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Relation between ischemic preconditioning and the duration of sustained ischemia.

机译:缺血预处理与持续缺血持续时间之间的关系。

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摘要

It has been reported that repetitive brief periods of ischemia and reperfusion (ischemic preconditioning, IP) cause a significant reduction in the extent of myocardial necrosis or in the incidence of reperfusion arrhythmias in rat heart. However, recent reports have stated that IP effect is diminished or lost in the canine or bovine heart if ischemia (mostly regional) is sustained for 40 min or longer. The main objective of this study is to assess whether IP provides myocardial protection in prolonged sustained ischemia under the condition of global ischemia in isolated rabbit heart. The hearts were subjected to 10-60 min sustained ischemia (SI) followed by 60 min reperfusion with (IP heart) or without IP (ISCH heart). IP was induced by 4 cycles of 5 min global ischemia and 5 min reperfusion. Left ventricular function (LVF), extent of infarction (EI) and ultrastructural changes were examined. As a whole, the LVF began to recover on reperfusion but there was no significant difference in the functional parameters. However, extracellular Ca2+ concentration was lower in the ISCH hearts (p < 0.05) and the EI was significantly different between the hearts which had received 60 min SI (67% in the ISCH versus 32% in the IP heart, p < 0.01). Ultrastructural changes were homogeneous in the ISCH hearts and became irreversible in accordance with increase of the duration of ischemia, while these changes were heterogeneous and restricted in the IP heart. These results suggest that IP does not attenuate the postischemic dysfunction in prolonged ischemia but it can provide an infarct size-limiting effect and delay ultrastructural changes. This cardioprotective effect may be related to calcium homeostasis.
机译:据报道,反复短暂的局部缺血和再灌注(缺血预处理,IP)可导致大鼠心肌缺血性坏死的程度或再灌注心律失常的发生率显着降低。但是,最近的报道表明,如果持续40分钟或更长时间(局部),则犬或牛心脏的IP效应会减弱或消失。这项研究的主要目的是评估在离体兔心脏的整体缺血情况下,IP在长期持续缺血中是否提供心肌保护。对心脏进行10-60分钟的持续缺血(SI),然后在有IP心脏或无IP(ISCH心脏)的情况下再灌注60分钟。通过5分钟的整体缺血和5分钟的再灌注的4个周期来诱导IP。检查左心室功能(LVF),梗死程度(EI)和超微结构改变。总体而言,LVF在再灌注后开始恢复,但功能参数无明显差异。但是,在接受了60分钟SI的心脏中,ISCH心脏中的细胞外Ca2 +浓度较低(EI )(I <67%,而在IP心脏中为32%,P <0.01)。在ISCH心脏中,超微结构变化是均匀的,并且随着缺血持续时间的增加而变得不可逆,而在IP心脏中,这些变化是异质的并且受到限制。这些结果表明,IP不能减轻长期缺血中的缺血后功能障碍,但可以提供梗死面积限制作用并延迟超微结构改变。这种心脏保护作用可能与钙稳态有关。

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