The effects of intravenous administration of propionyl-L-carnitine (PLC) were investigated in anesthetized dogs instrumented for the analysis of general hemodynamic and electrocardiographic data, peripheral blood flows, coronary blood flow and oxygen consumption, urine flow, and renal function. PLC was administered in bolus (20, 60, and 200 mg/kg) or by infusion (20 mg/kg/min * 15 min or 30 mg/kg/min * 10 min). In some cases also L-carnitine (LC) and L-carnitine+propionate (LC + P) were administered in doses equimolar to those of PLC. PLC elicited dose-dependent, short-lasting enhancements of cardiac output, both in open- and closed-chest conditions. Arterial blood pressure, heart rate, and contractility varied slightly and unpredictably; the substance did not elicit electrocardiographic effects. These responses were not changed by alpha- or beta-adrenergic blockade, nor by the administration of a calcium antagonist, but they were abolished or reversed by the combination of such blocking interventions. Mesenteric and iliac blood flows were increased by both PLC and LC; LC + P increased these, and in addition increased renal blood flow. A strong diuresis obtained with PLC, LC, and LC + P was due to osmotic clearance following the administration of hyperosmotic solutions. PLC elicited coronary vasodilation with reduced oxygen extraction; this effect lasted longer than the general hemodynamic effects and was not seen with LC. All the cardiovascular actions of PLC can be attributed to its pharmacologic properties, rather than to its role as a metabolic intermediate.
Short-term hemodynamic effects of intravenous propionyl-l-carnitine in anaesthetized dogs
Cevese A.;Schena F.;Cerutti G.
1991-01-01
Abstract
The effects of intravenous administration of propionyl-L-carnitine (PLC) were investigated in anesthetized dogs instrumented for the analysis of general hemodynamic and electrocardiographic data, peripheral blood flows, coronary blood flow and oxygen consumption, urine flow, and renal function. PLC was administered in bolus (20, 60, and 200 mg/kg) or by infusion (20 mg/kg/min * 15 min or 30 mg/kg/min * 10 min). In some cases also L-carnitine (LC) and L-carnitine+propionate (LC + P) were administered in doses equimolar to those of PLC. PLC elicited dose-dependent, short-lasting enhancements of cardiac output, both in open- and closed-chest conditions. Arterial blood pressure, heart rate, and contractility varied slightly and unpredictably; the substance did not elicit electrocardiographic effects. These responses were not changed by alpha- or beta-adrenergic blockade, nor by the administration of a calcium antagonist, but they were abolished or reversed by the combination of such blocking interventions. Mesenteric and iliac blood flows were increased by both PLC and LC; LC + P increased these, and in addition increased renal blood flow. A strong diuresis obtained with PLC, LC, and LC + P was due to osmotic clearance following the administration of hyperosmotic solutions. PLC elicited coronary vasodilation with reduced oxygen extraction; this effect lasted longer than the general hemodynamic effects and was not seen with LC. All the cardiovascular actions of PLC can be attributed to its pharmacologic properties, rather than to its role as a metabolic intermediate.
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
