The Effect of Lipopolysaccharide on Ischemic-Reperfusion Injury of Heart: A Double Hit Model of Myocardial Ischemia and Endotoxemia

Introduction: myocardial ischemia may coincide and interact with sepsis and inflammation. our objective was to examine the effects of bacterial endotoxin on myocardial functions and cell injury during acute ischemia. methods: rabbits were pretreated with incremental doses of e. coli lipopolysaccharide (lps) or normal saline. myocardial ischemia was induced by 50-minute occlusion of left anterior descending artery. s-tnfar was additionally used to block the effects lps. results: ventricular contractility as it was measured by dp/dt during systole decreased from 2445± 1298 to 1422 ± 944 mm hg/s, p = .019. isovolumetric relaxation time as an index of diastolic function was prolonged from 50±18 ms to 102± 64 ms following ischemia. pretreatment with low concentrations of lps (<1 μg) had no effect on dp/dt, while at higher concentrations it suppressed both contractility and prolonged ivrt. cell injury as measured by cardiac troponin i level increased to 15.1± 3.2 ng/dl following ischemia and continued to rise with higher doses of lps. while blocking tnfa did not improve the myocardial contractility after ischemia, it eliminated additional deleterious effects of lps. conclusion: lower doses of lps had no deleterious effect on myocardial function, whereas higher doses of this endotoxin cause cardiac dysfunction and increased extent of injury.