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Use of Insulin to Decrease Septic Shock-Induced Myocardial Depression in a Porcine Model

机译:在猪模型中使用胰岛素减少败血症性休克诱发的心肌抑郁

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摘要

Insulin is known to attenuate septic shock-induced myocardial depression. Possible mechanisms include an anti-inflammatory or inotropic effect of insulin. The objective of this study was to determine whether the mechanism of action of insulin in attenuating septic shock-induced myocardial depression is through an immunomodulatory effect. Fourteen pigs were assigned to one of two groups. Both groups received a 4-h infusion of lipopolysaccharide endotoxin from Escherichia coli 0111:B4. Group 2 additionally received insulin at 1.5 U/kg/h with infusions of D50 normal saline and KCl to maintain normal serum glucose and potassium levels. Cardiac function was measured with shortening fraction using transthoracic echocardiogram. Plasma TNF-α, IL-1β, and IL-6 levels were obtained every 30 min. Postmortem cytokine analysis and histomorphology were performed on the heart tissue. Although insulin attenuated septic shock-induced myocardial depression, this was not due to an anti-inflammatory effect and, therefore, likely resulted from an inotropic effect of insulin.
机译:已知胰岛素可以减轻败血性休克引起的心肌抑制。可能的机制包括胰岛素的抗炎或正性肌力作用。这项研究的目的是确定胰岛素在减轻败血性休克引起的心肌抑制中的作用机制是否是通过免疫调节作用。将十四头猪分为两组。两组均接受来自大肠杆菌0111:B4的脂多糖内毒素的4小时输注。第2组还接受1.5 U / kg / h的胰岛素注射,同时注入D50生理盐水和KCl以维持正常的血清葡萄糖和钾水平。使用胸腔超声心动图以缩短的分数测量心脏功能。每30分钟获得一次血浆TNF-α,IL-1β和IL-6水平。在心脏组织上进行死后细胞因子分析和组织形态学。尽管胰岛素减轻了败血性休克引起的心肌抑制,但这不是由于抗炎作用,因此很可能是由于胰岛素的正性肌力作用引起的。

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