Platelet adhesion and myointimal proliferation in canine pulmonary arteries.

Pulmonary arteries were studied by scanning and transmission electron microscopy in 15 preconditioned dogs. Five dogs were control animals, while 10 dogs were studied 4 and 30 days following transplantation of adult heartworms into the pulmonary arteries. Evan's blue dye was used to locate areas of vascular damage. Pulmonary arteries from control dogs exhibited no Evan's blue staining. The surface and ultrastructural characteristics of these blood vessels were comparable to normal peripheral blood vessels. Pulmonary arteries removed from dogs after 4 days of heartworm infection exhibited extensive staining with Evan's blue. These stained areas had disrupted endothelium with many platelets adhered to the exposed subendothelium. In addition, leukocytes were attached to adjacent areas of damaged endothelium. Pulmonary arteries of dogs infected with heartworms for 30 days also exhibited extensive staining with Evan's blue. The blue-stained areas in this group had two typical responses. On some portions the lesions were similar to those seen at 4 days (ie, loss of endothelium with platelet and leukocyte adhesion), while other stained areas had complex lesions that projected from the surface into the lumen of the blood vessel. These lesions were endothelialized, and transmission electron microscopy revealed that they consisted of large numbers of smooth muscle cells that had migrated through the internal elastic lamina. The findings in the 30-day infection group suggest that the proliferative lesion formation was a result of an ongoing active process of endothelial loss and plateletleukocyte adhesion. The characteristic response of canine pulmonary arteries to the presence of heartworms (endothelial loss, platelet-leukocyte adhesion, and development of myoproliferative intimal lesions) suggests that this condition is a potential model for study of the early vascular changes that produce myointimal proliferation.