Effects of induced tolerance to bacterial lipopolysaccharide on myocardial infarct size in rats

Abstract

LPS desensitization in rats for 1 week prior to coronary occlusion inhibited activation of circulating PMNs 3 days after reperfusion following 45 min of coronary occlusion. LPS also is well-known to induce heat stress proteins and may affect other protective mechanisms. These actions are associated with a significant reduction in myocardial infarct size in LPS-tolerant animals compared to untreated controls.