Right ventricular coronary flow in arterial hypertension

Right ventricular (RV) coronary circulation in systemic hypertension offers an opportunity to assess the effects of marked increases in coronary perfusion pressure in vivo without appreciable increases in workload or marked hypertrophy of the cardiac chamber. This study investigates RV coronary circulation in renal hypertensive rats (RHR). Mean arterial pressure rose by 50% to 60% in RHR as compared to control groups and RV mass increased by 15% (7.15 vs 6.19 mg/gm body weight, p less than 0.01). Coronary blood flow, which was measured by left atrial injection of microspheres in conscious rats, was not significantly different between study groups both at rest and after maximal coronary vasodilation with carbochrome (6 mg/kg). However, minimal RV coronary resistance level per gram were significantly elevated (p less than 0.05) in RHR. A second study was designed to further dissociate the effects of arterial hypertension from the effects of changes in RV mass in RHR. In one group, blood pressure was acutely reduced by 1 week of captopril therapy, while RV mass remained high. In the second group, captopril was discontinued after 14 weeks of treatment, allowing arterial pressure to rise, while RV mass, which had regressed with treatment, remained normal. After treatment, RV minimal coronary resistance levels remained high in the short-term-treated hypertensive rats, but returned to normal levels in the long-term-treated RHR. These results suggest the following possibilities: the RV is not immune to the effects of systemic hypertension, coronary structural changes are probably the main factor that accounts for the increase in RV coronary resistance levels, and coronary alterations are amenable to long-term antihypertensive therapy.