Authors: Chen, Bao-Ping¹; Mao, Hong-Jiao²; Fan, Fang-Yan³; Bruce, Iain¹; Xia, Qiang³

Source: Scandinavian Cardiovascular Journal, Volume 39, Number 6, Number 6/December 2005 , pp. 375-382(8)

Publisher: Informa Healthcare

Abstract:

Objectives. To determine whether the κ-opioid receptor agonist U50,488H affects electrical uncoupling during prolonged ischemia and, if so, whether the changes are associated with its cardioprotective action. Design. The isolated rat heart was perfused in a Langendorff apparatus. Formazan content, lactate dehydrogenase (LDH) and hemodynamic parameters were measured to confirm the cardioprotective effect of U50,488H. The effects of U50,488H on electrical coupling during prolonged ischemia were also measured. Results. U50,488H concentration-dependently increased formazan content and reduced LDH release, and the ameliorating effect of 10 −5 mol/L U50,488H was abolished by 5×10 −6 mol/L nor-binaltorphimine (nor-BNI), a selective κ-opioid receptor antagonist, or 10 −4 mol/L 5-hydroxydecanoate (5-HD), a selective mitochondrial ATP-sensitive K + (K ATP ) channel blocker. The onset of electrical uncoupling during prolonged ischemia was delayed by U50,488H, and the delay was not only abolished, but also advanced by nor-BNI or 5-HD relative to the control group. Conclusions. These results demonstrate that delayed uncoupling during prolonged ischemia is associated with the cardioprotection of U50,488H, and these effects of U50,488H are mediated by mitochondrial K ATP channels.

Keywords: κ-opioid receptor; electrical uncoupling; ischemia/reperfusion; whole-tissue resistance; cardioprotection

Document Type: Research article

DOI: http://dx.doi.org/10.1080/14017430500293056

Affiliations: 1: Department of Physiology, the University of Hong Kong, Hong Kong, China 2: Department of Physiology, Shaoxing University School of Medicine, Shaoxing, 312000, China 3: Department of Physiology, Zhejiang University School of Medicine, Hangzhou, 310031, China

Publication date: 2005-12-01

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