Microvascular permeability during experimental human endotoxemia: an open intervention study.
Microvascular permeability during experimental human endotoxemia: an open intervention study.
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DOI：
10.1186/cc3050
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发表时间：
2005-04
期刊：
影响因子：
--
通讯作者：
van der Hoeven JG
中科院分区：
文献类型：
--
作者：
van Eijk LT;Pickkers P;Smits P;van den Broek W;Bouw MP;van der Hoeven JG
感染性休克与微血管通透性增加有关。作为研究脓毒症病理生理学的模型，内毒素对人体的给药促进了对炎症、凝血和心血管效应的研究。本研究旨在确定是否可以将内毒素给予人类志愿者作为研究脓毒症相关微血管通透性增加的模型。在一所大学医疗中心进行的一项开放干预研究中，16名健康志愿者在重症监护室的研究室接受了评估。8人静脉注射内毒素（2 ng/kg大肠杆菌O 113），8人作为对照组。在给予内毒素（n = 8）或安慰剂（n = 8）之前和之后5小时，通过三种不同的方法评估微血管渗透性：I125-白蛋白的跨毛细血管逃逸率;静脉闭塞应变计体积描记术以确定过滤能力;和生物电阻抗分析以确定细胞外和总身体水分。给予内毒素导致促炎细胞因子、体温、流感样症状和心血管变化的预期增加。与对照组比较，差异均有统计学意义。在内毒素组中，所有微血管通透性参数与基线相比均无变化：I125-白蛋白的跨毛细血管逃逸率从7.2 ± 0.6%/h变为7.7 ± 0.9%/h，滤过能力从5.0 ± 0.3 ml/min/100 ml mmHg × 10-3变为4.2 ± 0.4 ml/min/100 ml mmHg × 10-3;细胞外/全身水从0.42 ± 0.01升/升变为0.40 ± 0.01升/升（所有差异均不显著）。虽然实验性人类内毒素血症经常被用作研究脓毒症相关病理生理学的模型，但使用三种不同的方法无法检测到内毒素诱导的体内微血管通透性增加。对人类志愿者给予内毒素不适合作为研究微血管通透性变化的模型。
Septic shock is associated with increased microvascular permeability. As a model for study of the pathophysiology of sepsis, endotoxin administration to humans has facilitated research into inflammation, coagulation and cardiovascular effects. The present study was undertaken to determine whether endotoxin administration to human volunteers can be used as a model to study the sepsis-associated increase in microvascular permeability. In an open intervention study conducted in a university medical centre, 16 healthy volunteers were evaluated in the research unit of the intensive care unit. Eight were administered endotoxin intravenously (2 ng/kg Escherichia coli O113) and eight served as control individuals. Microvascular permeability was assessed before and 5 hours after the administration of endotoxin (n = 8) or placebo (n = 8) by three different methods: transcapillary escape rate of I125-albumin; venous occlusion strain-gauge plethysmography to determine the filtration capacity; and bioelectrical impedance analysis to determine the extracellular and total body water. Administration of endotoxin resulted in the expected increases in proinflammatory cytokines, temperature, flu-like symptoms and cardiovascular changes. All changes were significantly different from those in the control group. In the endotoxin group all microvascular permeability parameters remained unchanged from baseline: transcapillary escape rate of I125-albumin changed from 7.2 ± 0.6 to 7.7 ± 0.9%/hour; filtration capacity changed from 5.0 ± 0.3 to 4.2 ± 0.4 ml/min per 100 ml mmHg × 10-3; and extracellular/total body water changed from 0.42 ± 0.01 to 0.40 ± 0.01 l/l (all differences not significant). Although experimental human endotoxaemia is frequently used as a model to study sepsis-associated pathophysiology, an endotoxin-induced increase in microvascular permeability in vivo could not be detected using three different methods. Endotoxin administration to human volunteers is not suitable as a model in which to study changes in microvascular permeability.
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影响因子：
38.9
作者：
CHIOLERO, RL;GAY, LJ;SCHUTZ, Y
通讯作者：
SCHUTZ, Y
影响因子：
8.8
作者：
Holbeck, S;Grände, PO
通讯作者：
Grände, PO
影响因子：
2.8
作者：
MARTICH, GD;BOUJOUKOS, AJ;SUFFREDINI, AF
通讯作者：
SUFFREDINI, AF
影响因子：
11.8
作者：
Bethell, DB;Gamble, J;Day, NPJ
通讯作者：
Day, NPJ
影响因子：
5
作者：
LASZLO, F;WHITTLE, BJR;MONCADA, S
通讯作者：
MONCADA, S