Smooth muscle proliferation in chronically injured canine pulmonary arteries is reduced by a potent platelet aggregation inhibitor U-53,059.

Abstract

Dirofilaria immitis (DI) infection chronically injures canine pulmonary arteries. This injury produces endothelial cell loss, platelet/leukocyte adhesion, and smooth muscle proliferation. In the present study we assessed the effect of the cyclooxygenase inhibitor, U-53,059, on platelet function, platelet kinetics, coagulation, and smooth muscle proliferation in DI infected dogs. Platelet aggregation to the combination of arachidonic acid/ADP was significantly inhibited by U-53,059. Coagulation and hematologic parameters were not effected by either DI infection or U-53,059 treatment. Platelet survival and the number of platelet dense granules were reduced in DI infection. Quantification of the lesions demonstrated that U-53,059 reduced both severity and density compared to non-treated dogs. U-53,059 is a potent and effective inhibitor of platelet aggregation which modifies smooth muscle proliferation produced by chronic vascular injury.

• Authors: R G Schaub, J C Keith Jr, C A Simmons, C A Rawlings
• Journal: Thrombosis and haemostasis (Thromb Haemost) Vol. 53 Issue 3 Pg. 351-5 (Jun 24 1985) ISSN: 0340-6245 [Print] Germany
• PMID: 4049309 (Publication Type: Journal Article)

Chemical References

• Thiazoles
• itazigrel

Topics

• Animals
• Blood Platelets (drug effects, ultrastructure)
• Cell Division (drug effects)
• Dirofilaria immitis (pathogenicity)
• Dirofilariasis (blood, pathology, physiopathology)
• Dogs
• Female
• Male
• Microscopy, Electron
• Muscle, Smooth, Vascular (drug effects, pathology, ultrastructure)
• Platelet Aggregation (drug effects)
• Pulmonary Artery (drug effects, pathology, ultrastructure)
• Thiazoles (pharmacology)