tbzmedTabriz University of Medical SciencesJCVTRJournal of Cardiovascular and Thoracic ResearchOriginal ArticleJournal of Cardiovascular and Thoracic ResearchThe Effect of Lipopolysaccharide on Ischemic-Reperfusion Injury of Heart: A Double Hit Model of Myocardial Ischemia and EndotoxemiaMyocardial Ischemia and EndotoxemiaD. NaderNaderProfessor at University at Buffalo, Department of AnesthesiologyAsgeriMehrdad, Davari-FaridSina, PourafkariLeili, AhmadpourFaraz, PorhomayonJahan, JavadzadeghanHassan, NegargarSohrab, R. Knight IIIPaul, 92015292015732572015Tabriz University of Medical Sciences2015The Effect of Lipopolysaccharide on Ischemic-Reperfusion Injury of Heart: A Double Hit Model of Myocardial Ischemia and Endotoxemia

<em><strong>Introduction:</strong></em> 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.<em><strong><br /> Methods:</strong></em> 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.<br /> <em><strong>Results:</strong></em> Ventricular contractility as it was measured by dp/dt during systole decreased from 2445&plusmn;1298 to 1422&plusmn;944 mmHg/s, P​=.019. Isovolumetric relaxation time as an index of diastolic function was prolonged from 50&plusmn;18 ms to 102&plusmn;64 ms following ischemia. Pretreatment with low concentrations of LPS (&lt;1 &micro;g) 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&plusmn;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.<em><strong><br /> Conclusion:</strong></em> 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.