Nitric oxide and fetal coronary regulation.

The determinants of coronary flow in the heart were studied using the chronic near-term fetal sheep model. Coronary flows were measured using implanted Doppler probes on the fetal circumflex artery calibrated with radiolabelled microspheres. Experiments were conducted to calculate maximal coronary flow under conditions of systolic work, chronic, and acute hypoxemia. Pressure-flow conductance curves were also constructed during adenosine administration. These studied showed that maximal right ventricular systolic work increases flow from a resting level of some 200 mL x min(-1) x 100 g(-1) to only about 60% of the maximal coronary flow under chemical vasodilation with adenosine (800 mL x min(-1) x 100 g(-1)). Chronic hypoxemia leads to a resting flow of some 800 mL x min(-1) x 100 g(-1) but with a remaining reserve of some 400 mL x min(-1) x 100 g(-1). Nitric oxide synthase blockade with N(ú)-nitro-L-arginine (L-NNA) depresses coronary flow at all levels of oxygen content and depresses myocardial oxygen consumption even under normoxemic conditions. Fetal coronary flow increases dramatically during severe acute hypoxemia and may exceed the maximal levels found during adenosine administration without a loss of ventricular function. However, in the presence of L-NNA and severe hypoxemia, coronary flow does not exceed flows found during adenosine administration.