Effect of Heart Rate Increase on Dorsal Aortic Flow in the Stage 24 Chick Embryo

Abstract

ABSTRACT. We evaluated the effect of increased heart rate on cardiac output and stroke volume in the stage 24 chick embryo (day 4 of a 21-day incubation). Blood flow was measured with a 20 MHz pulsed-Doppler flowmeter. Heart rate was increased by pacing with square wave stimuli (1 ms duration, <4 mA). The sinus venosus was paced from bipolar Teflon-coated silver electrodes in eight embryos and the ventricular apex was paced in three embryos. The pacing rates were at the intrinsic heart rate (P:I); 125% of intrinsic heart rate (P:125%1); and 150% of intrinsic heart rate (P:150%1). Physiologic measurements during pacing were compared to those obtained at the control intrinsic rate (I). We also evaluated the velocity profile of atrioventricular inflow and conotruncal outflow at intrinsic rate and during sinus venosus and ventricular pacing. With sinus venosus pacing, mean dorsal aortic blood flow was similar at control (1.07 f 0.05 mm3/s) and P:I (1.06 2 0.06 mm3/s) (2 f SEM). However, at P:125%I and P:150%1, mean dorsal aortic blood flow decreased significantly (P:125%1,0.88 f 0.05 mm3/s; P:150%I, 0.67 f 0.07 mm3/s) (p < 0.05). Stroke volume per beat also decreased with increasing heart rates (I, 0.41 2 0.02 mm3; P:I, 0.39 2 0.02 mm3; P:125%I, 0.28 f 0.02 mm3; P:150%I, 0.18 f 0.02 mm3) (p < 0.05). With rapid sinus venosus pacing, the atrioventricular blood flow velocity profile showed a rate-dependent decrease in passive ventricular filling while active filling remained the same or increased slightly. Thus, rate-dependent passive ventricular filling may be one reason for relatively slow heart rates during early embryonic development. During ventricular pacing at the intrinsic heart rate, mean dorsal aortic blood flow decreased to near zero presumably secondary to loss of normal atrioventricular synchrony. We speculate that atrial or ventricular tachycardia would be lethal to an embryo. (Pediatr Res 22: 442-444,1987) The heart begins to function early in embryonic development. In the chick embryo, heart rate is 90 bpm at the onset of blood flow and gradually increases during development to 2 10 bpm at hatching.The mechanisms that control heart rate in the embryo are not well defined. At the early stages, the sinus node and specialized conduction system are not histologically identifiable nor is the heart innervated by the autonomic nervous system. Yet, a chick embryo's heart rate responds to environmental factors. The heart rate slows with hypothermia (1) and increases with hyperthermia I?\ 1L.hWe hypothesized that heart rate and cardiac output are directly related to the preinnervated embryonic circulation. However, we found that a paced increase in heart rate decreased cardiac output and stroke volume by compromising the passive phase of ventricular filling. METHODSFertile white Leghorn chick eggs were incubated to Hamburger-Hamilton stage 24 (3). The shell and its membranes were opened to expose the embryo. Blood flow velocity was measured with a 20 MHz pulsed-Doppler meter from a 750 piezoelectric crystal po...

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