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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.
Although studies indicate that 17
-estradiol administration following trauma-hemorrhage (T-H) improves cardiac and hepatic functions, the underlying mechanisms remain unclear. Since the induction of heat shock proteins (HSPs) can protect cardiac and hepatic functions, we hypothesized that these proteins contribute to the salutary effects of estradiol following T-H. To test this hypothesis, male Sprague-Dawley rats (~300g) underwent laparotomy and hemorrhagic shock (35-40 mmHg for ~90min) followed by resuscitation with 4 x the shed blood volume in the form of Ringer's lactate. 17-estradiol (1mg/kg BW) was administered at the end of the resuscitation. Five hours after T-H and resuscitation there was a significant decrease in cardiac output, positive and negative dp/dt(max). Liver function as determined by bile production and ICG clearance was also compromised following T-H and resuscitation. This was accompanied by an increase in plasma ALT levels and liver perfusate LDH levels. Furthermore, circulating levels of TNF-
, IL-6 and IL-10 were also increased. In addition to decreased cardiac and hepatic function, there was an increase in cardiac HSP32 expression and a reduction in HSP60 expression following T-H. In the liver, HSP32 and HSP70 were increased following T-H. There was no change in heart HSP70 and liver HSP60 following T-H and resuscitation. Estradiol administration at the end of T-H and resuscitation increased heart/liver HSPs expression, ameliorated the impairment of heart/liver functions and significantly prevented the increase in plasma levels of ALT, TNF- and IL-6. The ability of estradiol to induce HSPs expression in the heart and liver suggests that HSPs in part mediate the salutary effects of 17-estradiol on organ functions following T-H.
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