111In-platelet and 125I-fibrinogen deposition in the lungs in experimental acute pancreatitis

An experimental model of acute pancreatitis in rats has been used to study intrapulmonary 125I-fibrinogen and 111In-platelet deposition. Pancreatitis caused a significant increase in wet lung weight compared to normal, and this could be abolished by heparin or aspirin pretreatment. 125I-fibrinogen was deposited in the lungs of animals to a significantly greater degree than in controls (P less than 0.01). 125I-fibrinogen deposition was reduced to control levels by pretreatment with aspirin or heparin (P less than 0.05). The uptake of radiolabeled platelets was greater in pancreatitis than in controls (P less than 0.001). Pancreatitis appears to be responsible for platelet entrapment in the lungs. Platelet uptake was reduced by heparin treatment but unaffected by aspirin therapy.