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在人类脓毒症犬类模型中,大肠杆菌攻击下的心血管功能表现

Cardiovascular performance with E. coli challenges in a canine model of human sepsis.

作者信息

Natanson C, Danner R L, Fink M P, MacVittie T J, Walker R I, Conklin J J, Parrillo J E

机构信息

Critical Care Medicine Department, National Institutes of Health, Bethesda 20892.

出版信息

Am J Physiol. 1988 Mar;254(3 Pt 2):H558-69. doi: 10.1152/ajpheart.1988.254.3.H558.

DOI:10.1152/ajpheart.1988.254.3.H558
PMID:3279822
Abstract

We investigated cardiovascular dysfunction by injecting lethal and nonlethal bacterial challenges into conscious dogs. E. coli bacteria of varying numbers were placed in a peritoneal clot. Cardiovascular function was studied with simultaneous radionuclide scans and thermodilution cardiac outputs. In surviving animals, the number of bacteria in the clot increased as the corresponding systolic cardiac function decreased (P = 0.01). Cardiac function was measured by left ventricular (LV) ejection fraction (EF) and LV function curves [LV stroke work index (LVSWI) vs. end-diastolic volume index (EDVI), and peak systolic pressure vs. end-systolic volume index]. Furthermore, the diastolic volume-pressure relationship of survivors shifted progressively to the right [i.e., increasing EDVI (P less than 0.02) with minimal change (P = NS) in LV filling pressure]. This increase in LV size was associated with maintenance of measures of cardiac performance [stroke volume index (SVI) and stroke work index (SWI)] at similar levels. Death occurred only in the group with the highest bacterial dose. Compared with survivors receiving the same number of bacteria, nonsurvivors had a decrease in (P less than 0.05) LV size, a leftward shift (P less than 0.01) in LV diastolic volume-pressure relationship, and a decrease in both LVSWI and SVI (possibly related to volume and/or LV functional status). Data from survivors suggest that increasing the number of bacteria produces changes in myocardial compliance and contractility. These changes increase LV size (preload), a major determinant of cardiac performance that possibly enhances survival.

摘要

我们通过向清醒的犬类注射致死性和非致死性细菌刺激来研究心血管功能障碍。将不同数量的大肠杆菌置于腹腔血凝块中。通过同步放射性核素扫描和热稀释心输出量来研究心血管功能。在存活的动物中,血凝块中的细菌数量随着相应的心脏收缩功能下降而增加(P = 0.01)。心脏功能通过左心室(LV)射血分数(EF)和左心室功能曲线[左心室每搏功指数(LVSWI)与舒张末期容积指数(EDVI),以及收缩压峰值与收缩末期容积指数]来测量。此外,存活动物的舒张期容积 - 压力关系逐渐向右移动[即,EDVI增加(P小于0.02),而左心室充盈压变化最小(P =无显著性差异)]。左心室大小的这种增加与心脏性能指标[每搏量指数(SVI)和每搏功指数(SWI)]维持在相似水平有关。仅在细菌剂量最高的组中发生死亡。与接受相同数量细菌的存活者相比,非存活者的左心室大小减小(P小于0.05),左心室舒张期容积 - 压力关系向左移动(P小于0.01),并且LVSWI和SVI均降低(可能与容量和/或左心室功能状态有关)。来自存活者的数据表明,增加细菌数量会导致心肌顺应性和收缩性发生变化。这些变化增加了左心室大小(前负荷),这是心脏性能的一个主要决定因素,可能会提高生存率。

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