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Endothelial regeneration. IX. Arterial injury followed by rapid endothelial repair induces smooth-muscle-cell proliferation but not intimal thickening.

Rat thoracic aortas were denuded of endothelial cells with a fine nylon filament, which removed a row of endothelium approximately 100 mu in width and caused platelets to adhere to the exposed subendothelium. A further group of rats was subjected to a sham operation where only the abdominal aorta was injured, and another group of rats was used as controls. Each animal was continuously labeled with 3H-thymidine (6.7 Ci/mM, 10 microCi/hr) for 7 days, at which time they were killed and the aortas perfusion-fixed with aldehydes. Sections of each aorta were processed for autoradiography. The thoracic aortas from animals subjected to the nylon filament injury showed no intimal thickening, but there was a significant increase in the thymidine index of the medial smooth muscle cells (SMCs) as compared with aortas from sham operation or control animals (1.02% +/- 0.44% versus 0.19% +/- 0.13% versus 0.15% +/- 0.12%). This experiment showed that continuous administration of 3H-thymidine permitted the detection of a small but significant increase in replication rates that could not be detected by the standard bolus administration of 3H-thymidine, and that selected loss of endothelium with minimal trauma to the vessel wall caused SMC proliferation without intimal thickening. These findings suggest that platelets may indeed provide SMC proliferation, but that migration of these cells into the intima may be controlled by different factor(s).