Abstract
Proliferation of arterial smooth muscle cells is an important feature of atherosclerosis, and a well documented reaction to intimal injury. To assess the influence of the intensity of injury to rat thoracic aorta, we studied the effects of a soft or hard friction with a moderately or tightly inflated ballon catheter at 2, 14 and 30 d after operation. As compared with soft injury, hard injury (1) strongly enhanced the proliferating response of the aortic intima and media (median incorporation of tritiated thymidine into deoxyribonucleic acid on day 2 increased 2.8-fold, 95% confidence interval 2.3–3.3; median deoxyribonucleic acid content on day 14: 102.1 v 72.1 μg); (2) markedly delayed endothelial regeneration (median percentage of intimal area stained by Evans blue on day 14: 33.1 v 0.6%). On day 2, transmission and scanning electron microscopy showed that endothelial denudation was complete after a hard injury, but only partial after a soft one. However, macroscopic staining of the intima with Evans blue was complete in both instances. The extent of endothelial denudation appears to be a major determinant of the mitotic reaction of arteries to injury. In the experimental search for drugs to reduce muscular proliferation (of potential value in the prevention of restenosis after percutaneous transluminal angioplasty), endothelial injury with balloon catheters should be carefully standardised, and applied “blindly” to afford valid comparisons between treated and control groups of animals.

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