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严重烧伤后多器官功能障碍综合征(MODS)发病机制的系列实验与临床研究

Serial experimental and clinical studies on the pathogenesis of multiple organ dysfunction syndrome (MODS) in severe burns.

作者信息

Huang Y S, Yang Z C, Liu X S, Chen F M, He B B, Li A, Crowther R S

机构信息

Institute of Burn Research, Southwestern Hospital, Third Military Medical University, Chongqing, People's Republic of China.

出版信息

Burns. 1998 Dec;24(8):706-16. doi: 10.1016/s0305-4179(98)00123-5.

DOI:10.1016/s0305-4179(98)00123-5
PMID:9915670
Abstract

These serial clinical and experimental studies were designed to clarify the pathogenesis of postburn MODS. Both animal and clinical studies were performed. In animal experiments, 46 male cross-bred dogs were cannulated with Swan-Ganz catheters and 39 of them were inflicted with 50% TBSA third degree burns (7 were used as controls). The burned dogs were randomly divided into 4 groups: immediate infusion, delayed infusion, delayed fast infusion and delayed fast infusion combined with ginsenosides. All dogs were kept under constant barbiturate sedation during the whole study period. Hemodynamics, visceral MDA, mitochondrial respiratory control rate (RCR) and ADP/O ratio, ATP, succinic dehydrogenase (SDH), organ water content as well as light and electron microscopy of visceral tissues were determined. In the clinical study, 61 patients with extensive deep burns were chosen, of which 16 sustained MODS. Plasma TXB2/6-keto-PGF1alpha ratio, TNF, SOD, MDA, circulatory platelet aggregate ratio (CPAR), PGE2, interleukin-1, total organ water content and pathological observations of visceral tissues from patients who died of MODS were carried out. Results demonstrated that ischemic-reperfusion damage due to severe shock, sepsis and inhalation injury are three main causes of postburn death. All inflammatory mediators increased markedly in both animals and patients who sustained organ damage or MODS. SDH, RCR, ADP/O and ATP decreased significantly. These findings suggested that ischemic damage and systemic inflammatory response syndrome (SIRS) initiated by mediators or cytokines might be important in the pathogenesis of postburn MODS.

摘要

这些系列临床和实验研究旨在阐明烧伤后多器官功能障碍综合征(MODS)的发病机制。同时进行了动物和临床研究。在动物实验中,46只雄性杂种犬插入了Swan-Ganz导管,其中39只遭受了50%体表面积的三度烧伤(7只作为对照)。烧伤犬被随机分为4组:即刻输液组、延迟输液组、延迟快速输液组和延迟快速输液联合人参皂甙组。在整个研究期间,所有犬均持续接受巴比妥类药物镇静。测定血流动力学、内脏丙二醛(MDA)、线粒体呼吸控制率(RCR)和ADP/O比值、三磷酸腺苷(ATP)、琥珀酸脱氢酶(SDH)、器官含水量以及内脏组织的光镜和电镜检查。在临床研究中,选择了61例大面积深度烧伤患者,其中16例发生了MODS。对死于MODS患者的血浆TXB2/6-酮-PGF1α比值、肿瘤坏死因子(TNF)、超氧化物歧化酶(SOD)、MDA、循环血小板聚集率(CPAR)、前列腺素E2(PGE2)、白细胞介素-1、总器官含水量以及内脏组织进行了病理观察。结果表明,严重休克、脓毒症和吸入性损伤所致的缺血-再灌注损伤是烧伤后死亡的三个主要原因。在发生器官损害或MODS的动物和患者中,所有炎症介质均显著增加。SDH、RCR、ADP/O和ATP显著降低。这些发现提示,由介质或细胞因子引发的缺血损伤和全身炎症反应综合征(SIRS)可能在烧伤后MODS的发病机制中起重要作用。

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