European Journal of Cardio-Thoracic Surgery, Vol 7, 26-33, Copyright © 1993 by European Association for Cardio-thoracic Surgery
Changes in coronary vasodilatory reserve induced by pressure overload during post-natal development: effects on post-ischemic perfusion
H Yamamoto and M Avkiran
Cardiovascular Research, Rayne Institute, St. Thomas' Hospital, London, UK.
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)
