Injury of an artery by passage of a balloon catheter causes both endothelial denudation and medial damage and produces a marked smooth muscle cell (SMC) proliferative response. In this study, the endothelium from rat carotid arteries was removed by use of a rotating loop of 5/0 monofilament suture (gentle denudation technique), which did not cause any detectable damage to the underlying medial cells but did cause platelet adherence. Expression of platelet-derived growth factor (PDGF) A-chain and PDGF receptor mRNA was comparable to that seen in ballooned carotids, but the medial SMC proliferative response to gentle denudation was markedly reduced when compared to that observed after balloon denudation (1.4% vs. 13.6%). Intimal lesions were only observed in those zones that remained denuded for more than 7 days. These results demonstrate that a denuding injury with no medial trauma is sufficient to induce intimal lesions and that the significantly higher proliferation seen in ballooned vessels might reflect a response of the medial cells to trauma that occurred during denudation. (Arteriosclerosis 10:1082-1087, November/December 1990) T he balloon catheter-injured artery has become the standard model for studying smooth muscle cell (SMC) proliferation in vivo, 123 and yet there is still little information as to what factors are involved in this process. One early hypothesis was that smooth muscle replication, which occurs soon after denudation, is initiated by platelet factors, but work by several groups has shown that platelet adherence to exposed subendothelium causes neither SMC replication nor intimal lesion formation.4 -9 Furthermore, in the total absence of platelets, balloon-injured arteries show a dramatic increase in SMC proliferation similar to that found in denuded arteries from control animals.10 These data strongly suggest that the SMC proliferation induced by mechanical injury is modulated by other, undetermined factors.A recent study by Majesky et al. 11 has shown that within hours after balloon injury, rat carotid arteries increase their expression of mRNA for platelet-derived growth factor (PDGF) A-chain and for the PDGF receptor. Therefore, injury to the arterial wall might induce an autocrine pathway in which SMC stimulate their own proliferation by synthesis of PDGF. Yet another explanation for the rapid increase in SMC proliferation might be

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We review the long-term results of carotid endarterectomy in 200 consecutive patients operated on from 1980 to 1987. The patients were part of an ongoing study using duplex scanning to assess the status of the carotid bifurcation before and after endarterectomy. The average follow-up for the patients was 31 months. The indications for surgery were transient ischemic attacks in 87 (43.5%) and stroke in 36 (18%) patients; 77 patients (38.5%) were asymptomatic. In 176 sides (88%), the degree of stenosis exceeded 50% in terms of diameter reduction. The perioperative stroke rate was 2.3% in patients with transient ischemic attacks, 2.8% in patients with strokes, and 1.3% in asymptomatic patients. There was one perioperative death (0.5%). There were five occlusions of the internal carotid artery, one during the perioperative period and four after discharge; in three patients the occlusion was associated with the development of a stroke. There was a restenosis rate of 19.7% secondary to myointimal hyperplasia; such lesions did not appear to contribute to new ischemic events during or after their development. The mean stroke incidence after the decision was made for carotid endarterectomy was 2.8%/yr in the patients with transient ischemic attacks, 6.2%/yr in the patients with stroke, and 0.65%/yr in the asymptomatic patients. The annual death rate was 6% for the entire group, 5.5%/yr in the patients with transient ischemic attacks, 9.2%/yr in the patients with stroke, and 4.6%/yr in the asymptomatic patients. (Stroke 1989;20:1138-1142)

This study describes the distribution of heparan sulfate proteoglycan ( HSPG ) within the rat aorta using immunocytochemical (biotin-avidin-peroxidase) and immuno-electron microscopy (125I-autoradiography). Heparan sulfate proteoglycan was isolated from a basement membrane producing mouse EHS sarcoma ( Hassell et al. 1980) and used to generate antisera in rabbits. Light microscopic observations revealed intense immunostaining of the intima and media of normal aorta, adventitial vasa vasorum, and aortic intimal fibromuscular thickenings induced by experimental injury (balloon de-endothelialization). Immunoelectron microscopy using 125I labeled antibodies to HSPG revealed that proteoheparan sulfate was localized to the amorphous layer of basement membrane below aortic and capillary endothelium. In addition, labeled anti- HSPG could be localized to the external lamina surrounding the smooth muscle cells in the hyperplastic intima. These studies reveal that antibodies prepared against a proteoheparan sulfate isolated from a basement membrane producing EHS sarcoma cross react with basement membrane structures within the aortic wall. Furthermore, these results demonstrate that the basement membranes beneath aortic and capillary endothelium and the external lamina surrounding aortic smooth muscle cells contain a heparan sulfate proteoglycan that is antigenically similar.

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