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Center for Surgical Research and Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence, Rhode Island 02903
Although studies have shown that
induction of the heat shock proteins (HSPs), such as HSP-70, has
various beneficial effects after ischemia-reperfusion, it
remains unknown whether prior induction of HSP-70 has any salutary
effects on cardiovascular and hepatocellular functions after
trauma-hemorrhage and resuscitation. Male rats were exposed to heat
stress (41°C, 15 min) and then allowed to recover for 24 h at room
temperature (21°C). The rats then underwent laparotomy (i.e.,
trauma induced) and were bled 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. Animals were then resuscitated
with four times the volume of shed blood with Ringer lactate over 60 min. The maximal rate of the left ventricular pressure increase or
decrease was measured up to 4 h after resuscitation. Cardiac output,
hepatocellular function, plasma levels of tumor necrosis factor-
(TNF-), and interleukin-6 (IL-6) were determined at 4 h after
resuscitation. Cardiac and hepatic tissue were examined for HSP-70 by
Western blot analysis. Left ventricular performance, cardiac output,
and hepatocellular function decreased significantly following
trauma-hemorrhage. Plasma levels of TNF- and IL-6 were also
significantly increased. However, prior heat stress attenuated
cardiovascular and hepatocellular dysfunction, decreased circulating
levels of proinflammatory cytokines following trauma-hemorrhage, and
was associated with an increased abundance of HSP-70 in the heart and
liver. Our data, therefore, suggest that preinduction of HSP-70
protects cardiovascular and hepatocellular functions following
trauma-hemorrhage and resuscitation.
heat shock protein-70; cardiac performance; cardiac output; hepatocellular function; hemorrhagic shock; tumor necrosis factor-; interleukin-6
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