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1 Center for Surgical Research and 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.
A growing body of evidence indicates that heme degradation products may counteract the deleterious consequences of hypoxic- and/or ischemia-reperfusion injury. Since hemeoxygenase (HO)-1 induction following adverse circulatory conditions is known to be protective, and since females in the proestrus cycle (with high estrogen) have better hepatic function and lesser hepatic damage than males following trauma-hemorrhage, we hypothesized that estrogen administration in males following trauma-hemorrhage will upregulate HO activity and protect the organs against dysfunction and injury. To test this hypothesis, male Sprague-Dawley rats underwent 5cm laparotomy and approximately 90 min of hemorrhagic shock (35-40 mmHg, for 93±2), followed by resuscitation with four times the shed blood volume in the form of Ringer's lactate. 17
-estradiol and/or the specific HO enzyme inhibitor chromium-mesoporphyrin (CrMP) were administered at the end of resuscitation and the animals were sacrificed 24 hr thereafter. Trauma-hemorrhage reduced cardiac output, myocardial contractility and serum albumin levels. Portal pressure and serum ALT levels were markedly increased under those conditions. These parameters were significantly improved in the 17-estradiol-treated rats. Estradiol treatment also induced increased HO-1 mRNA expression, HO-1 protein levels and HO enzymatic activity in cardiac and hepatic tissue as compared to vehicle treated trauma-hemorrhaged rats. Administration of the HO inhibitor, CrMP prevented the estradiol-induced attenuation of shock-induced organ dysfunction and damage. Thus, the salutary effects of estradiol administration on organ function following trauma-hemorrhage are mediated in part via upregulation of HO-1 expression and activity.
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