Varela A, Dalamon V, Sacks S, Carregal M, Savino E A
Catedra de Fisiologia, Facultad de Farmacia y Bioquimica, y PROSIVAD - CONICET, Buenos Aires, Argentina.
Rev Esp Fisiol. 1995 Dec;51(4):201-6.
The aim of the investigation was to assess whether L-carnitine, an essential cofactor in the mitochondrial transfer of fatty acids, would ameliorate the hypoxic-induced disturbances in the isolated rat atria. During hypoxia, the atria released lactate into the bathing medium and underwent a rise in resting tension and a decline of the peak developed tension and pacemaker frequency. The atria from 24-h fasted rats, which oxidize faster their endogenous triacylglycerol stores>> exhibited greater functional disturbances during hypoxia and a smaller recovery after reoxygenation, with respect to the fed rats' atria. Furthermore, at the end of the hypoxic incubation the fasted rats atria displayed a reduction of the free CoA content together with a 3-fold increase in the content of long-chain fatty-acyl CoA, in comparison with those of fed rats. The addition of 5 mM L-carnitine 60 min before the onset of hypoxia did not exert any effect on the hypoxic atria. In contrast, 20 mM L-carnitine accelerated the decline of the pacemaker activity in the fasted rat atria and worsened the contracture development in both nutritional states. The fall of the peak tension and the posthypoxic recovery as well as the levels of free CoA and long-chain fatty-acyl CoA, and lactate output, were not affected by 20 mM L-carnitine treatment. These data suggest that L-carnitine is not beneficial for the hypoxic rat atria, even in the fasted state, wherein the atrial fatty acid catabolism is increased.
