Abstract

Scanning electron microscopy (SEM) was used to study pulmonary artery injury 4 days (10 dogs) and 30 days (8 dogs) after transplantation of 6-8 adult canine heartworms (HW) into the pulmonary arteries. Worms were introduced into the jugular vein and allowed to float into position in the main pulmonary artery, where HW are found in naturally occurring infections. One half the dogs in each group were given 323 mg aspirin (ASA)/day starting 3 days before infection. At the end of the 4 or 30 day period all dogs were given 1% Evan’s blue dye (2 ml/kg i.v.), heparin (3,000 units i.v.) and anesthetized. The lungs were perfused at 15 mmHg pressure with Tyrode’s solution followed by 1% glutaraldehyde. Evan’s blue stained areas of pulmonary arteries were dissected and processed for SEM. Dogs were compared for the percentage of surface with endothelial damage, white blood cell and platelet adhesion, and myointimal proliferation. All numerical values show treated dogs vs non-treated dogs (mean ± SE). After 4 days of HW infection the blood vessels of both ASA treated and non-treated dogs exhibited extensive endothelial damage (51 ± 8% vs 81 ± 6%), white blood cell adhesion (56 ± 15% vs 60 ± 12%) and platelet adhesion (36 ± 6% vs 51 ± 9%). Neither group exhibited formation of myointimal proliferation. After 30 days of HW infection blood vessels from ASA treated dogs had less endothelial cell damage (15 ± 6% vs 33 ± 14%), less white blood cell adhesion (13 ± 2% vs 45 ± 9%) and less platelet adhesion (0% vs 25 ± 9%) than non-treated dogs. Myointimal proliferation was observed in both groups (50 ± 16% vs 61 ± 14%), however, the lesions were smaller and less complex in ASA treated dogs. These results suggest that after 4 days of HW infection ASA was ineffective in preventing vascular damage and platelet-leukocyte adhesion. However, continuous ASA therapy during the chronic vascular injury produced by a 30 day HW infection reduced platelet-leukocyte adhesion and the severity of myointimal proliferation. These findings support the suggestion that aspirin protects against formation of atherosclerotic lesions.

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