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

Abstract

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.

Analysis of vascular mechanical properties from the yellow anaconda indicates increased elasticity and distensibility of the pulmonary artery during digestion

“…However, snakes typically experience visceral organ volume growth of severalfold during the postprandial period (Secor and Diamond, 1998;Beese, 2001, 2002) the heart being an exception (Hansen et al, 2013;Slay et al, 2014;Henriksen et al, 2015) followed by large increases in cardiac output through heart rate and stroke volume modulation (Secor et al, 2000;Secor and White, 2010;Zerbe et al, 2011;Enok et al, 2016). As we did not observe any change in the arterial composition, the increased distensibility of the pulmonary artery is probably due to a structural modification to accommodate this higher cardiac output, while the increased elasticity probably improves the Windkessel effect, thus providing a proper blood perfusion for the lungs during digestion.…”

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

“…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).…”

The use of echocardiography as a health assessment tool in green sea turtles (Chelonia mydas)

“…To maintain adequate cardiac output, an appropriate heart rate and stroke volume are required, and increases in heart size and rate have been documented to compensate for an experimentally induced oxygen supply–demand mismatch in reptiles 28 . This was not seen in this study as, although heart rate in reptiles is variable 10 and can be affected by a range of factors, including handling, 29 no significant difference in heart rate was observed between groups.…”