Cardiorespiratory response to progressive hypoxia and hypercapnia in the turtle Trachemys scripta

The ventilatory responses of chelonian reptiles to hypoxic and hypercapnic stress have been fairly well described. As turtles are capable of large cardiac shunts, changes in pulmonary perfusion may be an equally viable and potent response to these stressors, To test this hypothesis, conscious unrestrained turtles were unidirectionally ventilated while blood flow in the left pulmonary artery ((Q) over dot(LPA)) and left aortic arch ((Q) over dot(LAo)) was monitored. Turtles were exposed to step changes (2.5 h step(-1)) in O-2 tension (30, 15, 5, 2.5 or 0 % O-2; CO2 inflow maintained constant) on day 1 followed by step changes in CO2 tension (0, 2, 4, 8 % CO2; O-2 inflow maintained constant) on day 2. Steady-state cardiorespiratory variables were recorded for the last 30 min of each step change in gas tension. Progressive hypoxia resulted in progressive increases in ventilation, (Q) over dot(LPA) and (Q) over dot(LAo) and a small, but non-significant, increase in heart rate. Progressive hypercapnia resulted in a progressive increase in ventilation, white (Q) over dot(LPA) and (Q) over dot(LAo) did not change at any level of CO2. These results suggest that information from the O-2-sensitive chemoreceptors appears to be stimulatory to both the cardiovascular and ventilatory control systems, while CO2 chemoreception appears to affect primarily the ventilatory control system. These results also suggest that, in animals capable of intracardiac shunting, increasing pulmonary perfusion may be an integral component of the reflex response to hypoxia.