Tabriz University of Medical Sciences Journal of Cardiovascular and Thoracic Research 2008-5117 7 3 2015 09 02 The Effect of Lipopolysaccharide on Ischemic-Reperfusion Injury of Heart: A Double Hit Model of Myocardial Ischemia and Endotoxemia 81 86 10.15171/jcvtr.2015.19 EN Nader D. Nader Mehrdad Asgeri Sina Davari-Farid Leili Pourafkari Faraz Ahmadpour Jahan Porhomayon Hassan Javadzadeghan Sohrab Negargar Paul R. Knight III Journal Article 10.15171/jcvtr.2015.19 2015 07 13 2015 08 01 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 mmHg/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.