Arteriosclerosis, thrombosis, and vascular biology
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Arterioscler. Thromb. Vasc. Biol. · Sep 1999
Endotoxin induces a second window of protection in the rat heart as determined by using p-nitro-blue tetrazolium staining, cardiac troponin T release, and histology.
Pretreatment of rats with small doses of lipopolysaccharide (LPS), eg, for 24 hours, attenuates the cardiac dysfunction caused by subsequent period of myocardial ischemia. This phenomenon of enhanced tolerance to an ischemic insult has been termed "second window of protection." Although the cardioprotective effects of LPS were first reported in 1989, it is still unclear whether the observed attenuation by LPS of the ischemia-induced cardiac dysfunction is indeed secondary to the protection of cardiac myocytes against ischemic cell injury and death. This study was designed to investigate the effects of "preconditioning" with LPS on cell injury caused by regional myocardial ischemia and reperfusion in the anesthetized rat. ⋯ Pretreatment (24 hours, as above) of rats with LPS also reduced the release of cardiac troponin T from 58+/-13 ng/mL (saline-control) to 16+/-9 ng/mL. In contrast, pretreatment of rats with LPS (2 hours, as above) did not affect infarct size (56+/-8%, n=6), cardiac troponin T release, or the histological parameters of cell injury. These data provide the first conclusive evidence that pretreatment of rats with a bolus of LPS 24 hours before intervention reduces the cell injury and death caused by a subsequent period of myocardial ischemia and reperfusion.