Abstract
The cholinergic effect of carnitine (β-hydroxy, γ-trimethylammonium butyrate) on the cardiovascular and digestive systems has been well-established by several investigators (1-8). Recently, physiological existence of carnitine in the heart muscle has attracted notice and carnitine has been regarded as a heart hormone which may contribute to regulate the contraction of the heart muscle and the coronary flow. The addition of carnitine to an incubation medium resulted in enhanced oxidation of long-chain fatty acids by heart muscle preparation (9) as well as by liver slices and homogenates (10, 11) and skeletal muscle particulates (12). Fritz et al. (9) showed that the activity of carnitine derivatives required to enhance fatty degradation was abolished by replacement of the carboxyl group with an ester grouping. Furthermore, Fritz and Yue (13) demonstrated that carnitine enhanced the conversion of acetyl-CoA to CO2 and augmented oxygen consumption by heart muscle mitochondria when acetyl-CoA was the substrate. Acetylcarnitine decreased the carnitine enhancement of acetyl-CoA conversion to CO2, via operation of the carnitine acetyltransferase reaction: acetyl-CoA+ carnitine⇔acetylcarnitine+CoA. They concluded that carnitine acetyltransferase and carnitine might function as a shuttle system to facilitate acetylgroup movement across the mitochondria membrane.
The present experiments were therefore designed to study the effects of carnitine and its methylester on the spontaneous contraction and the transmembrane potential in the isolated rabbit's atrium as a preliminary investigation to correlate the pharmacodynamic effects of carnitine on the heart with the above-mentioned biochemical effects.
