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The role of internal elastic laminae damage in the development of canine arteriosclerosis.

This study was designed to test the hypothesis that the extent of damage to the internal elastic lamina (IEL) may be a factor in determining the development of atheromatous lesions (lesion area). A bilateral iliac artery arteriosclerotic (AS) model in seven dogs prepared by intimal denudation and fracture of the IEL plus 5% cholesterol diet was investigated. The animals were sacrificed at 10-52 weeks (10, n = 1; 16, n = 3; 20, n = 1; 32, n = 1; 52, n = 1). Histologic analysis of sections (n = 42) of 14 canine iliac AS arteries harvested bilaterally from identical locations along the vessels (2, 7, and 12 cm from the aortic bifurcation) were compared with control segments of caudal and femoral arteries (n = 12) that had intact lamina and no luminal trauma. AS segments at all sites along the length of the traumatized iliac vessels demonstrated significant lesions, while control vessels had no arteriosclerotic changes. AS lesion area was calculated using ocular micrometry and a multiple regression model to test the predictability of the lesion area from the following independent variables: (1) proportion of intact IEL to total IEL (IEL/IELt), (2) sacrifice intervalens (3) frequency of disruptions to the IEL, (4) side and level of the arterial lesion, and (5) respective animals. This analysis revealed that none of the coefficients for the independent variables used in the multiple regression model was significant, suggesting that the extent of AS lesions is not related to the size, frequency, or location of breaks in the IEL, although a break in IEL is required to initiate the lesions. This observation suggests that the migration of cells from the arterial media through the broken laminae or the release of medial biochemical mediators which are normally contained by the elastic lamina is required to develop the AS lesions in this canine model, and that any size break in the lamina initiates the process.