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激活心脏 δ-阿片受体可增加心脏对再灌注的耐受性。

Activation of Cardiac δ-Opioid Receptors Increases Heart Tolerance to Reperfusion.

机构信息

Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.

Branch of Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Pushchino, Moscow region, Russia.

出版信息

Bull Exp Biol Med. 2024 Mar;176(5):539-542. doi: 10.1007/s10517-024-06063-6. Epub 2024 May 8.

Abstract

Coronary occlusion (45 min) and reperfusion (120 min) in male Wistar rats in vivo, as well as total ischemia (45 min) of an isolated rat heart followed by reperfusion (30 min) were reproduced. The selective δ-opioid receptor agonist deltorphin II (0.12 mg/kg and 152 nmol/liter) was administered intravenously 5 min before reperfusion in vivo or added to the perfusion solution at the beginning of reperfusion of the isolated heart. The peripheral opioid receptor antagonist naloxone methiodide and δ-opioid receptor antagonist naltriben were used in doses of 5 and 0.3 mg/kg, respectively. It was found that the infarct-limiting effect of deltorphin II is associated with the activation of δ-opioid receptors. We have demonstrated that deltorphin II can improve the recovery of the contractility of the isolated heart after total ischemia.

摘要

在体雄性 Wistar 大鼠冠状动脉闭塞(45 分钟)及再灌注(120 分钟),以及分离大鼠心脏总缺血(45 分钟)后继以再灌注(30 分钟)均被复制。选择性 δ 阿片受体激动剂δ- 脑啡肽 II(0.12 毫克/千克和 152 纳摩尔/升)在体内再灌注前 5 分钟静脉内给予,或在分离心脏再灌注开始时加入灌流液。外周阿片受体拮抗剂纳洛酮甲碘化物和 δ 阿片受体拮抗剂纳曲酮分别以 5 毫克/千克和 0.3 毫克/千克的剂量使用。研究发现,δ- 脑啡肽 II 的梗死限制作用与 δ 阿片受体的激活有关。我们已经证明,δ- 脑啡肽 II 可以改善总缺血后分离心脏收缩性的恢复。

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