CLOTTING AND FIBRINOLYTIC-ACTIVITY OF PLEURAL FLUID IN A MODEL OF PLEURAL ADHESIONS

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Abstract
To understand better the transition from pleural inflammation to pleural adhesions, to clotting and fibrinolytic systems in a model of sterile pleural inflammation was studied. New Zealand white rabbits (6) received an intrapleural instillation of 0.3 ml of turpentine. Four of these received 0.2 additional ml of turpentine 96 h after the initial instillation to produce a low-glucose, low-pH effusion to study the clotting and fibrinolytic systems in this setting. The other 2 rabbits received an intrapleural instillation of 0.2 ml of saline and served as control animals. Serial pleural fluid fibrinogen, prothrombin time, partial thromboplastin time, euglobulin lysis time and fibrin plate analyses for fibrinolysis were determined. In all pleural effusions, the largest leukocyte count, greatest fibrinogen concentration, and shortest prothrombin time occurred 24 h after initial instillation or reinstillation of turpentine. All of the partial thromboplastin times were greater than 150 s. No fibrinolytic activity by euglobulin lysis test or fibrin plate method was demonstrated. Autopsies were performed either 2 or 5 wk after initial pleural injury with fibrous adhesions being most impressive in those rabbits reinjected with turpentine and autopsied during the 5th wk. After acute pleural injury, pleural fluid apparently has clotting capacity and undetectable fibrinolytic activity. Although these findings are associated with formation of pleural adhesions, their causative role remains speculative.

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