Abstract

We are studying control mechanisms in the embryonic cardiovascular system. We hypothesize that stroke volume increases directly with preload as the chick embryo develops from stage 18 (3 days) to 29 (6 days), a 16-fold increase in embryo weight. Mean dorsal aortic blood velocity (V) was measured with a 20 MHz pulsed-Doppler velocity meter; mean blood flow (Q) was calculated using V and aortic diameter. Q+HR equals stroke volume index. dV/dt was electronically derived. Peak stroke volume was measured in response to intravenous injection of increasing volumes of chick Ringer's solution. Volumes ranged from 6.8 to 157 μL per gram embryo wet weight, permitting comparison of the volume response at different stages. A minimum of 5 embryos were studied for each volume. Data were tested by ANOVA and regression analysis. Heart rate decreased less than 6% for all stages. Stroke volume changed less than 3% in controls. With volume infusion maximum peak stroke volume increased 29% for stage 18, 83% for stage 24, and 46% for stage 29. Stroke volume increased linearly in all stages with slopes of 3.9 at stage 18, 4.7 at stage 24, and 5.5 at stage 29. dV/dt increased with volume infusion for all 3 stages. Although there is considerable change in embryo and ventricular weight, heart geometric shape, and myofibril myocyte volume and alignment, the relationship between preload and stroke volume is similar at each stage. We conclude that the Frank-Starling mechanism functions over a broad range of development in the preinnervated embryonic heart.

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