Changes in coronary vasodilatory reserve induced by pressure overload during post-natal development: effects on...

Several congenital heart defects result in increased hemodynamic load on one or both ventricles. We have investigated the effects of left ventricular (LV) pressure overload during post-natal development on the coronary vasodilatory reserve in isolated rat hearts (i) during aerobic perfusion, and (ii) following cardioplegic arrest and hypothermic ischemia. The LV pressure overload was induced in 1-week-old Wistar rats by abdominal aortic constriction (AC), with controls (C) undergoing sham operations. Relative to C, the LV weight/body weight in AC increased by 45% and 100% at 3 and 6 weeks of age, respectively. At these ages, the hearts (n = 8/group) were isolated and Langendorff-perfused. Minimal coronary vascular resistance per gram dry weight (MCVR/g) was measured during maximal vasodilation with adenosine (10 mumol/l) before cardioplegic arrest and hypothermic (15 degrees C) ischemia (210 min) and again after reperfusion (45 min). Before ischemia, MCVR/g was greater in AC than in C both at 3 weeks of age (0.48 +/- 0.03 vs 0.31 +/- 0.01 mmHg/ml per min/g dry wt) and at 6 weeks of age (1.20 +/- 0.05 vs 0.46 +/- 0.01 mmHg/ml per min/g dry wt). In the post-ischemic period, MCVR/g increased in all groups. Post-ischemic MCVR/g was similar in C and AC at 3 weeks of age (0.52 +/- 0.12 and 0.66 +/- 0.05 mmHg/ml per min/g dry wt, respectively) but was significantly greater in AC than in C at 6 weeks of age (2.42 +/- 0.22 vs. 0.54 +/- 0.02 mmHg/ml per min/g dry wt).(ABSTRACT TRUNCATED AT 250 WORDS)