0000000000803458
AUTHOR
Josef Moravec
Assessment of the cardiostimulant action of propionyl-L-carnitine on chronically volume-overloaded rat hearts.
Chronic volume overload was induced in young rats of Wistar strain by surgical opening of the aorto-caval fistula. Three months later, during in vitro perfusion with exogenous palmitate, left ventricular function and energy turnover (QO2) of hypertrophied hearts were severely depressed. This seemed to be related to impaired long-chain fatty acid utilization, as reflected by decreased 14CO2 production from U-14C-palmitate and decreased tissue levels of L-carnitine. Another group of rats exposed to chronic volume overload was pretreated for 2 weeks before sacrifice with propionyl-L-carnitine (250 mg/kg/day), and the hearts were perfused with 1.2 mM palmitate and 10 mM propionyl-L-carnitine. I…
Carnitine transport in volume-overloaded rat hearts
Carnitine concentration in tissue is generally related to mitochondrial volume-density and ability to oxidize fatty acids. The highest tissue carnitine has been detected in ventricular myocardium which, compared to other tissues, presents elevated rates of oxidative phosphorylation [1]. The ability of cardiac mitochondria to oxidize long chain fatty acids is also much higher when compared to skeletal muscle or liver sarcosomes (Table 1). Paradoxically enough, it has been known for many years [3–5] that the heart is missing γ-butyrobetaine hydroxylase [6, 7], the last enzyme of carnitine synthesizing pathway, and that in the myocardium of different species including man, the carnitine synthe…