Staphylococcus aureus and human platelets cause pulmonary hypertension and thromboxane generation in isolated saline-perfused rabbit lungs.
The 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. We found that the addition of Staphylococcus aureus, 502A to isolated rabbit lungs perfused with saline, 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. In contrast, 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. The results suggest that 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.
D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D001794:Blood Pressure; D006976:Hypertension, Pulmonary / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D008168:Lung / Q000378:metabolism*; D010976:Platelet Count; D011651:Pulmonary Artery / Q000503:physiopathology; D011817:Rabbits; D013211:Staphylococcus aureus; D013931:Thromboxanes / Q000378:metabolism*
D013931:Thromboxanes