Nader Nader D, Asgeri Mehrdad, Davari-Farid Sina, Pourafkari Leili, Ahmadpour Faraz, Porhomayon Jahan, Javadzadeghan Hassan, Negargar Sohrab, Knight Paul R
Department of Anesthesiology, University at Buffalo, Buffalo, NY, USA.
Private Practicing Gastroenterologist, Cleveland Area, OH, USA.
J Cardiovasc Thorac Res. 2015;7(3):81-6. doi: 10.15171/jcvtr.2015.19.
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.
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.
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.
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.
心肌缺血可能与脓毒症和炎症同时发生并相互作用。我们的目的是研究细菌内毒素在急性缺血期间对心肌功能和细胞损伤的影响。
给兔子递增剂量的大肠杆菌脂多糖（LPS）或生理盐水进行预处理。通过结扎左前降支动脉50分钟诱导心肌缺血。另外使用可溶性肿瘤坏死因子受体（S-TNFaR）来阻断LPS的作用。
收缩期dp/dt测定的心室收缩力从2445±1298mmHg/s降至1422±944mmHg/s，P = 0.019。缺血后作为舒张功能指标的等容舒张时间从50±18ms延长至102±64ms。低浓度LPS（<1μg）预处理对dp/dt无影响，而高浓度时它会抑制收缩力并延长等容舒张时间。缺血后心肌肌钙蛋白I水平测定的细胞损伤增加至15.1±3.2ng/dL，并随着更高剂量的LPS持续升高。虽然阻断肿瘤坏死因子α（TNFα）不能改善缺血后的心肌收缩力，但它消除了LPS的额外有害作用。
较低剂量的LPS对心肌功能没有有害影响，而较高剂量的这种内毒素会导致心脏功能障碍和损伤程度增加。
