Estimation of pulmonary interstitial fluid space compliance in isolated perfused rabbit lung

Magno, Michael G.; Atkinson, Beryl A.; Katz, Adam J.; Fishman, Alfred P.

doi:10.1152/jappl.1980.48.4.677

Cited by 12 publications

(2 citation statements)

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“…1; Table 1). The values of Kf,c and vascular compliance ( Table 2) corresponded to those previously described for this model (Seeger et al, submitted) and were in the same range as the values given from other laboratories for similar isolated-lung preparations (0.8 [31], 1.2 [58], 3.4 [37], and 4.7 cm3 per cm H20 per s per g [wet weight] of the lung x 10-4 [D. F. Kern, C. Kilven, and A. G. Malik, Microvasc. Res.…”

supporting

confidence: 77%

Pulmonary microvascular injury induced by Pseudomonas aeruginosa cytotoxin in isolated rabbit lungs

Seeger¹,

Walmrath²,

Neuhof³

et al. 1986

Infect Immun

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The effects of Pseudomonas aeruginosa cytotoxin on the pulmonary microvasculature were studied in blood-free, perfused, isolated rabbit lungs. Cytotoxin was administered to the recirculating Krebs Henseleit albumin (1%) buffer during two consecutive 30-min-perfusion phases (phases 1 and 2) at a concentration of 13 ,ug/ml, followed by a third perfusion phase (phase 3) without toxin. After perfusion phases 2 and 3, the capillary filtration coefficient (Kf,c) and vascular compliance were determined gravimetrically from two-step microvascular pressure increments under zero-flow conditions. Cytotoxin caused a continuous release of K+ and lactate dehydrogenase, which started within the first 5 min and amounted to about 50% of the total lung cellular K+ and 5 to 7% of the total lactate dehydrogenase by the end of the experiment. The toxin caused the continuous generation of prostaglandin 12, which was detectable in the perfusates of all perfusion phases at maximum values five times above the control values and which was measured in the bronchoalveolar lavage fluid at the end of the experiment. Thromboxane generation in toxin-treated lungs did not significantly exceed that of control lungs or of lungs with mechanically induced edema. Cytotoxin caused a gradual increase in pulmonary vascular resistance, to maximum values 2.5 times above the control, starting within 1 min; the increase was partially reversible after washout of the toxin. After a lag period of 20 to 30 min, the lungs gained weight, amounting to a mean gain of 9.1 g at the end of the experiments. After perfusion phases 2 and 3, an almost fourfold increase in Kf1,, which was not reversible after washout of the toxin, was measured, whereas the values of vascular compliance were not altered. We conclude that pseudomonal cytotoxin may be an important factor in the pathogenesis of prolonged microvascular injury, encountered in states of P. aeruginosa sepsis or acute lung failure with secondarily acquired P. aeruginosa pneumonia.

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supporting

confidence: 77%

Pulmonary microvascular injury induced by Pseudomonas aeruginosa cytotoxin in isolated rabbit lungs

Seeger¹,

Walmrath²,

Neuhof³

et al. 1986

Infect Immun

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“…In particular, when inflow rises above outflow, interstitial compliance determines how much interstitial fluid pressure rises. Increases in interstitial hydrostatic pressure not only act to decrease flow into the interstitium, but also increase flow out via the lymphatics (48). Even though these are relatively well-understood phenomena and their interaction is governed by conservation of mass, the resulting behavior can be exceedingly complex.…”

mentioning

confidence: 99%

Edemagenic gain and interstitial fluid volume regulation

Dongaonkar

Quick²,

Stewart³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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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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Pulmonary Interstitial Spaces and Lymphatics

Taylor

Parker

1985

Comprehensive Physiology

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Estimation of pulmonary interstitial fluid space compliance in isolated perfused rabbit lung

Cited by 12 publications

References 0 publications

Pulmonary microvascular injury induced by Pseudomonas aeruginosa cytotoxin in isolated rabbit lungs

Pulmonary microvascular injury induced by Pseudomonas aeruginosa cytotoxin in isolated rabbit lungs

Edemagenic gain and interstitial fluid volume regulation

Pulmonary Interstitial Spaces and Lymphatics

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