AREGU July 46/1

Davis, Lowell E., A. Roger Hohimer, and Mark J. Morton. Myocardial blood flow and coronary reserve in chronically anemic fetal lambs. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R306–R313, 1999.— Chronic fetal anemia produces large compensatory increases in coronary blood flow in the near-term fetal lamb. To determine if increased coronary flow in anemic fetuses is associated with decreased coronary flow reserve or, alternatively, an increase in coronary conductance, we measured maximal coronary artery conductance during adenosine infusion before and during anemia. Isovolemic hemorrhage over 7 days reduced hematocrit from 30.6 6 2.7 to 15.8 6 2.4% (P , 0.02) and the oxygen content from 7.3 6 1.4 to 2.6 6 0.4 ml/dl (P , 0.001). Coronary blood flow increased from control (202 6 60) to 664 6 208 ml·min21 ·100 g21 with adenosine to 726 6 169 ml·min21 ·100 g21 during anemia and to 1,162 6 250 ml·min21 ·100 g21 (left ventricle) during anemia with adenosine infusion (all P , 0.001). Coronary conductance, determined during maximal vasodilation, was 18.2 6 7.7 before and 32.8 6 11.9 ml·min21 ·100 g21 ·mmHg21 during anemia (P , 0.001). Coronary reserve, the difference between resting and maximal myocardial blood flow interpolated at 40 mmHg, was unchanged in control and anemic fetuses (368 6 142 and 372 6 201 ml/min). Because hematocrit affects viscosity, anemic fetuses were transfused with blood to acutely increase the hematocrit back to control, and conductance was remeasured. Coronary blood flow decreased 57.3 6 18.9% but was still 42.6 6 18.9% greater than control. We conclude that in chronically anemic fetal sheep coronary conductance is increased and coronary reserve is maintained, and this is attributed in part to angiogenesis as well as changes in viscosity.