期刊
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
卷 294, 期 2, 页码 R651-R659出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00354.2007
关键词
Starling-Landis equation; mathematical model; edematogenic
类别
资金
- NHLBI NIH HHS [K25 HL 070608] Funding Source: Medline
- PHS HHS [CDC 620069, CDC 623086] Funding Source: Medline
Under physiological conditions, interstitial fluid volume is tightly regulated by balancing microvascular filtration and lymphatic return to the central venous circulation. Even though microvascular filtration and lymphatic return are governed by conservation of mass, their interaction can result in exceedingly complex behavior. Without making simplifying assumptions, investigators must solve the fluid balance equations numerically, which limits the generality of the results. We thus made critical simplifying assumptions to develop a simple solution to the standard fluid balance equations that is expressed as an algebraic formula. Using a classical approach to describe systems with negative feedback, we formulated our solution as a gain relating the change in interstitial fluid volume to a change in effective microvascular driving pressure. The resulting edemagenic gain is a function of microvascular filtration coefficient (K-f), effective lymphatic resistance (R-L), and interstitial compliance (C). This formulation suggests two types of gain: multivariate dependent on C, R-L, and K-f, and compliance-dominated approximately equal to C. The latter forms a basis of a novel method to estimate C without measuring interstitial fluid pressure. Data from ovine experiments illustrate how edemagenic gain is altered with pulmonary edema induced by venous hypertension, histamine, and endotoxin. Reformulation of the classical equations governing fluid balance in terms of edemagenic gain thus yields new insight into the factors affecting an organ's susceptibility to edema.
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