Plante G E, Chakir M, Lehoux S, Lortie M
Department of Medicine, University of Sherbrooke, Quebec.
Can J Cardiol. 1995 Oct;11(9):788-802.
To review the mechanisms of disease on the basis of dysfunction in body fluid distribution secondary to abnormalities in capillary permeability and plasma membrane transport disorders, leading to quantitative and qualitative alterations of the interstitial space, a mainly strategic compartment positioned between the microcirculation and cell mass.
The recent literature on the mechanisms involved in the control of body fluid balance, with special reference to microcirculation and interstitial compartment physiology, as well as published and unpublished original data from the authors laboratory.
To illustrate the importance of capillary permeability dysfunction in the development of disease, animal (rat and dog) models of chronic renal failure, acute diuretic-induced fluid depletion, diabetes mellitus, arterial hypertension and ischemia-reperfusion of the kidney were used in an attempt to show that in all these experimental models, basic capillary permeability dysfunction (measured by the extravasation of Evans blue, a marker of albumin leakage) develops in specific microcirculation beds. As a consequence, tissue edema (interstitial and/or cellular) develops and likely impairs the traffic of nutrients and waste products to and from the cellular mass, and/or challenges the microcirculation, leading to organ damage. Kidney dysfunction is measured by conventional clearance methods (renal hemodynamics and tubular function). In some models, the eventual mediators of vascular abnormality are examined by use of pharmacological tools.
The critical role of microcirculation dysfunctions, in particular capillary permeability, resulting in interstitial compositional changes is presented as the basis of disease. The apparent specificity of target organ damage may represent the nonspecific result of physicochemical alteration in the strategic interstitial fluid compartment.
基于毛细血管通透性异常和质膜转运障碍继发的体液分布功能障碍，探讨疾病机制，这种功能障碍会导致间质间隙（微循环与细胞群之间的一个主要关键区域）在数量和质量上发生改变。
近期有关体液平衡调控机制的文献，特别参考了微循环和间质区生理学，以及作者实验室已发表和未发表的原始数据。
为阐明毛细血管通透性功能障碍在疾病发生中的重要性，使用了慢性肾衰竭、急性利尿导致的体液耗竭、糖尿病、动脉高血压和肾脏缺血再灌注的动物（大鼠和狗）模型，试图表明在所有这些实验模型中，特定微循环床会出现基本的毛细血管通透性功能障碍（通过伊文思蓝外渗来测量，伊文思蓝是白蛋白渗漏的标志物）。结果，组织水肿（间质和/或细胞性）形成，可能会损害营养物质和代谢废物进出细胞群的运输，和/或对微循环造成挑战，导致器官损伤。通过传统清除方法（肾血流动力学和肾小管功能）来测量肾功能障碍。在一些模型中，使用药理学工具研究血管异常的最终介质。
微循环功能障碍，尤其是毛细血管通透性导致间质成分改变的关键作用，被视为疾病的基础。靶器官损伤的明显特异性可能代表了关键间质液区物理化学改变的非特异性结果。
