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瑞芬太尼诱导的预处理与缺血再灌注大鼠心脏中的 A1 和 A2B 腺苷受体存在相互作用。

Remifentanil-induced preconditioning has cross-talk with A1 and A2B adenosine receptors in ischemic-reperfused rat heart.

作者信息

Lee Yong-Cheol, Jung Jiyoon, Park Sang-Jin

机构信息

Department of Anesthesiology and Pain Medicine, School of Medicine, Keimyung University.

出版信息

Bosn J Basic Med Sci. 2016 Jan 1;16(1):64-70. doi: 10.17305/bjbms.2016.738.

Abstract

The purpose of this study was to determine whether there is a cross-talk between opioid receptors (OPRs) and adenosine receptors (ADRs) in remifentanil preconditioning (R-Pre) and, if so, to investigate the types of ADRs involved in the cross-talk. Isolated rat hearts received 30 min of regional ischemia followed by 2 hr of reperfusion. OPR and ADR antagonists were perfused from 10 min before R-Pre until the end of R-Pre. The heart rate, left ventricular developed pressure (LVDP),velocity of contraction (+dP/dtmax), and coronary flow (CF) were recorded. The area at risk and area of necrosis were measured. After reperfusion, the LVDP, +dP/dtmax,and CF showed a significant increase in the R-Pre group compared with the control group (no intervention before or after regional ischemia). These increases in the R-Pre group were blocked by naloxone, a nonspecific ADR antagonist, an A1 ADR antagonist, and an A2B ADR antagonist. The infarct size was reduced significantly in the R-Pre group compared with the control group. The infarct-reducing effect in the R-Pre group was blocked by naloxone, the nonspecific ADR antagonist, the A1 ADR antagonist, and the A2B ADR antagonist. The results of this study demonstrate that there is cross-talk between ADRs and OPRs in R-Pre and that A1 ADR and A2B ADR appear to be involved in the cross-talk.

摘要

本研究的目的是确定在瑞芬太尼预处理(R-Pre)过程中阿片受体(OPRs)与腺苷受体(ADRs)之间是否存在相互作用;如果存在,则研究参与这种相互作用的ADR类型。将离体大鼠心脏进行30分钟的局部缺血,随后再灌注2小时。从R-Pre前10分钟至R-Pre结束期间灌注OPR和ADR拮抗剂。记录心率、左心室舒张末压(LVDP)、收缩速度(+dP/dtmax)和冠状动脉血流量(CF)。测量危险区域和坏死区域。再灌注后,与对照组(局部缺血前后均无干预)相比,R-Pre组的LVDP、+dP/dtmax和CF显著增加。R-Pre组的这些增加被纳洛酮、非特异性ADR拮抗剂、A1 ADR拮抗剂和A2B ADR拮抗剂阻断。与对照组相比,R-Pre组的梗死面积显著减小。R-Pre组的梗死面积减小效应被纳洛酮、非特异性ADR拮抗剂、A1 ADR拮抗剂和A2B ADR拮抗剂阻断。本研究结果表明,在R-Pre过程中ADRs与OPRs之间存在相互作用,且A1 ADR和A2B ADR似乎参与了这种相互作用。

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