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

• Published in: Molecular and cellular biochemistry Vol. 156; no. 1; p. 87
• Main Authors: Hulsmann, W C, Peschechera, A, Serafini, F, Ferrari, L E
• Format: Journal Article
• Language: English
• Published: Netherlands 09.03.1996
• Subjects: Aerobiosis; Animals; Cardiac Pacing, Artificial; Carnitine - analogs & derivatives; Carnitine - chemistry; Carnitine - pharmacology; Carnitine - physiology; Carnitine - therapeutic use; Cations; Cell Membrane - physiology; Cells, Cultured; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; Glucagon - pharmacology; Glycerol - metabolism; Heart - drug effects; Lactates - metabolism; Lactic Acid; Lipolysis; Lysophosphatidylcholines - metabolism; Male; Myocardial Ischemia - drug therapy; Myocardial Ischemia - metabolism; Organ Culture Techniques; Perfusion; Rats; Rats, Wistar; Uric Acid - metabolism
• ISSN: 0300-8177
• DOI: 10.1007/BF00239323

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 Iysophosphatidyl-choline (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 (Biochim 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.