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在食蟹猴中,高动力型严重血管内脓毒症依赖于液体输注。

Hyperdynamic severe intravascular sepsis depends on fluid administration in cynomolgus monkey.

作者信息

Carroll G C, Snyder J V

出版信息

Am J Physiol. 1982 Jul;243(1):R131-41. doi: 10.1152/ajpregu.1982.243.1.R131.

Abstract

A new model of high cardiac output septic shock in primates is presented that includes hemodynamic and metabolic effects of separate and combined infusions of normal saline and live Escherichia coli. In monkeys receiving ketamine anesthesia, cardiac output (QT) increased with saline loading but not significantly with bacterial infusion, and bacterial infusion without saline never significantly increased QT. Depressed oxygen consumption (VO2) was reversed with saline loading. In spite of continuing E. coli infusion, radiolabeled microspheres showed no increase in systemic anatomic shunt when QT was elevated. It is perceived that the tissue dysfunction associated with sepsis, which is called septic shock, and elevation of cardiac output are related only indirectly. High cardiac output only reflects an adequate volume status in a stressed individual; some of the afferent stress signals can be related to the septic state, but no specific or direct relationship is involved. In general, shock as indicated by a depression of VO2 does not appear to occur when QT is increased.

摘要

本文提出了一种灵长类动物高心输出量脓毒性休克的新模型,该模型包括单独和联合输注生理盐水和活大肠杆菌的血流动力学和代谢效应。在接受氯胺酮麻醉的猴子中,心输出量(QT)随生理盐水输注而增加,但随细菌输注无显著增加,且无生理盐水的细菌输注从未显著增加QT。生理盐水输注可逆转氧耗(VO2)降低的情况。尽管持续输注大肠杆菌,但当QT升高时,放射性微球显示全身解剖分流并未增加。据认为,与脓毒症相关的组织功能障碍(即脓毒性休克)与心输出量升高仅间接相关。高心输出量仅反映了应激个体的充足容量状态;一些传入应激信号可能与脓毒症状态有关,但不存在特定或直接关系。一般来说,当QT增加时,似乎不会出现VO2降低所表明的休克。

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