[阿片受体在心脏抵抗缺血再灌注影响中的调节作用]。

A V Krylatov, O E Vaizova, M V Belousov, S V Poznyakova, P G Madonov
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引用次数: 0

摘要

m-, d1-, d2-和k1-阿片受体的激活增加心脏缺血再灌注的抵抗。在许多情况下,阿片类药物的心脏保护作用似乎与外周OR的激活有关。然而,当涉及到非肽激动剂或能够穿过血脑屏障时,我们不能排除中枢阿片受体参与心脏保护。内源性阿片类药物不参与非适应性动物心脏缺血再灌注耐受的调节。刺激k1-和d1-OP可能发挥迟发性心脏保护作用。激活d-和k1-OP可降低心肌细胞再灌注后的凋亡强度。有关阿片类药物在心脏再灌注时的肌力作用的研究结果仍然存在很大争议。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[ROLE OF OPIOID RECEPTORS IN THE REGULATION OF RESISTANCE OF HEART TO IMPACT OF ISCHEMIA-REPERFUSION].

Activation of m-, d1-, d2- and k1-opioid receptors increases cardiac resistance to ischemia-reperfusion. The cardioprotective effect of opioids in many cases appears to be associated with the activation of the peripheral OR. However, when it comes to non-peptide agonists OR able to cross the blood-brain barrier, we cannot exclude the involvement of central opioid receptors in cardioprotection. Endogenous opioids are not involved in the regulation of cardiac tolerance to ischemia- reperfusion in non-adapted animals. Stimulation of k1- and d1-OP may exert delayed cardioprotective effect. Activation d- and k1-OP reduces the intensity of cardiomyocyte apoptosis after reperfusion. The results of studies related to the inotropic effect of opioids during reperfusion of the heart remain highly controversial.

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