Acute treatment with vitamin E does not protect the regionally ischemic, reperfused porcine heart.

Thirty pigs were randomly assigned to a blind treatment with vitamin E or placebo. Ten animals each received 0.5 g d-alpha tocopherol intravenously before ischemia (group 1) or before reperfusion (group 2). Ten control pigs were treated with a lipid emulsion as placebo. The left anterior descending coronary artery was distally ligated for 45 min followed by 3 days of reperfusion. Infarct size was determined as ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was assessed by sonomicrometry. Myocardial and plasma concentrations of vitamin E were determined by high-performance liquid chromatography. Global hemodynamic parameters and estimated left ventricular oxygen consumption did not differ among the three groups. Intravenous treatment with vitamin E raised the plasma levels of this vitamin from 1 +/- 0.3 mg/l (control group) to 21 +/- 6 mg/l before ischemia, to 4 +/- 2 mg/l before reperfusion and to 2 +/- 0.6 mg/l at the end of the experiments in group 1. In group 2, vitamin E plasma levels increased from 1 +/- 0.3 mg/l to 24 +/- 13 mg/l before reperfusion and to 2 +/- 0.6 mg/l after 3 days of reperfusion. At the end of the experiments, myocardial vitamin E concentrations amounted to 4.2 +/- 0.7 ng/mg fresh weight (control group), 9.7 +/- 2.1 ng/mg (group 1), and to 8.7 +/- 1.4 ng/mg (group 2). The increase in vitamin E plasma concentration was not associated with a cardioprotective effect. Infarct sizes of the three groups (group 1: 68 +/- 12%, group 2: 66 +/- 15%, control group: 69 +/- 8%) were almost identical. Furthermore, recovery of systolic shortening was not improved by the acute vitamin E treatment. Mean systolic shortening of the reperfused segment amounted to 4% in the two treatment groups and 3% in the control group after 3 days of reperfusion. These results suggest that an acute increase in vitamin E plasma concentration before ischemia or during the early phase of reperfusion does not protect the ischemic, reperfused porcine heart.