Ischaemic preconditioning of skeletal muscle 2. Investigation of the potential mechanisms involved
Ischaemic preconditioning of skeletal muscle 2. Investigation of the potential mechanisms involved
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DOI：
10.1302/0301-620x.84b8.9362
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发表时间：
2002-11-01
影响因子：
--
通讯作者：
Jackson, MJ
中科院分区：
文献类型：
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作者：
Bushell, AJ;Klenerman, L;Jackson, MJ
我们之前已经证明，预先将大鼠后肢暴露于缺血五分钟和再灌注五分钟，可以减少随后的缺血四小时和再灌注一小时后骨骼肌的结构损伤。我们现在已经研究了这种缺血预处理方案可能有效减少长期缺血和再灌注引起的骨骼肌损伤的潜在机制。预先将后肢暴露于缺血 5 分钟并再灌注 5 分钟并不能阻止胫骨前肌 ATP 含量的下降，这种下降是在随后的缺血 4 小时和再灌注 1 小时后发生的。同样，预处理方案对升高的肌肉髓过氧化物酶没有影响，表明中性粒细胞含量升高或肌肉阳离子含量异常。还发现再灌注缺血肌肉的热休克蛋白 (HSP) 72 含量增加，但预处理方案没有进一步增加该或其他 HSP 的含量，表明它不是通过增加这些细胞保护蛋白的表达来发挥作用。预处理的保护作用似乎可以通过在暴露于四小时期间之前立即向动物输注腺苷来模仿，这表明可以对骨骼肌进行预处理以维持结构活力的潜在机制。
We have previously shown that prior exposure of rat hind limbs to ischaemia for five minutes and reperfusion for five minutes reduced the structural damage to skeletal muscle which followed a subsequent period of ischaemia for four hours and reperfusion for one hour. We have now examined the potential mechanisms by which this ischaemic preconditioning protocol may be effective in reducing damage to skeletal muscle induced by prolonged ischaemia and reperfusion. Prior exposure of the hindlimb to ischaemia for five minutes and reperfusion for five minutes did not prevent the fall in the ATP content of tibialis anterior which occurred after a subsequent period of ischaemia for four hours and reperfusion for one hour. Similarly, no effect of the preconditioning protocol was seen on the elevated muscle myeloperoxidase, indicative of an elevated neutrophil content, or abnormal muscle cation content. Reperfused ischaemic muscle was also found to have an increased content of heat-shock protein (HSP) 72, but the preconditioning protocol did not further increase the content of this or other HSPs indicating that it was not acting by increasing the expression of these cytoprotective proteins. The protective effects of preconditioning appeared to be mimicked by the infusion of adenosine to animals immediately before exposure to the four-hour period, indicating a potential mechanism by which skeletal muscle may be preconditioned to maintain structural viability.