Arterial hemodynamics and mechanical properties after circulatory intervention in the chick embryo

Abstract

Altered blood pressure and flow impact cardiac function during morphogenesis. How the arterial system supports cardiac morphogenesis after circulatory disruptions is not well characterized. We manipulated arterial flow via left atrial ligation (LAL) or arterial load via right vitelline artery ligation (VAL) in HamburgerHamilton (HH) stage 21 chick embryos. Embryos were reincubated for 1·h (HH21), 14·h (HH24) or 30·h (HH27). At each stage we measured simultaneous dorsal aortic blood pressure and flow, and calculated arterial compliance, impedance and hydraulic power. LAL acutely reduced stroke volume (VS), cardiac output (Q) and hydraulic power. Arterial pressure was preserved by a compensatory increase in characteristic impedance and decrease in compliance. Impedance parameters and compliance normalized by HH24 and all parameters normalized by HH27. VAL acutely increased arterial resistance. Embryos maintained arterial pressure by decreasing VS and Q. These parameters remained altered through HH27. In summary, despite the intervention, compensatory alterations in VS and arterial resistance maintained arterial pressure and fraction of oscillatory power within a narrow range. These results suggest that the maintenance of arterial pressure and circulatory energy efficiency, but not arterial flow, is critical to embryogenesis.

Impact of Hypoxia on Early Chick Embryo Growth and Cardiovascular Function

“…response to hypoxia noted in fetal and adult vertebrates and is consistent with published data in the early embryo (10,13,14,18,24,28,35,36). In contrast to the mid-and lategestation fetus, the early embryo does not compensate for impaired CV function by adjusting HR.…”

“…In the current study, we tested the hypothesis that hypoxia alters both embryonic ventricular and vascular function and growth in the early embryo during the critical period of early morphogenesis when changes in ventricular and arterial function can produce permanent structural and functional alterations (12,13,24,(27)(28)(29). In response to chronic hypoxia from the onset of incubation, we noted decreased ventricular systolic function, increased arterial impedance, reduced arterial blood flow, and reduced embryo growth and survival.…”

“…Input impedance spectra were generated as previously described (10,24). We defined total vascular resistance (TVR) as the impedance modulus at 0 Hz, (Z 1 ) as the impedance modulus at the first harmonic, characteristic impedance (Z C ) as the average of the impedance moduli from the third harmonic up to 10 Hz and peripheral impedance (Z P ) as the difference between TVR and Z C .…”

Dependence of Aortic Arch Morphogenesis on Intracardiac Blood Flow in the Left Atrial Ligated Chick Embryo

“…Furthermore, the aortic arches are part of a system which includes the entire embryo and vitelline vasculature. Even a small amount of vascular reactance to pulsatile flow will become significant when summed over such a large circulation (Lucitti et al, 2005). The dynamic component of the forces impeding blood flow must also be taken into account.…”

Computational hemodynamic optimization predicts dominant aortic arch selection is driven by embryonic outflow tract orientation in the chick embryo

“…Extensive studies using the chick embryo model have shown that epigenetic perturbations in blood flow can also lead to altered cardiovascular morphogenesis and congenital defects, implicating hemodynamics as a major environmental, epigenetic factor (deAlmeida et al 2007;Gessner 1966;Hogers et al 1999;Lucitti et al 2005;Reckova et al 2003;Sedmera et al 1999;Tobita et al 2005). This relationship has been validated for the global growth of the aortic arches by several studies, where changes in aortic arch perfusion by occlusion of a vitelline vein (Hogers et al 1999;Rychter and Lemez 1965), left atrial ligation (Hu et al 2009), manipulation of the outflow tract (Gessner 1966), or ligation of individual aortic arches (Rychter 1962) generated abnormal arch growth and defects in arch derivatives.…”