Although studies indicate that 17beta-estradiol administration after
trauma-
hemorrhage (T-H) improves cardiac and hepatic functions, the underlying mechanisms remain unclear. Because 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 after T-H. To test this hypothesis, male Sprague-Dawley rats ( approximately 300 g) underwent
laparotomy and
hemorrhagic shock (35-40 mmHg for approximately 90 min) followed by
resuscitation with four times the shed blood volume in the form of Ringer
lactate. 17beta-estradiol (1 mg/kg body wt) 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 maximal rate of left ventricular pressure. Liver function as determined by bile production and
indocyanine green clearance was also compromised after T-H and
resuscitation. This was accompanied by an increase in plasma
alanine aminotransferase (ALT) levels and liver perfusate lactic
dehydrogenase levels. Furthermore, circulating levels of
TNF-alpha,
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 after T-H. In the liver, HSP32 and HSP70 were increased after T-H. There was no change in heart HSP70 and liver HSP60 after 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-alpha, and
IL-6. The ability of
estradiol to induce HSPs expression in the heart and the liver suggests that HSPs, in part, mediate the salutary effects of 17beta-estradiol on organ functions after T-H.