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Increased Intimal Hyperplasia After Carotid Endarterectomy in Spontaneously Hypertensive Rats

Fred Southern, MD

Department of Surgery, Division of Vascular Surgery, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR

D. Keith Williams, PhD

Department of Biometry, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR

Aliza T. Brown, PhD

John Eidt, MD

Department of Surgery, Division of Vascular Surgery, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR

Mohammed M. Moursi, MD

Department of Surgery, Division of Vascular Surgery; University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, AR MoursiMohammedM{at}exchange.uams.edu

This study evaluated the effects of hypertension on postoperative intimal hyperplasia using a rat carotid endarterectomy (CEA) model with spontaneously hypertensive rats (SHR) and normotensive Sprague-Dawley rats (SD). SHR and SD rats underwent left carotid exposure and CEA via an arteriotomy, scoring and removal of the intima, followed by arteriotomy closure. The rats were then sacrificed two weeks postoperatively. The left carotid artery was harvested and underwent elastin and double immunohistochemical staining. The percent of lumenal stenosis was calculated using morphometric measurements, and stained cells within the intimal hyperplasia were counted. The means and standard deviation of the means were calculated, and the two groups were compared using a 2-sample t test. The systolic blood pressure was 228 +35 mm Hg in the SHR group and 108 ±8 mm Hg in the SD group (p < 0.00001). The percent of lumenal stenosis was 82.6 ±17.l10% in the SHR group and 21.2 ±¹3.7% in the SD rats (p value <0.0001). The percentage of cells staining for aSM actin was equal in the SHR group and the SD group (> 91%) but the percentage of these cells staining for BrdU was 38.2 +8.4% in the SHR group and 10.7 +5.8% in the SD group (p<0.0000 1). Hypertension in the SHR rats was associated with an increased lumenal stenosis due to increased intimal hyperplasia. The increased intimal hyperplasia was due to enhanced and accel-erated replication of smooth muscle cells. Hypertension may be associated with increased restenosis rates after CEA.

Vascular and Endovascular Surgery, Vol. 35, No. 1, 11-18 (2001)
DOI: 10.1177/153857440103500103


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