Differential effect of short-term ethanol on cardiac and vascular growth responses

To determine in rats the acute effect of ethanol on the activity of a marker of cardiac and vascular growth processes (ornithine decarboxylase) and on alpha 1-adrenergic-induced vascular trophic responses, and whether ethanol-induced sympathoadrenal hyperactivity stimulated vascular structural changes after a more prolonged treatment.

Acute treatment was as follows: ethanol (5 g/kg, intubation), alpha 1-adrenergic agonist (10 mg/kg methoxamine subcutaneously), methoxamine plus ethanol, or control. Left ventricular, aortic and mesenteric vascular ornithine decarboxylase activity was determined 4 h later by measuring 14CO2 evolved from [14C]-ornithine. Three-day treatment was as follows: ethanol (every 8 h, intubation, 5 g/kg initial dose, subsequent doses based on intoxication level) or isocaloric quantities of maltose dextrin. The left ventricular: body weight ratio, hindlimb vascular resistance properties and indices of cardiac and vascular hypertrophy were determined.

In the acute treatment methoxamine-induced pressor responses and the activation of vascular ornithine decarboxylase were both inhibited by ethanol treatment. Ethanol alone elevated the heart rate and decreased mean arterial pressure while stimulating left ventricular but not vascular ornithine decarboxylase activity. Methoxamine did not alter left ventricular ornithine decarboxylase activity. Three-day ethanol treatment induced cardiac hypertrophy but had no effect on the hindlimb vascular resistance properties measured at maximum dilation and maximum constriction.

Acute and short-term ethanol exposure induces cardiac growth processes. Ethanol prevents alpha 1-adrenergic activated vascular growth response by a mechanism that may be similar to the attenuation of alpha 1-adrenergic-induced elevation of arterial pressure.