The pulmonary interstitium in capillary exchange.
ABSTRACT When capillaries filter excessive fluid, tissue fluid pressure increases, tissue colloid osmotic pressure decreases, and lymph flow increases. The change in tissue forces and flows have been termed edema safety factors since they act to oppose alterations in pulmonary capillary pressure. It is well known that pulmonary capillary pressure can be acutely increased by approximately 20 mm Hg before fluid enters the alveoli, and that the changes in the tissue forces are responsible for this phenomenon. The decrease in interstitial colloid osmotic pressure appears to account for approximately 50% of the tissue's ability to oppose increases in pulmonary capillary pressure. The tissue colloids change because the capillaries filter a protein-poor fluid, and the exclusion of plasma proteins decreases with increasing interstitial volume. Tissue pressure, at least in the perivascular regions, increases with tissue hydration and provides another major tissue force opposing capillary filtration. The contribution of lymph flow to the overall edema safety factor is difficult to estimate at the present time. However, it is possible that the pressure drop associated with the flow of interstitial fluid between the alveolar septal interstitium and the larger perivascular spaces could serve as an edema safety factor, rather than the standard lymphatic flow pressure drop across the capillary membrane. To calculate the standard lymph flow contribution to the total edema safety factor, total lymph flow [LF] and the filtration coefficient of the capillaries [Kf,c] must be known, i.e., Capillary Wall Drop = LF/Kf,c. For normal lung lymph flows and Kf,c's, it would appear that this factor is small. However, if the total pressure drop for fluid movement through the entire lung tissue is used to estimate the lymphatic factor, then it may represent a major portion of the edema safety factor, i.e., Total Pressure Drop = LF/[Kf,cKf,t]/Kf,c + Kf,t] where Kf,t is the filtration coefficient of the tissues. Tissue forces at different site within the lung tissue are presently under intense investigation in serveral laboratories. The next years should provide the necessary information to discuss fluid accumulation in lung tissue in terms of local transcapillary forces rather than the average forces that are now the "present state of the art."
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ABSTRACT: Pulmonary edema results from increases in pulmonary capillary hydrostatic pressure and microvascular protein permeability. Mediators that induce pulmonary edema can be subdivided into two classes: (1) mediators that alter pulmonary hydrostatic pressure such as serotonin and (2) mediators that increase capillary permeability and result in increased transport of protein. A recognized important permeability increasing factor in the pulmonary microcirculation is the process of neutrophil activation and concomitant mediator release subsequent to neutrophil sequestration. Increased pulmonary capillary pressure occurring concomitantly with increased permeability greatly enhances protein flux and extravascular fluid accumulation. The rise in capillary hydrostatic pressure is determined by precapillary and postcapillary vessel resistances. Recent data indicate that pulmonary veins are not inert conduits but possess active smooth muscle components which respond to vasoactive agents such as histamine and arachidonic acid metabolites through venoconstriction. It appears that few humoral factors acting independently actually increase pulmonary capillary permeability. In comparison to the systemic microcirculation, the lung microcirculation appears to be more resistant to agents such as histamine and bradykinin which are known permeability-increasing agents in systemic microvessels. This may be important teleologically as the pulmonary microcirculation receives the entire cardiac output.Beiträge zur Klinik der Tuberkulose 02/1985; 163(4):193-219. DOI:10.1007/BF02713821 · 2.17 Impact Factor
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ABSTRACT: William of Ockham, 14th-century scholastic philosopher at Oxford and Munich, emphasized the principle of economy, "pleurality is not to be supposed without necessity" (Ockham's razor). Necessity is the key word. In the modeling of steady-state lung liquid and protein exchange, the desire for simplicity has sometimes outweighed good judgment. In fact, we and others have shown that simple models do not work. It is necessary to include several forms of inhomogeneity. The air-filled lung shows regional (top to bottom) variations of mass, microvascular pressure, and perimicrovascular protein concentration. Normally, the small longitudinal (arterioles to venules) gradient of microvascular and perimicrovascular pressures is not a major concern, but in nonuniform disease processes, such as microembolism, longitudinal inhomogeneity, and parallel inhomogeneity are dominant. Multiple pores should also be considered a form of inhomogeneity. The effect on liquid and protein exchange, when plasma protein concentration or microvascular pressure change, can be readily explained using pore heterogeneity. The model I am currently using consists of a large number of discrete compartments (18), rather than a continuous distribution. We have recently identified a fifth inhomogeneity, which is that lung lymph flow might not always represent steady-state transvascular filtration because interstitial liquid may leak through the pleura or along the bronchovascular liquid cuffs into the mediastinum.Annals of Biomedical Engineering 02/1987; 15(2):115-26. DOI:10.1007/BF02364048 · 3.23 Impact Factor
Article: Lung water during the puerperium[Show abstract] [Hide abstract]
ABSTRACT: An alteration in pulmonary water balance might be expected during pregnancy and the puerperium, as a result of the physiological adaptations to pregnancy. A preliminary investigation of this hypothesis was conducted using a radiological method of lung water measurement in 20 normal primigravidae during the early puerperium. Evidence of interstitial lung water was found in seven of the 20 mothers. There was a significant correlation with plasma volume (p less than 0.05) and fluid turnover (p less than 0.05) in the group with excess lung water. The implications of increased interstitial lung water and its possible causes during pregnancy are discussed.Anaesthesia 03/1987; 42(2):141-7. DOI:10.1111/j.1365-2044.1987.tb02986.x · 3.85 Impact Factor