TURPENTINE PLEURISY IN RABBITS - MODEL OF PLEURAL FLUID ACIDOSIS AND LOW PLEURAL FLUID GLUCOSE

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Abstract
Pleural fluid acidosis occurs in several pleural inflammatory states, but the mechanisms responsible for this phenomenon were not clearly defined. A rabbit model of acidic, low glucose, pleural effusions included with turpentine was developed to study the contribution of pleural fluid per se to pleural fluid acidosis. A single injection of 0.3 ml of turpentine into the rabbit pleural space produced an exudative pleural effusion. The rate of acid generation in vitro of the resultant pleural fluid had a significant inverse correlation with pleural fluid pH and glucose concentration in vivo (in both cases, P < 0.05). A significant direct correlation between acid generation in vitro and pleural fluid leukocyte count was found (P < 0.01). A 2nd intrapleural turpentine injection produced pleural fluid that had a low pH, low glucose concentration and a high lactate concentration and was significantly different from control fluids (in all cases, P < 0.05). A significant correlation was found between simultaneously determined pleural fluid pH and glucose concentration after reinjection of turpentine (P < 0.01). At 3 and 6 h after a 2nd intrapleural injection of turpentine, there was no demonstrable acid generation in vitro by the pleural fluid (P < 0.01). In the present model, after a single intrapleural injection of turpentine, pleural fluid acid generation made a contribution to pH in vivo. After reinjection utilization of glucose by metabolically active pleural surface cells was apparently responsible for the low glucose concentration and the increased lactate production and pleural fluid acidosis, because the pleural fluid per se showed no acid generation during the time when acid generation was occurring in vivo and at the time of maximal acidosis and low glucose concentration.