Maximal myocardial blood flow is enhanced by chronic hypoxemia in late gestation fetal sheep

The measurement of maximal myocardial blood flow gives information about the total cross-sectional area of the coronary resistance vessels. During a continuous left atrial infusion of adenosine (60 μg · kg^-1 · min^-1), maximal myocardial blood flow was measured in 4 fetuses hypoxemic for a minimum of 5-8 days (pH = 7.33 ± 0.01, arterial PCO₂ = 49.8 ± 4.2 Torr, arterial PO₂ = 16.1 ± 1.3 Torr, and arterial concentration of O₂ = 5.3 ± 1.2 ml/dl). These data were compared with an identically instrumented group of normoxemic fetuses (n = 7) following the same study protocol (pH = 7.38 ± 0.02, arterial PCO₂ = 43.1 ± 3.8 Torr, arterial PO₂ = 19.8 ± 2.0 Torr, and arterial concentration of O₂ = 7.9 ± 1.0 ml/dl) (P < 0.05). At comparable arterial pressures, the maximal myocardial flow (ml · min^-1 · 100 g tissue^-1) for hypoxemic vs. normoxemic fetuses was 974 ± 273 and 630 ± 181 for the total myocardium, 986 ± 367 and 602 ± 192 for the left ventricular free wall, 1,025 ± 346 and 614 ± 178 for the septum, and 1,231 ± 274 and 757 ± 269 for the right ventricular free wall, respectively (P < 0.01). These data suggest that hypoxemia in the fetus can significantly alter the coronary vascular bed, which, if confirmed, would represent an important adaptation in the developing fetus.