Heat-shock. has been reported to induce tolerance for subsequent ische
mia. We wished to determine whether thermal stress is protective for h
ypothermic storage. Three groups of Sprague-Dawley rats were studied (
n = 8 per group). Control animals received routine care (CONT) while a
naesthetized rats were either warmed to 42 degrees C for 20 min (HEAT)
or maintained at room temperature (SHAM). Twenty-four hours later, he
arts were mounted on a Langendorff apparatus with an intraventricular
balloon. Hearts were then flushed and stored in UW solution for 8 hr a
t 0 degrees C and reperfused for 45 min. Data are reported as a percen
tage of the prestorage results or as the absolute value (mean +/- SD).
Recovery of developed pressure was significantly greater (P < 0.05) i
n the heat-shocked animals (79.5 +/- 10.2%) than in the SHAM (63.6 +/-
17.2%) or CONT groups (59.0 +/- 10.8%). Coronary how was similarly en
hanced (P < 0.05) in the HEAT group (86.8 +/- 5.5%) vs the CONT (77.0
+/- 12.3%) or SHAM hearts (74.5 +/- 10.2%). Diastolic compliance as as
sessed by evaluation of the end-diastolic pressure-volume curves was r
educed in all groups (P < 0.0001) but not different among groups. Card
iac creatine kinase release during reperfusion was greater in the CONT
and SHAM groups (CONT: 726.9 +/- 297.8 IU/g; SHAM: 548.9 +/- 420.9 IU
/g) than in the heat-shocked rodents (282.3 +/- 175.5 IU/g, P < 0.05 H
EAT vs CONT). Cardiac biopsies were performed sequentially in separate
animals (n = 6 per group). Tissue levels of ATP and total adenine nuc
leotides were greater in the heat-shacked or SHAM hearts following rep
erfusion compared with controls (P < 0.05). Thermal stress provides ad
ditional protection for prolonged hypothermic storage. (C) 1996 Academ
ic Press, Inc.