Preinduction of heat shock proteins protects cardiac and hepatic functionsfollowing trauma and hemorrhage

Although studies have shown that induction of the heat shock proteins (HSPs ), such as HSP-70, has various beneficial effects after ischemia-reperfusio n, it remains unknown whether prior induction of HSP-70 has any salutary ef fects on cardiovascular and hepatocellular functions after trauma-hemorrhag e and resuscitation. Male rats were exposed to heat stress (41 degrees C, 1 5 min) and then allowed to recover for 24 h at room temperature (21 degrees C). The rats then underwent laparotomy (i.e., trauma induced) and were ble d to and maintained at a mean arterial pressure of 40 mmHg until 40% of the maximal shed blood volume was returned in the form of Ringer lactate. Anim als were then resuscitated with four times the volume of shed blood with Ri nger lactate over 60 min. The maximal rate of the left ventricular pressure increase or decrease was measured up to 4 h after resuscitation. Cardiac o utput, hepatocellular function, plasma levels of tumor necrosis factor-alph a (TNF-alpha), and interleukin-6 (IL-6) were determined at 4 h after resusc itation. Cardiac and hepatic tissue were examined for HSP-70 by Western blo t analysis. Left, ventricular performance, cardiac output, and hepatocellul ar function decreased significantly following trauma-hemorrhage. Plasma lev els of TNF-alpha and IL-6 were also significantly increased. However, prior heat stress attenuated cardiovascular and hepatocellular dysfunction, decr eased circulating levels of proinflammatory cytokines following trauma-hemo rrhage, and was associated with an increased abundance of HSP-70 in the hea rt and liver. Our data, therefore, suggest that preinduction of HSP-70 prot ects cardiovascular and hepatocellular functions following trauma-hemorrhag e and resuscitation.