T. Tveita et al., EXPERIMENTAL HYPOTHERMIA - EFFECTS OF CORE COOLING AND REWARMING ON HEMODYNAMICS, CORONARY BLOOD-FLOW AND MYOCARDIAL-METABOLISM IN DOGS, Anesthesia and analgesia, 79(2), 1994, pp. 212-218
Conflicting results have been reported as to the extent that cardiovas
cular function can be reestablished after rewarming from hypothermia.
We measured hemodynamic function, myocardial metabolism and tissue wat
er content in dogs core-cooled to 25 degrees C and later rewarmed. At
25 degrees C left ventricular (LV) systolic pressure (LVSP) was 54% +/
- 4%, maximum rate of LV pressure rise (LV dP/dt(max)) 44% +/- 5%, aor
tic pressure (AOP) 50% +/- 6%, heart rate (HR) 40% +/- 0%, cardiac out
put (CO) 37% +/- 5%, myocardial blood flow (MBF) 34% +/- 5%, and myoca
rdial oxygen consumption (MVo(2))8% +/- 1%, compared to precooling. St
roke volume (SV) and LV end-diastolic pressure (LVEDP) were unchanged.
As normothermia (37 degrees C) was reestablished, the depression of c
ardiac function and myocardial metabolism remained the same as that at
25 degrees C:LVSP 71% +/- 6%, LV dP/dt(max) 73% +/- 7%, SV 60% +/- 9%
, AOP 70% +/- 6%, CO 57% +/- 9%, MBF 53% +/- 8%, and MVo(2) 44% +/- 8%
. HR, in contrast, recovered to precooling values. The arterial concen
trations of glucose and free fatty acids (FFA) did not change signific
antly during the experimental period, whereas an increase in lactate o
f nonmyocardial origin appeared after rewarming. Increased myocardial
contents of creatine phosphate and water were found during both hypoth
ermia and rewarming. The present study demonstrates a persistent depre
ssion of cardiac function after hypothermia and rewarming in spite of
adequate energy stores. Thus, a direct influence on myocardial contrac
tile function by the cooling and rewarming process is suggested.