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首页> 外文期刊>American Journal of Physiology >Attenuation of heat shock-induced cardioprotection by treatment with the opiate receptor antagonist naloxone.
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Attenuation of heat shock-induced cardioprotection by treatment with the opiate receptor antagonist naloxone.

机译：通过使用阿片受体拮抗剂纳洛酮治疗减轻热休克诱导的心脏保护作用。

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Whole body hyperthermia induces heat shock proteins (HSPs), which confer cardioprotection. Several opioid receptor subtypes are expressed in the heart and are linked to cardioprotection; however, no one has attempted to link the protection elicited by heat stress (HS) to opioids. Therefore, we investigated the effect of an opiate receptor antagonist, naloxone, on HS-induced cardioprotection. Anesthetized Sprague-Dawley rats were subjected to HS (42 degrees C for 20 min) with and without naloxone pretreatment and were allowed to recover for 48 h. They then underwent 30 min of ischemia followed by 2 h of reperfusion. An acute HS group was given an intravenous bolus of naloxone (3 mg/kg) 10 min before index ischemia. Infarct size (IS), expressed as a percentage of the area at risk (IS/AAR), was determined. The right heart was excised for analysis of HSP content by Western blot. Heat-shocked rats showed significant reductions in IS/AAR versus control (16 +/- 3 vs. 58 +/- 4%, P < 0.001). Pretreatment with naloxone before HS attenuated the protective effects in a dose-dependent fashion, with significant attenuation of protection occurring at 15 mg/kg naloxone versus heat shock (42 +/- 6 vs. 16 +/- 3%, P < 0.001). Acute treatment with naloxone (3 mg/kg) 48 h after recovery from HS also significantly attenuated the delayed protective effect (47 +/- 4 vs. 16 +/- 3%, P < 0.001). No difference was seen in the level of HSP70 induced in the different groups. We conclude that heat shock-induced cardioprotection can be attenuated by naloxone, an opiate receptor antagonist, without reducing the levels of certain HSPs. These results suggest there may be a link between the endogenous release of opioids and HS that mediates cardioprotection.
机译：全身热疗诱导热休克蛋白（HSP），赋予心脏保护作用。心脏中表达了几种阿片受体亚型，它们与心脏保护作用有关。然而，没有人试图将由热应激（HS）引起的保护作用与阿片类药物联系起来。因此，我们研究了阿片受体拮抗剂纳洛酮对HS诱导的心脏保护作用。麻醉的Sprague-Dawley大鼠在接受和不接受纳洛酮预处理的情况下接受HS（42摄氏度，持续20分钟），并恢复48小时。然后，他们经历了30分钟的缺血，然后再灌注2小时。急性HS组在指数缺血前10分钟静脉给予纳洛酮（3 mg / kg）静脉推注。确定梗塞面积（IS），以占危险区域的百分比（IS / AAR）表示。切下右心脏以通过蛋白质印迹分析HSP含量。与对照组相比，热休克大鼠的IS / AAR明显降低（16 +/- 3 vs. 58 +/- 4％，P <0.001）。 HS前用纳洛酮预处理以剂量依赖性方式减弱保护作用，相对于热休克，纳洛酮在15 mg / kg时显着减弱保护作用（42 +/- 6对16 +/- 3％，P <0.001） 。从HS恢复后48小时，用纳洛酮（3 mg / kg）进行的急性治疗也显着减弱了延迟的保护作用（47 +/- 4对16 +/- 3％，P <0.001）。在不同组中诱导的HSP70水平没有差异。我们得出的结论是，阿片受体拮抗剂纳洛酮可以减弱热休克诱导的心脏保护作用，而不降低某些HSP的水平。这些结果表明，阿片类药物的内源性释放与介导心脏保护作用的HS之间可能存在联系。

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