Cellular mediation of respiratory distress syndrome induced by fragment D.
The serum concentration of fibrinogen degradation product D (Fg D) is elevated after injury and sepsis. Purified human Fg D infused into awake rabbits causes progressive thrombocytopenia, complement depletion, hypoxia, vascular permeability to albumin and neutrophil congestion. In previous work experimentally induced thrombocytopenia protected lungs of rabbits against the effects of Fg D. The present study was designed to determine the role of the neutrophil in the development of Fg D-induced respiratory distress by rendering rabbits neutropenic with antiserum. Neutrophil depletion offered some, but not total, protection of the lungs against the toxic effects of Fg D infusion. Only one neutropenic rabbit became hypoxic. Vascular leak to albumin and water was diminished. Platelet and white blood cell counts decreased. However, complement activity was unaffected. The results suggest that neutrophils, like platelets, also contribute to the onset of respiratory failure in this model.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects; D004195:Disease Models, Animal; D005338:Fibrin Fibrinogen Degradation Products / Q000494:pharmacology*; D005342:Fibrinolysis; D009504:Neutrophils / Q000187:drug effects*; D011817:Rabbits; D012128:Respiratory Distress Syndrome / Q000503:physiopathology*; D014947:Wounds and Injuries / Q000503:physiopathology
D005338:Fibrin Fibrinogen Degradation Products; C015214:fibrinogen D fragment