HEAT-SHOCK IMPROVES ISCHEMIC TOLERANCE OF HYPERTROPHIED RAT HEARTS
HEAT-SHOCK IMPROVES ISCHEMIC TOLERANCE OF HYPERTROPHIED RAT HEARTS
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DOI：
10.1152/ajpheart.1994.267.5.h1941
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发表时间：
1994-11-01
影响因子：
4.8
通讯作者：
SNOECKX, LHEH
中科院分区：
文献类型：
--
作者：
CORNELUSSEN, R;SPIERING, W;SNOECKX, LHEH
观察全身热疗24 h后肥厚心脏的缺血后恢复情况。为此，将麻醉后的大鼠和假手术大鼠分别进行热休克（AoB（HS）和Sham(HS)）。8周前诱导心肌肥厚。在离体射血心脏中，非加热（对照）肥厚（AoB(C)）和非加热（对照）非肥厚（羞耻）心脏在缺血45分钟后功能恢复较差，而非加热（对照）肥厚（羞耻）心脏功能恢复中等。热休克显著改善AoB（HS）和Sham（HS）心脏缺血后恢复。这种功能恢复的改善与心律失常持续时间的显著缩短有关。此外，两种热休克心脏在缺血前和缺血后的冠状动脉血流均明显高于相应的对照心脏。使用放射性微球评估，AoB（HS）心脏的缺血后心内膜血流明显改善。与相应的对照心脏相比，AoB（HS）心脏的内源性过氧化氢酶活性没有变化，而Sham（HS）心脏的内源性过氧化氢酶活性显著升高。目前的研究结果表明，全身热疗后的缺血后功能改善可以通过心肌灌注增加和更均匀来解释，这也可能缩短缺血后心律失常的持续时间。这种作用对肥大的心脏尤其有益，因为肥大的心脏极易受到可能由心内膜下灌注不足引起的缺血性损伤。
The postischemic recovery of hypertrophied hearts was studied 24 h after total body hyperthermia. To this end, anesthetized aortic-banded and sham-operated rats were subjected to heat shock (AoB(HS) and Sham(HS), respectively). Cardiac hypertrophy was induced 8 wk earlier. In isolated ejecting hearts, functional recovery after 45 min of global ischemia was poor and moderate in nonheated (control) hypertrophied (AoB(C)) and nonheated (control) nonhypertrophied (Shame) hearts, respectively. Heat shock significantly improved postischemic recovery in both AoB(HS) and Sham(HS) hearts. This improvement of functional recovery was associated with a significant reduction of the duration of arrhythmias. In addition, coronary flow was significantly higher in both types of heat-shocked hearts than in the corresponding control hearts during the preischemic as well as the postischemic period. Postischemic endocardial flow, assessed using radioactive microspheres, was significantly improved in AoB(HS) hearts. Compared with the corresponding control hearts, the native endogenous catalase activity was not changed in AoB(HS) hearts but was significantly increased in Sham(HS) hearts. The present findings suggest that the postischemic functional improvement after total body hyperthermia can be explained by increased and more homogeneous myocardial perfusion, which may also reduce the duration of postischemic arrhythmias. This effect is especially beneficial for the hypertrophied heart, which is known to be extremely vulnerable to the ischemic insult probably caused by subendocardial underperfusion.