Control of ventricular fibrillation during induced hypothermia in cats after differential depletion of cardiac catecholamine stores with prenylamine (Segontin).

The role of adrenergic mechanisms for the development of ventricular fibrillation during induced hypothermia was studied in cats. Prenylamine (60 mg/kg) caused a disappearance of the adrenergic transmitter in the muscular nerves; those to the vessels were only slightly affected. Thus pretreated, animals can be cooled to 17.8 to 17°C rectal temperature, and subsequently rewarmed, without developing ventricular fibrillation. Blood pressure was maintained with metaraminol. Without pretreatment the animals constantly develop ventricular fibrillation at 23 to 18.6°C. When prenylamine was given in a dose (20 mg/kg) that does not overtly affect the norepinephrine content of the cardiac adrenergic nerves, ventricular fibrillation was not prevented. In one group of animals receiving 60 mg/kg of prenylamine, norepinephrine instead of metaraminol was infused to maintain the blood pressure during cooling. These animals developed ventricular fibrillation (or cardiac standstill). Fluorescence microscopy showed that the infusion had restored the norepinephrine content in the cardiac nerves previously depleted of their endogenous transmitter by prenylamine. The incidence of ventricular fibrillation seems to be related to the number of intact adrenergic nerves present in relation to the cardiac muscles. Hypothermia caused a distinct release of transmitter from the cardiac adrenergic nerves. ADDITIONAL