This study investigated the role of nitric oxide (NO) in the control of right coronary (RC) blood flow at rest and during acute pulmonary hypertension. Experiments were performed in seven chronically instrumented, conscious dogs. NO synthesis was inhibited by systemic administration of Nω-nitro-L-arginine (LNA, 35 mg/kg). Inflation of a balloon in the main pulmonary artery raised right ventricular (RV) peak systolic pressure from 34 ± 2 to 47 ± 3 mmHg before LNA and from 37 ± 2 to 47 ± 3 mmHg after LNA, but did not affect mean systemic arterial pressure. RV O2 consumption (MVO2) increased from 4.4 ± 0.7 to 6.1 ± 0.7 ml/min/100 g. 82% of the elevated RV MVO2 was provided by RC blood flow, which increased from 46 ± 7 to 61 ± 8 ml/min/100 g. After LNA, resting RV MVO2 and RC flow fell. RC venous PO2 fell, but RV lactate uptake was not altered. During pulmonary hypertension, the increase in RC blood flow was blunted by LNA, so that only 66% of the elevated RV MVO2 was supplied by increased RC flow. Analysis of O2 supply variables as functions of RV MVO2 further demonstrated a significant role of NO in regulating RC flow at rest and during moderate pulmonary hypertension. Conclusions: NO is required for the RC hyperemic response to acute pulmonary hypertension as well as for normal resting RC blood flow. After blockade of NO synthesis, RV O2 supply at rest and during pulmonary hypertension was sustained by increased RV O2 extraction.
- Coronary circulation
- Myocardial oxygen consumption
- Nitric oxide
- Pulmonary hypertension
- Right ventricle