Effect of changes in circulating blood volume on cardiac output and arterial and ventricular blood pressure in the stage 18, 24, and 29 chick embryo.

We studied the hemodynamic effects of changing volume loading in the chick embryo, before autonomic innervation, to test the hypothesis that the Frank-Starling mechanism functions in the embryonic myocardium. Dorsal aortic blood velocity was measured by pulsed Doppler. Heart rate and aortic diameter were also measured to calculate cardiac output and stroke volume index. Vitelline arterial and ventricular pressures were measured with a servo-null micropressure system in stage 24 embryos. Infusing isotonic solution intravenously resulted in linear increases in stroke volume index for stages 18 (y = 388x + 6.89), 24 (y = 466x + 7.86), and 29 (y = 549x + 4.96). The slopes and intercepts were statistically the same for all three stages. Similar volume loading in stage 24 embryos initially increased mean arterial pressure linearly, but at higher loading conditions, the rate of rise lessens. Thus, volume loading resulted in a decrease in vascular resistance. Withdrawing blood from stage 24 embryos resulted in a decrease in ventricular peak systolic and end-diastolic pressures. With reinfusion of the blood, systolic and end-diastolic pressures initially rose above baseline levels and later returned to normal. We conclude that a length-tension relation is present in the preinnervated embryonic heart and that vascular resistance changes inversely with loading conditions. We speculate that these mechanisms are the primary hemodynamic control mechanism in the early chick embryo.