Cellular and humoral mediators of pulmonary edema
| Autor: | K. E. Burhop, Asrar B. Malik, W. M. Selig |
|---|---|
| Rok vydání: | 1985 |
| Předmět: |
Blood Platelets
Pulmonary and Respiratory Medicine Pulmonary Circulation Serotonin Cardiac output Neutrophils Hydrostatic pressure Bradykinin Pulmonary Edema Vascular permeability Arachidonic Acids In Vitro Techniques Pharmacology Biology Microcirculation Capillary Permeability chemistry.chemical_compound Catecholamines Dogs Hydrostatic Pressure medicine Animals Arachidonic Acid Sheep Lung Thrombin Pulmonary edema medicine.disease medicine.anatomical_structure chemistry Immunology Histamine |
| Zdroj: | Lung. 163:193-219 |
| ISSN: | 1432-1750 0341-2040 |
| DOI: | 10.1007/bf02713821 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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