Effect of Angiotensin II on the Left Ventricular Function in a Near-Term Fetal Sheep with Metabolic Acidemia

Ganesh Acharya,Tiina Erkinaro,James C Huhta,Mervi Haapsamo,Ole-Jakob How,Juha Räsänen

doi:10.1155/2011/634240

Abstract

We tested the hypothesis that, in acute metabolic acidemia, the fetal left ventricle (LV) has the capacity to increase its contractility in response to angiotensin II infusion. Eleven ewes and their fetuses were instrumented at 127–138/145 days of gestation. The effect of angiotensin II on fetal LV function was assessed using intraventricular pressure catheter and tissue Doppler imaging (TDI). Angiotensin II increased fetal arterial blood pressure, whereas pH and pO2 decreased. The heart rate and systemic venous pressure were not affected significantly. The LV end-diastolic and end-systolic pressures, as well as dP/dtmax, increased. The TDI-derived LV longitudinal myocardial isovolumic contraction velocity and its acceleration and velocity during early filling were higher than those at baseline. The incidence of absent isovolumic relaxation velocity was greater during angiotensin II infusion. In summary, during acute metabolic acidemia, the fetal left ventricle could increase its contractility in response to inotropic stimulus even in the presence of increased afterload. The diastolic LV function parameters were altered by angiotensin II.

Highlights

Experimental studies have shown that sheep fetuses with increased placental vascular resistance and acute metabolic acidosis are able to maintain right and left ventricular (LV) cardiac outputs [1]
We tested the hypothesis that, in acute metabolic acidemia, the fetal left ventricle (LV) has the capacity to increase its contractility in response to angiotensin II infusion
The LV isovolumic myocardial acceleration demonstrated over a two-fold increase (P < 0.02) during angiotensin II infusion

Summary

Introduction

Experimental studies have shown that sheep fetuses with increased placental vascular resistance and acute metabolic acidosis are able to maintain right and left ventricular (LV) cardiac outputs [1]. They show signs of impaired myocardial contractility during the isovolumic contraction phase and impaired relaxation during the isovolumic and early diastolic filling phases of the cardiac cycle. It is evident that angiotensin II, in addition to its peripheral vasoconstrictive effect, has positive inotropic and chronotropic effects on the heart independent of arterial blood pressure [2]. Several pregnancy complications including placental insufficiency are associated with fetal

Methods

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Conclusion