Effect of Heart Rate Increase on Dorsal Aortic Flow before and after Volume Loading in the Stage 24 Chick Embryo

Abstract

ABSTRACT. In the stage 24 chick embryo, a paced increase in heart rate reduces stroke volume, presumably by rate-dependent decrease in passive filling. We hypothesized that rate-dependent stroke volume reduction could be abolished by volume loading. Dorsal aortic blood velocity was measured with a 20 mHz pulsed-Doppler meter from a 0.75-mm piezoelectric crystal (eight embryos), and atrioventricular velocity was simultaneously measured from the ventricular apex (six embryos). Sinus venosus pacing (stimuli of 1 ms duration and <4 mA) was performed at intrinsic rate ( P I ) and at 150% of intrinsic rate (P:150%I). Volume loading was performed during P:150%I by intravenous injection of 7.5 pL of chick Ringer's solution. Using atrioventricular velocity profile, stroke volume was divided into the proportion due to passive (E-phase) and active (Aphase) filling. Stroke volume was compared during P I , P:150%I, immediately (P:150%If) and 30 s after (P:150%IU) volume loading. Data (mean + SEM) were compared by ANOVA. During pacing, stroke volume (mm2/cycle) decreased but increased after volume loading (I, 0.43 2 0.03; P I , 0.37 k 0.03; P:150%1, 0.19 f 0.03; P:150%If, 0.24 + 0.05; P:150%1", 0.28 f 0.04 (p < 0.005).During P:150%I, E-phase filling disappeared and was not restored by volume loading, whereas, A-phase filling diminished but was restored by volume loading. In stage 24 chick embryos, rate-dependent stroke volume decrease is reversed by volume loading that restores stroke volume due to an increase in active filling but not passive filling. Thus, even at rapid heart rate, the embryonic ventricle responds to volume loading, indicating that the FrankStarling relationship functions during tachycardia in the embryonic heart. (Pediatr Res 26: 438-441,1989) Abbreviations I, intrinsic heart rate P:I, pacing at rate slightly faster than I P:150%I, pacing at 150% of I P:150% If, P:150%1 immediately after volume loading P:150%1", P:150%1 15-30s after volume loading I", P:150%1 after cessation of pacing Received December 28, 1988; accepted June 28, 1989 Heart rate change is integrally involved in cardiovascular development, but little is known regarding adaptation of the developing cardiovascular system to heart rate change. In the stage 24 chick embryo, a paced increase in heart rate resulted in decreased cardiac output and stroke volume, presumably by altering the passive phase of ventricular filling (1).Inasmuch as the Frank-Starling relationship has been shown to function in the developing chick embryo (2), we hypothesized that volume loading would augment cardiac output and stroke volume during pacing-induced tachycardia. We found that in the stage 24 chick embryo, volume loading reversed the pacinginduced reduction in cardiac output and stroke volume. MATERIALS AND METHODSFertile White Leghorn chicken eggs were incubated to Hamburger-Hamilton stage 24 (3). The embryo was exposed by opening the shell and its membranes. Blood flow velocity was measured with a 20 mHz pulsed-Doppler meter from a 0.75-mm piezoelectric cr...

Validating the Paradigm That Biomechanical Forces Regulate Embryonic Cardiovascular Morphogenesis and Are Fundamental in the Etiology of Congenital Heart Disease

“…Changes in embryo temperature showed that heart rate and cardiac output are temperature dependent and that peripheral resistance changed inversely to cardiac output [ 65 , 66 ]. Normal heart rate and normal AV conduction are required for optimal cardiac output [ 67 , 68 , 69 ], and SV changes in response to altered circulating blood volume [ 70 ]. A range of pharmacologic and metabolic treatments confirmed the impact of acute changes in myocardial contractility on embryonic CV function [ 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 ] and that the embryonic myocardial response to beta-adrenergic receptor stimulation was due to changes in peripheral vascular resistance rather than to changes in heart rate or contractility [ 80 ] prior to functional innervation [ 81 ].…”

“…Altered ventricular loading conditions have also been used to determine the relationship between mechanical load and the induction and maturation of the conducting fibers within the developing heart. Elegant pulse-chase, retroviral marking, optical mapping experiments documented the withdrawal of myocytes from proliferation at the tips of the embryonic ventricular trabeculae, forming the initial Purkinje fibers within the embryonic heart [ 192 , 193 , 194 ] with changes in myocardial activation patterns [ 30 , 68 , 195 , 196 ]. LAL also alters aortic arch morphogenesis [ 183 ] via changes in shear stress [ 164 ].…”

Biomechanics of early cardiac development

“…Cardiac rate can alternatively be quantified from arterial or ventricular pressure measurements (Hu and Clark, 1989; Hochel et al, 1998). A comparison of the cardiac rates in the literature (Benson et al, 1989; Hu and Clark, 1989; Keller et al, 1991; Cuneo et al, 1993; Keller et al, 1996; Ishiwata et al, 2003) reveals that at the same developmental stages, reported cardiac rates vary widely. These differences are most likely the result of different temperatures and the invasive nature of some of the techniques employed.…”

“…Increasing temperature leads to an increase in cardiac rate and a decrease in stroke volume (Cuneo et al, 1993; Phelan et al, 1995). Similarly, an increase in cardiac rate achieved by pacing also reduces stroke volume (Benson et al, 1989) (see Table 3). Injection of saline or plasma leads to a transient increase in preload (Keller et al, 1994) and a maintained, linear increase in stroke volume (Faber et al, 1974; Wagman et al, 1990) (see Table 3).…”

Cardiac Enlargement in the Chick Embryo Induced by Hypothermic Incubation Is Due to a Combination of Hyperplasia and Hypertrophy of Cardiomyocytes

“…Chick embryonic heart rate shows a nearly linear response to variations in temperature around the physiological optimum both in vitro and in vivo (Vostarek et al, 2014). Variations in the heart rate are compensated for by changes in the stroke volume in order to maintain cardiac output even in the embryonic heart using (although within rather narrow limits) the Frank-Starling relationship (Benson et al, 1989). A chronic decrease in the heart rate at lower temperatures leads to increased end-diastolic volume, which in general is compensated for by eccentric hypertrophy (Hutchins et al, 1978;Benes et al, 2011).…”