Protection of primate lung from stored-blood perfusion by peptidase inhibition and target membrane stabilization.
Microaggregate filtration and separation of the cellular components of stored autologous blood have not changed the functional and morphological damage in primate lungs from stored-blood perfusion. Pharmacologic prevention of these "shock lung" changes was attempted with trasylol and with methylprednisolone pretreatment. In an in situ primate lung perfusion model, fresh and stored blood was perfused in untreated baboons and in groups of seven animals each pretreated with Trasylol or methylprednisolone. Pulmonary damage from stored-blood perfusion was evident by pulmonary edema, increase in pulmonary vascular resistance, decreases in effective compliance and arteriovenous pO2 gradient as well as by morphological criteria. Some protection was afforded by methylprednisolone and, to a lesser extent, trasylol pretreatment against this damage in primate lung form and function induced by stored-blood perfusion.
D000818:Animals; D007611:Aprotinin / Q000627:therapeutic use*; D006439:Hemodynamics; D008297:Male; D008566:Membranes / Q000187:drug effects / Q000502:physiology; D008775:Methylprednisolone / Q000031:analogs & derivatives*; D008776:Methylprednisolone Hemisuccinate / Q000627:therapeutic use*; D010215:Papio; D010477:Perfusion; D011654:Pulmonary Edema / Q000517:prevention & control; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000517:prevention & control*; D065227:Transfusion Reaction
D008776:Methylprednisolone Hemisuccinate; D007611:Aprotinin; D008775:Methylprednisolone