STAPHYLOCOCCUS-AUREUS AND HUMAN-PLATELETS CAUSE PULMONARY-HYPERTENSION AND THROMBOXANE GENERATION IN ISOLATED SALINE-PERFUSED RABBIT LUNGS

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Abstract
Potential contributions of bacterial-platelet interactions to the development of acute edematous lung injury, such as that seen in the adult respiratory distress syndrome (ARDS), remains unknown. Addition of S. aureus, 502A to isolated rabbit lungs perfused with saline, albumin and human platelets rapidly decreased the number of circulating platelets, increased pulmonary artery perfusion pressures and generated thromboxane B2, the stable derivative of thromboxane A2. Increases in perfusion pressures or thromboxane levels did not occur when platelets treated with acetylsalicylic acid (ASA) were used, even though ASA-treated platelets disappeared from the perfusates. Activation of platelets by bacteria may account for thrombocytopenia, platelet microemboli and/or contribute to increases in pulmonary artery pressures seen in some patients with ARDS.