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[外科重症监护中的感染性休克与多器官功能衰竭。关于肺和肠道功能障碍分析的动物实验模型]

[Septic shock and multiple organ failure in surgical intensive care. An animal experiment model on the analysis of pulmonary and intestinal dysfunction].

作者信息

Töns C, Klosterhalfen B, Klinge U, Kirkpatrick C J, Mittermayer C, Schumpelick V

机构信息

Chirurgische Klinik, RWTH Aachen.

出版信息

Langenbecks Arch Chir. 1993;378(4):217-32. doi: 10.1007/BF00184364.

Abstract

The study deals with an animal model for the problems of surgical intensive care patients. Following repeated applications of E. coli endotoxin WO 111:B4 under standard conditions, specific hemodynamic and biochemical (TNF, TXA2, PGI2, IL-6, PAF) and morphological (endothelium of the lung) alterations were detected. ARDS patterns induced by the sepsis were analyzed by high-frequency measurement of pressure and flow (385 measurements per breathing cycle). The role of the intestine in sepsis was investigated by ion-selective monitoring of surface potassium activity comparing mucosa and serosa. Every injection of endotoxin was followed by a selective increase of the potassium activity revealing relative ischemia induced by the endotoxin. The profile of the potassium levels on the surface correlates both with the cardiac output and with the prostacyclin levels. The continuous narrowing of the difference between mucosa and serosa, potassium during the period of investigation can be regarded as evidence for pathologic change in permeability fostering the septic course.

摘要

该研究涉及一种针对外科重症监护患者问题的动物模型。在标准条件下反复应用大肠杆菌内毒素WO 111:B4后,检测到特定的血流动力学和生化指标(肿瘤坏死因子、血栓素A2、前列环素、白细胞介素-6、血小板活化因子)以及形态学变化(肺内皮)。通过高频测量压力和流量(每个呼吸周期385次测量)分析脓毒症诱导的急性呼吸窘迫综合征模式。通过离子选择性监测黏膜和浆膜表面钾活性来研究肠道在脓毒症中的作用。每次注射内毒素后,钾活性选择性增加,揭示了内毒素诱导的相对缺血。表面钾水平的变化曲线与心输出量和前列环素水平均相关。在研究期间,黏膜和浆膜之间钾差异的持续缩小可被视为促进脓毒症病程的通透性病理变化的证据。

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