Release of ischemia in paced rat Langendorff hearts by supply of L-carnitine: Role of endogenous long-chain acylcarnitine

Rat Langendorff hearts perfused with media that do not contain erythrocytes or fluorocarbon as oxygen carriers are borderline aerobic during 5 Hz pacing. This follows from the release of catabolic products measured: lactate, urate and lysophosphatidylcholine (IysoPC). Addition of L-carnitine to the perfusion medium reduced the level of these compounds, while the release of long-chain acylcarnitine (LCAC) increased. Previously, we found (Biochem Biophys Acta 847:62–66,1985) that micromolar LCAC protects membranes during reperfusion after ischemia, Therefore, the observed inverse relation between LCAC and the other compounds measured suggests that LCAC is the basis of an acute relief of imminent ischemia by carnitine addition. LCAC may be released from various cell types, including vascular endothelium, as demonstrated. The cationic amphiphilic nature of LCAC is responsible for protection of membrane functions in imminent ischemia. (Mol Cell Biochem 156: 87-91, 1996)