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J Thorac Cardiovasc Surg 2002;124:933-941
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Lipopolysaccharide pretreatment attenuates myocardial infarct size: A possible mechanism involving heat shock protein 70-inhibitory B complex and attenuation of nuclear factor B

From the Divisions of Cardiothoracic Surgery and Biochemical Genetics, Tokyo Medical and Dental University Graduate School of Medicine, Tokyo, Japan.

Received for publication Sept 24, 2001. Revisions requested Oct 25, 2001, revisions received Nov 9, 2001. Accepted for publication Dec 7, 2001. Address for reprints: Makoto Sunamori, MD, Professor and Chief, Division of Cardiothoracic Surgery, Tokyo Medical and Dental University Graduate School of Medicine, Bunkyo-ku yushima 1-5-45, Tokyo 113-8519, Japan (E-mail: sunamori.tsrg{at}tmd.ac.jp).

Objective: Lipopolysaccharide pretreatment is known to reduce myocardial infarct size, but the mechanism has not been elucidated. We hypothesized that heat shock protein 70, induced by lipopolysaccharide pretreatment, formed complexes with inhibitory B, thereby inhibiting degradation and attenuating activation of nuclear factor B and cellular injury in rat myocardium.
Methods: Fifteen Sprague-Dawley rats were given saline solution (control group) or lipopolysaccharide. After 48 hours, 5 hearts in each group were excised without ischemia for examination of heat shock protein 70 and inhibitory B levels and detection of heat shock protein 70-inhibitory B complexes. Myocardium from the remaining 10 rats in each group was exposed to 30 minutes of ischemia and 30 minutes of reperfusion (n = 5) to evaluate nuclear factor B activity or to 24 hours of reperfusion (n = 5) to evaluate infarct size.
Results: Infarct size was reduced in the lipopolysaccharide group (P < .05). Nuclear factor B was activated in the control ischemia group and attenuated in the lipopolysaccharide group (P < .05). Heat shock protein 70 levels were increased in the lipopolysaccharide group (P < .05), but inhibitory B levels were similar in both groups. Heat shock protein 70-inhibitory B complexes were detected only in the lipopolysaccharide group. Colocalization of the 2 proteins was observed in the lipopolysaccharide group.
Conclusions: Heat shock protein 70, induced by lipopolysaccharide pretreatment, forms complexes with inhibitory B and attenuates activation of nuclear factor B and myocardial infarct size. Our results suggest that attenuation of nuclear factor B through a mechanism forming heat shock protein 70-inhibitory B complexes might protect the myocardium from ischemia-reperfusion injury.

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