Time sequence and site of fluid accumulation in experimental neurogenic pulmonary edema

Hücker, H; Frenzel, H; Kremer, Bernd; Richter, I. E.

doi:10.1007/bf01851320

Cited by 9 publications

(2 citation statements)

References 22 publications

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“…These changes reflect an extensive transfer of blood from the systemic to the pulmonary circulation and are similar to the findings after a massive infusion of adrenaline (Luisada, 1967). During this early phase the pattern of interstitual fluid accumulation and the electron microscopic appearance are those characteristic of hydrostatic oedema (Hucker et al,1976). Pressures return to normal within a short time, but pulmonary oedema persists and increases in volume.…”

Section: Particular Types Of Pulmonary Oedemasupporting

confidence: 68%

Current views on the mechanisms of pulmonary oedema

1978

The Journal of Pathology

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Understanding of the causes of pulmonary oedema must be based on knowledge of the mechanism responsible for fluid exchange between the several compartments of the normal lung. Recent physiological studies have clarified the main features of these mechanisms. However in three areas knowledge is still incomplete--the magnitude of the hydrostatic and oncotic forces responsible for fluid movement within the lung, the means by which protein leaks across the wall of small pulmonary vessels and the routes by which fluid and protein pass between the interstitial tissues of the lung and the alveolar space. Further work is needed in these areas. On the basis of this physiological knowledge the mode of development of hydrostatic oedema, the role of lymphatics in pulmonary oedema, and the several stages of pulmonary oedema development that may culminate in alveolar flooding are now clearly understood. Knowledge is less complete about oedema due to increased vascular permeability. In some experimental models, such as alloxan, leakage is due to irreversible injury to the alveolar wall; in other models, including ANTU, oedema formation has been shown to depend upon minor and reversible changes in pulmonary vascular endothelium similar to those that cause exudate formation in areas of acute inflammation. In no instance is detailed information available of both the rate and magnitude of protein leakage and of the morphological basis of increased vascular permeability. Further work is required in this area. Present knowledge allows an adequate explanation of the changes that occur in many clinically important types of pulmonary oedema, including cardiac failure and neurogenic pulmonary oedema. Other types of oedema, notably that which may complicate traumatic shock or extrapulmonary sepsis and high altitude pulmonary oedema, are more complex and the details of their pathogenesis are still obscure.

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Section: Particular Types Of Pulmonary Oedemasupporting

confidence: 68%

Current views on the mechanisms of pulmonary oedema

1978

The Journal of Pathology

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“…The protein concentration of airway edema fluid in neurogenic pulmonary edema approached that of plasma (Theodore and Robin, 1976;Fein and Rackow, 1982), suggesting that increases in permeability of pulmonary capillaries and alveolar epithelium to proteins are prominently involved in the development of pulmonary edema. Morphological studies in experimental animal models have supported these clinical observations (Hucker et al, 1976;Minnear and Connell, 1981). Since pulmonary arterial hypertension has been observed with the pulmonary edema in experimental animals and patients after central nervous system (CNS) injury (Sarnoff and Sarnoff, 1952;Wray and Nicotra, 1978), a rise in Pc may also be an important factor in edema formation.…”

Section: Introductionmentioning

confidence: 94%