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J Cardiovasc Thorac Res. 2015;7(3):81-6. doi: 10.15171/jcvtr.2015.19.

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

Author information

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 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.

KEYWORDS:

Endotoxemia; Myocardium Ischemia; Reperfusion Injury; Tumor Necrosis Factor-Alpha

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