Myocardial blood flow and coronary reserve in chronically anemic fetal lambs

Chronic fetal anemia produces large compensatory increases in coronary bloo d flow in the near-term fetal lamb. To determine if increased coronary flow in anemic fetuses is associated with decreased coronary flow reserve or, a lternatively, an increase in coronary conductance, we measured maximal coro nary artery conductance during adenosine infusion before and during anemia. Isovolemic hemorrhage over 7 days reduced hematocrit from 30.6 +/- 2.7 to 15.8 +/- 2.4% (P < 0.02) and the oxygen content from 7.3 +/- 1.4 to 2.6 +/- 0.4 ml/dl (P < 0.001). Coronary blood flow increased from control (202 +/- 60) to 664 +/- 208 ml . min(-1). 100 g(-1) with adenosine to 726 +/- 169 m l . min(-1). 100 g(-1) during anemia and to 1,162 +/- 250 ml . min(-1). 100 g(-1) (left. ventricle) during anemia with adenosine infusion (all P < 0.0 01). Coronary conductance, determined during maximal vasodilation, was 18.2 +/- 7.7 before and 32.8 +/- 11.9 ml . min(-1). 100 g(-1). mmHg(-1) during anemia (P < 0.001). Coronary reserve, the difference between resting and ma ximal myocardial blood flow interpolated at 40 mmHg, was unchanged in contr ol and anemic fetuses (368 +/- 142 and 372 +/- 201 ml/min). Because hematoc rit affects viscosity, anemic fetuses were transfused with blood to acutely increase the hematocrit back to control, and conductance was remeasured. C oronary blood flow decreased 57.3 +/- 18.9% but was still 42.6 +/- 18.9% gr eater than control. We conclude that. in chronically anemic fetal sheep cor onary conductance is increased and coronary reserve is maintained, and this is attributed in part to angiogenesis as well as changes in viscosity.