Endotoxin induces cardiac heat shock protein 70 and resistance to
endotoxemic myocardial depression in the rat.
Meng, Xianzhong, James M. Brown, Lihua Ao, Steven K. Nordeen, Wilbur
Franklin, Alden H. Harken, Anirban Banerjee.
Departments of Surgery and Pathology, University of Colorado Health
Sciences Center, Denver, Colorado, 80262
APStracts 3:0153C, 1996.
Endotoxin (bacterial lipopolysaccharide, LPS) depresses myocardial
function. However, heat shock and sub-lethal LPS can confer cardiac
resistance to post-ischemic dysfunction. We hypothesized that a prior
exposure to LPS stress induces the expression of cardiac heat shock
protein (HSP) 70 and resistance to endotoxemic myocardial depression.
Moreover, induction of HSP70 by hyperthermia should also increase
cardiac resistance to LPS toxicity. LPS (500 [mu]g/kg, ip) depressed
rat left ventricular developed pressure (LVDP) maximally at 6 hours
(58.4 +/- 3.72 mmHg vs 101 +/- 1.46 mmHg in saline control,
P<0.01), and myocardial contractile function recovered at 24
hours. In rats pretreated with LPS 24 hours earlier, subsequent LPS
exposure did not depress LVDP (97.0 +/- 3.53 mmHg at 6 hours,
P<0.01 vs single exposure). Both LPS and hyperthermia (42 oC, 15
minutes) induced HSP72 mainly in the cardiac interstitial cells
including macrophages at 24 hours after treatment. When hyperthermia
-pretreated animals were similarly challenged with LPS, myocardial
depression at 6 hours was partially abrogated (LVDP 80.1 +/- 5.67
mmHg vs 62.2 +/- 4.91 mmHg in sham+LPS group, P<0.01). We
conclude that LPS induces HSP70 in rat heart, and that an exposure to
LPS or heat stress confers cardiac resistance to endotoxemic
myocardial depression.
Received 17 November 1995; accepted in final form 3 May 1996.
APS Manuscript Number C693-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96