To determine the importance of angiotensin converting enzyme (ACE) activity in the development of arterial proliferative lesions in a primate model, the response to vascular injury was studied in five baboons treated with oral cilazapril (20 mg/kg/day) and in five untreated control animals. Each animal underwent three procedures: 1) carotid artery endarterectomy, 2) balloon catheter deendothelialization of the superficial femoral artery, and 3) surgical placement of bilateral aorto-iliac expanded polytetrafluoroethylene (Gore-Tex) vascular grafts. Cilazapril therapy was initiated 1 week preoperatively and continued throughout the study interval. At 1 and 3 weeks postoperatively, plasma ACE activity was inhibited by more than 96% versus control values. After animals were killed at 3 months, injured vessel and graft segments were evaluated morphometrically. Although the response between animals was variable, average cross-sectional areas of neointima did not differ between the cilazapril-treated and control groups at sites of carotid endarterectomy (0.26±0.12 versus 0.34±0.17 mm2, respectively; p>0.5), femoral artery ballooning (0.15±0.08 versus 0.11±0.01 mm2;p>0.5), or at graft anastomoses (1.86±0.50 versus 1.72±0.50 mm2;p>0.5). Thus, cilazapril did not reduce intimai thickening over 3 months in these primate arterial injury models. However, a possible beneficial effect of cilazapril, which might be apparent at earlier time points or with larger animal groups, cannot be excluded.
|Original language||English (US)|
|Issue number||4 SUPPL.|
|State||Published - 1991|
- Angiotensin converting enzyme inhibitors
- Primate studies
ASJC Scopus subject areas
- Internal Medicine