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Submitted: 13 Jul 2015
Accepted: 01 Aug 2015
ePublished: 02 Sep 2015
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J Cardiovasc Thorac Res. 2015;7(3): 81-86.
doi: 10.15171/jcvtr.2015.19
PMID: 26430494
PMCID: PMC4586603
  Abstract View: 1444
  PDF Download: 1838

Original Article

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

Nader D. Nader 1 * , Mehrdad Asgeri 2, Sina Davari-Farid 1, Leili Pourafkari 3, Faraz Ahmadpour 4, Jahan Porhomayon 1, Hassan Javadzadeghan 1, Sohrab Negargar 3, Paul R. Knight III 1

1 Department of Anesthesiology, University at Buffalo, Buffalo, NY, USA
2 Private Practicing Gastroenterologist, Cleveland Area, OH, USA
3 Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
4 Virox Inc., Oakville, Ontario, Canada

Abstract

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.
Keywords: Myocardium Ischemia, Reperfusion Injury, Tumor Necrosis Factor-Alpha, Endotoxemia
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Abstract View: 1444

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