Hypothermia and ethanol are often closely linked and in hypothermic ac
cidents ethanol is often a contributing factor. To study the effects o
f ethanol on the circulation in hypothermic conditions, cardiac cathet
erization was carried out on 18 anaesthetized beagle dogs. They were d
ivided into two groups. One gram of ethanol/kg of b.wt, diluted in sal
ine was infused into the vena cava superior within 30 min to seven dog
s. The dogs were then cooled between ice bags until the blood temperat
ure in the ascending aorta was 25 degrees C and they were then rewarme
d. The control group of 11 dogs was cooled and rewarmed without ethano
l infusion. The heart rate first increased when cooling down to 33 deg
rees C and decreased thereafter in the control group. In the ethanol g
roup heart rate increased during the ethanol infusion and remained hig
h when cooling down to 33 degrees C and decreased thereafter. Heart ra
te was higher in the ethanol group throughout the experiments, and dur
ing rewarming the difference was significant. In the control group car
diac output first increased until a body temperature of 33 degrees C w
as achieved but then decreased. In the ethanol group cardiac output st
arted to decrease after ethanol infusion. During rewarming there was a
significantly higher cardiac output in the ethanol group, probably du
e to the higher heart rate. In the cardiac cycle the systolic period p
rolonged significantly (p < 0.001) in both groups when the body temper
ature decreased from 37 degrees C to 25 degrees C whereas the diastoli
c period remained quite stable. The contraction phase was also affecte
d by the cooling. The changes in contraction force cannot be seen in d
P/dt alone because dP/dt values first increased significantly when coo
ling from 37 degrees C to 33 degrees C but then decreased. Ejection fr
action, systolic period, and the systemic vascular resistance increase
d despite the reduction of the dP/dt and thus we conclude that the con
traction force is augmented in hypothermia. in the ethanol group the m
yocardium seems to be depressed due to ethanol. In the early phase of
cooling heart rate increased but cardiac output decreased in the ethan
ol group, indicating the decreased ability of the heart to respond to
cooling in the presence of ethanol. The time constant of exponential p
ressure fall (tau) increased linearly with cooling from 37 degrees C t
o 25 degrees C and recovered with rewarming in both groups. Changes in
negative dP/dt coincided with the changes in the time constant of exp
onential isovolumic pressure fall. Ethanol did nor influence relaxatio
n. All the parameters we checked recovered to normal during rewarming.