Effect of long-term aspirin treatment on platelet adhesion to chronically damaged canine pulmonary arteries.
The effect of aspirin on platelet adhesion to chronically damaged pulmonary arteries was studied in 18 dogs. Chronic injury was produced in all dogs by infection with the canine heartworm Dirofilaria immitis (DI). Ten dogs were subjected to 4 days of chronic injury. Eight dogs were subjected to 30 days of chronic injury. Five of the 4 day injury and 4 of the 30 day injury dogs received aspirin daily; (325 mg/day orally). Aspirin was started 3 days prior to infection with DI. Pulmonary arteries were perfusion fixed in situ at physiologic pressure. The damaged pulmonary arteries were located by Evan's blue staining (2 ml/kg of 1% dye given one hr prior to perfusion) and prepared for scanning electron microscopy. Both groups of dogs with 4 day DI infection had monolayers of platelets adhered to exposed subendothelium. Aspirin treated dogs had enhanced platelet adhesion to damaged arteries. Aspirin treatment for 33 days reduced platelet adhesion. The damaged arteries of treated dogs infected with DI for 30 days had very few platelets adhering to the damaged surface. However, non-treated dogs subjected to 30 days of infection had platelet adhesion equivalent to the 4 day non-treated infection group. These results suggest that although aspirin is ineffective in preventing platelet adhesion in short term therapy it is effective when given for longer time periods. This inhibitory effect may occur due to platelet membrane changes rather than because of aspirin inhibition of cyclooxygenase.
D000818:Animals; D001241:Aspirin / Q000009:adverse effects*; D001792:Blood Platelets / Q000648:ultrastructure; D004184:Dirofilariasis / Q000662:veterinary*; D004283:Dog Diseases / Q000097:blood*; D004285:Dogs; D010973:Platelet Adhesiveness / Q000187:drug effects*; D011651:Pulmonary Artery / Q000503:physiopathology* / Q000648:ultrastructure
D001241:Aspirin