Functional adaptations of the coronary microcirculation to anemia in fetal sheep

Abstract

Fetal anemia causes cardiac adaptations that have immediate and life-long repercussions on heart function and health. It is known that resting and maximal coronary conductance both increase during chronic fetal anemia, but the coronary microvascular changes responsible for the adaptive response are unknown. Until recently, technical limitations have prevented quantifying functional capillary-level adaptations in the in vivo fetal heart. Our objective was to characterize functional microvascular adaptations in chronically anemic fetal sheep. Chronically instrumented fetuses were randomized to a control group (n = 11) or were made anemic by isovolumetric hemorrhage (n = 12) for one week prior to myocardial contrast echocardiography at 85 % of gestation. Anemia augmented cardiac mass by 23 % without changing body weight. In anemic fetuses, microvascular blood flow per volume of myocardium was twice that of control fetuses at rest, during vasodilatory hyperemia, and during hyperemia plus increased aortic pressure. The elevated blood flow was attributable almost entirely to an increase in microvascular blood flux rate whereas microvascular blood volumes were not different between groups at baseline, during hyperemia, or with hyperemia plus increased aortic pressure. Increased coronary microvascular flux rate in response to chronic fetal anemia is consistent with expected reductions in capillary resistance from capillary diameter widening detected in earlier histological studies.

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