As for most ectothermic vertebrates, the breathing pattern of turtles is episodic, and pulmonary blood flow (Qpul) and heart rate (fH) normally increase several-fold during spontaneous ventilation. While some previous studies suggest that these cardiovascular changes are caused by stimulation of pulmonary stretch receptors (PSRs) during ventilation, it has been noted in other studies that blood flows often change prior to the initiation of breathing. Given the uncertainty regarding the role of PSRs in the regulation of central vascular blood flows, we examined the effect of manipulating lung volume (and therefore PSR stimulation) on blood flows and heart rate in the freshwater turtle Trachemys scripta. Turtles were instrumented with blood flow probes on the left aortic arch and the left pulmonary artery for measurements of blood flow, and catheters were inserted into both lungs for manipulation of lung volume. In both anaesthetized and fully recovered animals, reductions or increases in lung volume by withdrawal of lung gas or injection of air, N2, O2 or 10% CO2 (in room air) had no effect on blood flows. Furthermore, simulations of normal breathing bouts by withdrawal and injection of lung gas did not alter Qpul or fH. We conclude that stimulation of PSRs is not sufficient to elicit cardiovascular changes and that the large increase in Qpul and fH normally observed during spontaneous ventilation are probably caused by a simultaneous feedforward control of central origin.

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