Manipulation of myocardial alpha-tocopherol levels fails to affect reperfusion arrhythmias or functional recovery following ischemic challenge in the rat heart.

Antioxidants that act as free radical scavengers have the potential to inhibit lipid peroxidation. It has previously been proposed that a relationship exists between free radicals, lipid peroxidation and reperfusion-induced arrhythmias. We have therefore examined the ability of the lipid-soluble antioxidant, alpha-tocopherol, to decrease the incidence of reperfusion-induced arrhythmias. We have shown that the myocardial alpha-tocopherol content can be significantly increased from its control value of 65.3 +/- 5.6 nmoles/g wet wt of heart to 115.0 +/- 15.6 nmoles/g wet wt of heart (p less than 0.01) by chronic intraperitoneal pretreatment and that it can be decreased, to 21.1 +/- 3.7 nmoles/g wet wt of heart (p less than 0.01), by chronic dietary manipulation. Rat hearts isolated from either of these groups, or from placebo-treated control animals, were subjected to 5 or 10 min coronary artery occlusion and were subsequently reperfused; there were no significant differences between the incidence and duration of VF and VT or the incidence and number of VPBs in these three groups. The effect of alpha-tocopherol manipulation on metabolic and functional recovery of working hearts subjected to 20 min global ischemia was subsequently examined and no significant changes were observed. Cardiac output recovered to 82 +/- 4, 81 +/- 6 and 76 +/- 5% of its preischemic value in the control, enriched and depleted groups, respectively. In conclusion, myocardial alpha-tocopherol content appears to bear no relation to the severity of reperfusion-induced arrhythmias or to the resistance of the heart to ischemic injury.