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犬输注肿瘤坏死因子-α后左心室收缩力降低。

Decrease in left ventricular contractility after tumor necrosis factor-alpha infusion in dogs.

作者信息

Walley K R, Hebert P C, Wakai Y, Wilcox P G, Road J D, Cooper D J

机构信息

Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, British Columbia, Canada.

出版信息

J Appl Physiol (1985). 1994 Mar;76(3):1060-7. doi: 10.1152/jappl.1994.76.3.1060.

DOI:10.1152/jappl.1994.76.3.1060
PMID:8005845
Abstract

Whether systolic contractility or diastolic compliance changes soon after tumor necrosis factor-alpha (TNF-alpha) exposure is not known. Accordingly, we measured hemodynamics, left ventricular contractility using the slope of the end-systolic pressure-volume relationship, and diastolic pressure-volume relationships in six control dogs and in six dogs receiving 60 micrograms.kg-1.h-1 i.v. of TNF-alpha. Mean aortic pressure decreased by 22% 1 h after TNF-alpha infusion and remained decreased (P < 0.05). Cardiac output increased by 19% 1 h after TNF-alpha infusion and remained significantly greater than control values (P < 0.05). Left ventricular contractility decreased by 23% (P < 0.05) 1 h after TNF-alpha infusion and decreased by 52% (P < 0.01) 5 h after TNF-alpha infusion. The diastolic pressure-volume relationship did not change in the TNF-alpha group or the control group. Ejection fraction did not change after TNF-alpha infusion despite the decrease in contractility because afterload decreased. We conclude that TNF-alpha is important in causing the hypotensive, hyperdynamic circulation of sepsis. The new finding that left ventricular contractility is decreased shortly after TNF-alpha infusion suggests that TNF-alpha, or another mediator released very soon after TNF-alpha, is an important myocardial depressant factor.

摘要

肿瘤坏死因子-α(TNF-α)暴露后不久,心脏收缩力或舒张顺应性是否发生变化尚不清楚。因此,我们测量了6只对照犬和6只接受60微克·千克⁻¹·小时⁻¹静脉注射TNF-α的犬的血流动力学、用收缩末期压力-容积关系斜率表示的左心室收缩力以及舒张期压力-容积关系。TNF-α输注1小时后,平均主动脉压下降22%,并持续降低(P<0.05)。TNF-α输注1小时后,心输出量增加19%,且仍显著高于对照值(P<0.05)。TNF-α输注1小时后,左心室收缩力下降23%(P<0.05),TNF-α输注5小时后下降52%(P<0.01)。TNF-α组和对照组的舒张期压力-容积关系均未改变。尽管收缩力下降,但由于后负荷降低,TNF-α输注后射血分数未发生变化。我们得出结论,TNF-α在导致脓毒症的低血压、高动力循环中起重要作用。TNF-α输注后不久左心室收缩力下降这一新发现表明,TNF-α或TNF-α释放后很快释放的另一种介质是一种重要的心肌抑制因子。

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