et al. 2016

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“…While the tachycardia stems from a combination of NANC (non-adrenergicnon-cholinergic) factors and a withdrawal of cholinergic tone (Enok et al, 2012;Skovgaard et al, 2009), the rise in V S remains more enigmatic. The postprandial increase of V S in pythons was originally ascribed to a rapid and extensive growth of the heart allowing for an elevated end-diastolic volume (Andersen et al, 2005;Secor and White, 2010), but a number of recent studies clearly demonstrate that heart mass does not increase during digestion (Hansen et al, 2013;Henriksen et al, 2014;Jensen et al, 2011;Slay et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Improved cardiac filling facilitates the postprandial elevation of stroke volume inPython regius

Enok

Leite

et al. 2016

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To accommodate the pronounced metabolic response to digestion, pythons increase heart rate and elevate stroke volume, where the latter has been ascribed to a massive and fast cardiac hypertrophy. However, numerous recent studies show that heart mass rarely increases, even upon ingestion of large meals, and we therefore explored the possibility that a rise in mean circulatory filling pressure (MCFP) serves to elevate venous pressure and cardiac filling during digestion. To this end, we measured blood flows and pressures in anaesthetized Python regius. The anaesthetized snakes exhibited the archetypal tachycardia as well as a rise in both venous pressure and MCFP that fully account for the approximate doubling of stroke volume. There was no rise in blood volume and the elevated MCFP must therefore stem from increased vascular tone, possibly by means of increased sympathetic tone on the veins. Furthermore, although both venous pressure and MCFP increased during volume loading, there was no evidence that postprandial hearts were endowed with an additional capacity to elevate stroke volume. In vitro measurements of force development of paced ventricular strips also failed to reveal signs of increased contractility, but the postprandial hearts had higher activities of cytochrome oxidase and pyruvate kinase, which probably serves to sustain the rise in cardiac work during digestion.

“…The correlation between the magnitudes of SDA and postprandial cardiac hypertrophy is not well understood (Jensen et al, 2011). Thus, while V · O 2 consistently increases following feeding, the postprandial cardiac hypertrophy is inconsistent.…”

Section: Introductionmentioning

confidence: 99%

“…The universality and stimulus of the postprandial cardiac hypertrophy, however, remain unclear as Jensen et al found no postprandial cardiac hypertrophy in Burmese or Ball pythons (Python regius) under a similar experimental protocol (Jensen et al, 2011). They argued, therefore, that postprandial cardiac hypertrophy should be considered a 'facultative' rather than 'obligatory' response to feeding (Jensen et al, 2011), and the lack of postprandial cardiac hypertrophy was recently reported in two additional studies (Hansen et al, 2013;Enok et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…The rise in stroke volume has been linked with a 40% increase in ventricular mass within 48 h of eating (Andersen et al, 2005) that Riquelme et al described as being 'physiological' in nature and triggered by humoral factors, including increased levels of circulating free fatty acids (Riquelme et al, 2011). The universality and stimulus of the postprandial cardiac hypertrophy, however, remain unclear as Jensen et al found no postprandial cardiac hypertrophy in Burmese or Ball pythons (Python regius) under a similar experimental protocol (Jensen et al, 2011). They argued, therefore, that postprandial cardiac hypertrophy should be considered a 'facultative' rather than 'obligatory' response to feeding (Jensen et al, 2011), and the lack of postprandial cardiac hypertrophy was recently reported in two additional studies (Hansen et al, 2013;Enok et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Reduction of blood oxygen levels enhances postprandial cardiac hypertrophy in Burmese python (Python molurus)

Slay

Enok

Hicks

et al. 2013

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Physiological cardiac hypertrophy is characterized by reversible enlargement of cardiomyocytes and changes in chamber architecture, which increase stroke volume and V · O2,max via augmented convective oxygen transport. Cardiac hypertrophy is known to occur in response to repeated elevations of O 2 demand and/or reduced O 2 supply in several species of vertebrate ectotherms, including postprandial Burmese pythons (Python bivittatus). Recent data suggest postprandial cardiac hypertrophy in P. bivittatus is a facultative rather than obligatory response to digestion, though the triggers of this response are unknown. Here, we hypothesized that an O 2 supply-demand mismatch stimulates postprandial cardiac enlargement in Burmese pythons. To test this hypothesis, we rendered animals anemic prior to feeding, essentially halving blood oxygen content during the postprandial period. Fed anemic animals had heart rates 126% higher than those of fasted controls, which, coupled with a 71% increase in mean arterial pressure, suggests fed anemic animals were experiencing significantly elevated cardiac work. We found significant cardiac hypertrophy in fed anemic animals, which exhibited ventricles 39% larger than those of fasted controls and 28% larger than in fed controls. These findings support our hypothesis that those animals with a greater magnitude of O 2 supply-demand mismatch exhibit the largest hearts. The 'low O 2 signal' stimulating postprandial cardiac hypertrophy is likely mediated by elevated ventricular wall stress associated with postprandial hemodynamics.