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Studies on the Mechanism of Endotoxin-Induced Increase of Alveolocapillary Permeability
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1974
Year
Acute Lung InjuryLung InflammationBiomedical EngineeringPlasma MedicineInflammationPulmonary PharmacologyToxicologyEndotoxin-induced IncreaseCapillary NetworkAnimal PhysiologyVeterinary PhysiologyPulmonary CirculationAllergySmall Animal Internal MedicinePharmacologyPermeability IncreaseComplement SystemComplement InactivationPhysiologyPulmonary PhysiologyLung MechanicsWound HealingMedicineAnesthesiology
Using an isolated perfused dog lung system, studies were carried out to ascertain the role of plasma factors in the increase in alveolocapillary permeability induced by the administration of endotoxin. Heat treatment of dog serum (56° for 30 min) abolished the capacity of endotoxin to induce permeability increase. In contrast, serum treated with potassium thio-cyanate to inactivate the complement components C3, C4, and C5 did allow the increase in endotoxin-induced permeability, as did a 5.8% solution of human serum albumin and a 6% dextran solution. Pretreatment with a massive dose of hydrocortisone sodium succinate decreased, but did not abolish, the endotoxin-induced permeability increase in albumin-perfused lung. The studies suggest that endotoxin may affect the alveolocapillary membrane directly, by a process which is independent of the complement system. Heat treatment of serum impairs the endotoxin effect due to a mechanism other than complement inactivation.