Abstract

Low temperature directly alters cardiovascular physiology in freshwater turtles, causing bradycardia, arterial hypotension, and a reduction in systemic blood pressure. At the same time, blood viscosity and systemic resistance increase, as does sensitivity to cardiac preload (e.g., via the Frank-Starling response). However, the long-term effects of these seasonal responses on the cardiovascular system are unclear. We acclimated red-eared slider turtles to a control temperature (25°C) or to chronic cold (5°C). To differentiate the direct effects of temperature from a cold-induced remodeling response, all measurements were conducted at the control temperature (25°C). In anesthetized turtles, cold acclimation reduced systemic resistance by 1.8-fold and increased systemic blood flow by 1.4-fold, resulting in a 2.3-fold higher right to left (R-L; net systemic) cardiac shunt flow and a 1.8-fold greater shunt fraction. Following a volume load by bolus injection of saline (calculated to increase stroke volume by 5-fold, ∼2.2% of total blood volume), systemic resistance was reduced while pulmonary blood flow and systemic pressure increased. An increased systemic blood flow meant the R-L cardiac shunt was further pronounced. In the isolated ventricle, passive stiffness was increased following cold acclimation with 4.2-fold greater collagen deposition in the myocardium. Histological sections of the major outflow arteries revealed a 1.4-fold higher elastin content in cold-acclimated animals. These results suggest that cold acclimation alters cardiac shunting patterns with an increased R-L shunt flow, achieved through reducing systemic resistance and increasing systemic blood flow. Furthermore, our data suggests that cold-induced cardiac remodeling may reduce the stress of high cardiac preload by increasing compliance of the vasculature and decreasing compliance of the ventricle. Together, these responses could compensate for reduced systolic function at low temperatures in the slider turtle.

Highlights

  • REDUCTIONS IN AMBIENT TEMPERATURE have direct (i.e., Q10; the rate of change over 10°C) and immediate effects on the ectotherm heart and cardiovascular system

  • We found that Qsys. Net cardiac shunt flow (Qshunt) patterns were altered following cold acclimation, with a right to left (R-L; net systemic) Qshunt achieved by reducing Rsys and, increasing Qsys

  • As there was no effect of temperature acclimation on total cardiac output (Qtotal; Fig. 2C), pulmonary flow (Qpul; Fig. 2D) or systemic pressure (Psys; Fig. 2E), both groups had a right to left (R-L; net systemic) cardiac shunt (Qshunt; Fig. 2F)

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Summary

Introduction

REDUCTIONS IN AMBIENT TEMPERATURE have direct (i.e., Q10; the rate of change over 10°C) and immediate effects on the ectotherm heart and cardiovascular system. Cardiac stroke volume (VStot) is maintained at low temperatures, partly by reduced end-systolic volume and increased diastolic filling due to changes in vascular resistance, and the sensitivity of the turtle heart to cardiac preload is increased [15, 27] These temperature-induced responses and the direct effect of temperature on blood viscosity may alter hemodynamic load on the heart [44, 56, 62]. We found that Qshunt patterns were altered following cold acclimation, with a right to left (R-L; net systemic) Qshunt achieved by reducing Rsys and, increasing Qsys It appears that cold-induced cardiovascular remodeling increases ventricular stiffness and systemic vasculature compliance, which reduces the stress of high blood volume load and may compensate for decreased systolic function at low temperatures

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