AJP - Heart and Circulatory Physiology, Vol 259, Issue 3 879-H888, Copyright © 1990 by American Physiological Society
Transient hypothermic reperfusion and postischemic recovery in isolated rat heart
R. D. Kempsford, T. Murashita and D. J. Hearse
Rayne Institute, St. Thomas' Hospital, London, United Kingdom.
The potential benefit of transient hypothermic reperfusion of the ischemic
myocardium was investigated in isolated working rat hearts (n = 6/group)
subjected to 25 min of global ischemia at 37 degrees C. Hearts were
reperfused in the Langendorff mode at 5, 10, 20, 30, or 37 degrees C for 10
min plus 5 min at 37 degrees C before assessment of functional recovery
(working mode). Compared with normothermic reperfusion (recovery of cardiac
output = 42.3 +/- 6.1%), transient hypothermia failed to improve the
recovery of cardiac output, which was 47.9 +/- 12.7 (P = NS), 54.3 +/- 11.5
(P = NS), 25.3 +/- 2.7 (P = NS), and 6.4 +/- 3.8% (P less than 0.05) in the
30, 20, 10, and 5 degrees C groups, respectively. Reduced recovery in the 5
degrees C group was reflected in increased creatine kinase leakage from
0.26 +/- 0.04 IU.ml-1.g dry wt-1 (37 degrees C reperfusion) to 0.62 +/-
0.12 IU. ml-1.g dry wt-1 (5 degrees C reperfusion; P less than 0.05). Brief
periods (3 x 1 min) of hypothermic (5 degrees C) perfusion during
normothermic Langendorff reperfusion (15 min) also reduced recovery of
cardiac output to 12.1 +/- 7.2% (P less than 0.01). In additional studies,
hearts were subjected to a 2-min preischemic infusion with the St. Thomas'
Hospital cardioplegic solution before either 25 or 35 min of normothermic
ischemia and reperfusion with transient hypothermia at 5, 10, 20, or 30
degrees C. Once again hypothermic reperfusion failed to improve recovery
but detrimental effects were not observed in the 5 degrees C group. These
results indicate no beneficial effect of transient hypothermic reperfusion
on recovery of function measured following global normothermic ischemia.
