Recovery from reperfusion injury in intact canine heart by nifedipine

Effect of nifedipine post-treatment (100 micrograms/kg slow bolus followed by 3 micrograms/kg/min infusion) on the functional and metabolic changes of the heart after a brief regional ischemia (I) (20 min.) followed by 1 hr of reperfusion (R) was studied in pentobarbitone-anaesthetized open-chest coronary ligated dogs. In the control group, 1 hr of reperfusion failed to cause any significant recovery of the depressed LVdP/dtmax and that of the elevated LVEDP (LVdP/dtmax, pre-ischemic: 2720 +/- 90 mm Hg/sec., 20 min. of I: 2410 +/- 120 mm Hg/sec and 60 min. of R: 2210 +/- 130 mm Hg/sec. LVEDP, pre-ischemic: 5.25 +/- 0.2 mm Hg, 20 min. of I: 10.5 +/- 0.9 mm Hg and 60 min. of R: 7.5 +/- 0.5 mm Hg). However, 1 hr of reperfusion caused a significant recovery of ischemia-induced depletion of myocardial creatine phosphate (CP) content only, but not that of ATP. On post-treatment with nifedipine (i.e., infusion started just before reperfusion), there was a significant recovery in LVEDP (8.25 +/- 0.6 mm Hg after 20 min. of ischemia to 5.0 +/- 0.4 mm Hg after 1 hr of reperfusion) and there was no further deterioration in LVdP/dtmax, as observed in untreated dogs. More significantly, nifedipine caused a near normal recovery of both ATP and CP contents of the affected myocardium. Therefore, the present study shows that post-ischemic administration of nifedipine prevented reperfusion injury of the ischemic myocardium, as evidenced by both functional and metabolic recovery.