We have seen that while traversing the heart loop, the blood stream undergoes not only a complete reversal in direction of flow but, as it passes through the spongy endomyocardial trabeculations, also encounters a mechanical hindrance (Chap. 2). Additionally, the blood flow is subject to rhythmical interruption by the contracting heart, giving rise to upsurge and dissipation of pressure. Taken together, the morphologic and hemodynamic phenomena suggest that the heart, rather than being the source of flow, is an organ whose function is rhythmical generation of pressure. Of the total power produced by the ventricle, about 75% is expended on maintaining the pressure, and the balance is used for pulsatile distension of the arterial bed. This ratio appears to be tightly controlled and is preserved during perturbations of flow and volume [1]. In addition to promoting the endothelial cell division, the pulsatile flow at an increased mean pressure in the arterial loop of the circuit is the essential factor in normal development of organs and vascular beds. We have further seen that, at the early stage, the simple tube heart can do little more than interrupt the flow of blood, creating only minimal pressures. Essential components for generation of pressure appear to be the “priming” and the “pressure” chambers, i.e., the atrium and the ventricle of the primary myocardium , which convert the kinetic energy of the moving blood into hydraulic energy or pressure. The combination of flow-generated shear forces and genetic factors gives rise to the secondary myocardium, which, with its valves and septa, is better “equipped” to perform the pressure-generating function. Several studies have shown that any interference on the part of this essential task is met with an acute hemodynamic compensatory response and is followed, in due course, by structural remodeling.

Clark and colleagues studied the effect of increased functional load in HH stage 21 chick embryo hearts by constricting the conotruncus with a nylon loop. The embryos were incubated and evaluated at stage 24, 27, and 29 of successive development. Compared to normal controls, the artificially imposed obstruction to ventricular ejection caused increased peak ventricular systolic pressures by an average of 68% at stage 24. There was no change in cardiac output. The authors further noted a time-related increase in ventricular weight due to hyperplasia of the myocytes, however, without an increase in the total weight of the embryo [2].

Lucitti et al. measured hemodynamic response in stage 21, 24, and 29 chick embryos by left atrial ligation (LAL). Simultaneous dorsal aortic blood flow and pressure measurements were performed at 1 h, 14 h (stage 25), and 30 h (stage 29) after ligation and compared to sham-operated controls. In addition, the steady and the oscillatory hydraulic power were calculated from the hemodynamic data. One hour after ligation, the systolic, mean, and diastolic pressures remained similar to controls and increased appropriately with the developmental stage. Minute aortic flow (CO) and stroke volume (SV) initially dropped to about half, but recovered to control values by stage 29. The acute drop in flow-related parameters is brought about by the reduction of the effective chamber size to half its normal volume, thus reducing the total cross-sectional area available to flowing blood. By stage 29 significant remodeling of the existing chamber had occurred, thus allowing for normalization of flow-related parameters [3].

In a separate group of embryos (stage 21), Lucitti and coworkers ligated the left vitelline artery (VAL) and performed hemodynamic measurements, as was done in the left atrial ligation (LAL) group. Of note is the fact that at this stage, roughly 75% of cardiac output passes through the vitelline arteries and only a quarter (25%) through the embryo’s aortae [4]. Obstruction of the vitelline artery thus represents a significant increase in impedance to the embryo heart. One hour after ligation, there was an acute decline in stroke volume and aortic flow to about half of the control values; however, all pressure parameters remained similar to control values. By stage 29, stroke volumes and aortic flow remained reduced by an average of 23% and 70%, respectively. Of further significance is the fact that in both groups (LAL and VAL), the oscillatory and mean power parameters dropped significantly post-ligation, but were normalized by stage 29 [3] (Fig. 9.1). The authors concluded that the maintenance of arterial pressure, but not arterial flow, is crucial to embryo survival. Regardless of the acute compensatory changes brought about by atrial or vitelline artery ligation, the investigators maintain, “it is evident that rapid restoration of arterial pressure is a primary directive of the embryonic vascular system” [3].

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