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1 Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: Irshad.Chaudry{at}ccc.uab.edu.
Recent studies have shown that administration of dehydroepiandrosterone (DHEA) following trauma-hemorrhage (T-H) improves cardiovascular and hepatic function in male animals. Although androstenediol, one of the DHEA metabolites, has been recently reported to produce salutary effects on cardiac function and splanchnic perfusion following T-H, it remains unknown whether androstenediol per se has any salutary effects on hepatic function under those conditions. To study this, male Sprague-Dawley rats underwent laparotomy and ~90 min of hemorrhagic shock (35-40 mmHg), followed by resuscitation with four times the shed blood volume in the form of Ringer's lactate. Androstenediol (1mg/kg BW, iv.) was administered at the end of resuscitation and the animals were sacrificed at 24 hr thereafter. Trauma-hemorrhage significantly reduced portal blood flow, bile production, and serum albumin levels. Portal pressure, serum ALT, hepatic nitrate/nitrite, inducible nitric oxide synthase (iNOS) and endothelin-1 markedly increased following T-H. The alterations in these parameters induced by T-H- were significantly attenuated in rats treated with androstenediol. Endothelial NOS (eNOS) expression, which was not different between T-H and sham, was found to be significantly elevated in T-H androstenediol treated rats. These data suggest that improvement in hepatic perfusion by androstenediol following T-H is likely due to a decrease in endothelin-1 and induction of eNOS. Moreover, the decrease in hepatic damage after androstenediol administration is likely related to liver iNOS down-regulation. Thus, androstenediol appears to be a novel and useful adjunct for restoring hepatic function in male animals following adverse circulatory conditions.
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