• Mona M Soliman.
• Department of Physiology, College of Medicine, King Saud University, P.O. Box 29825 (29), Riyadh 11461, Saudi Arabia. monaslmn@yahoo.com
• Eur. J. Pharmacol. 2011 Jan 10;650(1):324-7.

AbstractNa(+)-H(+) exchanger activation on resuscitation following hemorrhagic shock has been shown to result in myocardial injury and dysfunction. Amiloride, an inhibitor of the Na(+)-H(+) exchanger has been shown to protect the myocardium against reperfusion injury in the ischemic hearts. However, the mechanism of protection remains unclear. Na(+)-H(+) exchanger blockers have been implicated in the regulation of inflammatory responses and chemokine production. The present study investigated the therapeutic anti-inflammatory value of amiloride on myocardial contractile function in post-resuscitation following hemorrhagic shock in rats. Male Sprague-Dawley rats were assigned into 3 groups: 1) hemorrhage, 2) hemorrhage treated with amiloride, and 3) sham hemorrhage (n=6 per group). Rats were hemorrhaged over 60min to reach a mean arterial blood pressure of 40mmHg. After 60min of hemorrhagic shock, rats were treated or not by injection of 1ml of 100μM amiloride (0.027mg/ml) intra-arterially. Resuscitation was made in vivo by reinfusion of the shed blood to restore norm tension for 30min. Left ventricular contractile function was measured in the isolated hearts following hemorrhage and in vivo resuscitation using the Langendorff apparatus. Arterial blood samples were collected from all groups at the end of the experimental period (90min) for cytokine measurements (TNF-α). Amiloride decreased the inflammatory response to hemorrhagic shock and resuscitation by lowering the levels of TNF. These results indicate that amiloride protects the myocardium by down regulating the inflammatory response to hemorrhagic shock and resuscitation.Copyright © 2010 Elsevier B.V. All rights reserved.

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