The mutual potentiation of the hepatotoxic effects of ethanol and hypoxia r
aised the question of whether such an interaction also occurs in the cardio
vascular system. Therefore, anaesthetized rats were infused intravenously w
ith ethanol (25 mg/kgxmin.) over 90 min. to reach blood ethanol concentrati
ons between 2.2 and 2.6 g/l and were ventilated artificially either with ro
om air, 10% O-2/90% N-2 or 100% O-2. Under normoxic conditions, ethanol pro
duced a slow decrease of mean arterial blood pressure from 130 to 100 mmHg
due to the decline in cardiac output and stroke volume (-20%) while heart r
ate and peripheral resistance remained unchanged. Hypoxia (arterial oxygen
tension 35-38 mmHg) without ethanol produced immediate hypotension (-60 mmH
g) without decreasing the cardiac output, i.e. by reducing peripheral resis
tance. In combination with ethanol, hypoxia produced an even stronger hypot
ension (-90 mmHg) due to reduction in both cardiac output and peripheral re
sistance. On the other hand, respiration with 100% O-2 (arterial oxygen ten
sion about 500 mmHg) elevated peripheral resistance, attenuated ethanol-ind
uced cardiodepression and prevented ethanol-induced hypotension. The lethal
doses of ethanol evaluated by infusing 75 mg/kgxmin. ethanol until death a
mounted to 4.1 g/kg with 10% O-2, to 5.5 g/kg with 20% O-2 (room air) arid
to 6.9 g/kg with 100% O-2. Thus decrease in vascular contractility induced
by hypoxia combined with ethanol-induced cardiodepression may result in let
hal cardiovascular failure. Hyperoxia, on the other hand, counteracts ethan
ol-induced cardiodepression and its acute toxicity by raising the vascular
contractility.