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Titolo:
Suppression of experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors
Autore:
Liao, SX; Miralles, M; Kelley, BJ; Curci, JA; Borhani, M; Thompson, RW;
Indirizzi:
Washington Univ, Sch Med, Dept Surg, Vasc Surg Sect, St Louis, MO 63130 USA Washington Univ St Louis MO USA 63130 c Surg Sect, St Louis, MO 63130 USA Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63130 USA Washington Univ St Louis MO USA 63130 Dept Radiol, St Louis, MO 63130 USA Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63130 USAWashington Univ St Louis MO USA 63130 l & Physiol, St Louis, MO 63130 USA
Titolo Testata:
JOURNAL OF VASCULAR SURGERY
fascicolo: 5, volume: 33, anno: 2001,
pagine: 1057 - 1064
SICI:
0741-5214(200105)33:5<1057:SOEAAA>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMINOGEN-ACTIVATOR INHIBITOR-1; SMOOTH-MUSCLE CELLS; FACTOR-KAPPA-B; MATRIX METALLOPROTEINASES; ENDOTHELIAL-CELLS; HEART-FAILURE; EXPRESSION; EXPANSION; RECEPTOR; GROWTH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Thompson, RW Washington Univ, Sch Med, Wohl Hosp 9901, Vasc Surg Sect, 4960 Childrens Pl, St Louis, MO 63110 USA Washington Univ 4960 Childrens Pl StLouis MO USA 63110 0 USA
Citazione:
S.X. Liao et al., "Suppression of experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors", J VASC SURG, 33(5), 2001, pp. 1057-1064

Abstract

Purpose: Pathologic remodeling of the extracellular matrix is a critical mechanism in the development and progression of abdominal aortic aneurysms (AAAs). Although angiotensin-converting enzyme (ACE) inhibitors are known toalter vascular wall remodeling in other conditions, their effects on AkAs are unknown. In this study we assessed the effect of ACE inhibitors in a rodent model of aneurysm development. Methods: Male Wistar rats underwent transient aortic perfusion with porcine pancreatic elastase, followed by treatment with one of three ACE inhibitors (captopril [CP], lisinopril [LP], or enalapril [Er]), an angiotensin (AT)(1) receptor antagonist (losartan [LOS]), or water alone (9 rats in each group). Blood pressure and aortic diameter (AD) were measured before elastase perfusion and on day 14, with an AAA defined as an increase in AD (Delta AD) of more than 100%. The structural features of the aortic wall were examined by means of light microscopy. Results: Aneurysmal dilatation consistently developed within 14 days of elastase perfusion in untreated rats, coinciding with the development of a transmural inflammatory response and destruction of the elastic media (mean Delta AD, 223% +/- 28%). Ah three ACE inhibitors prevented AAA development (mean Delta AD: CP, 67% +/- 4%; LP, 18% +/- 12%; and EP, 14% +/- 3%; each P < .05 vs controls). ACE inhibitors also attenuated the degradation of medial elastin without diminishing the inflammatory response. Surprisingly, the aneurysm-suppressing effects of ACE inhibitors were dissociated from their effects on systemic hemodynamics, and LOS had no significant effect on aneurysm development compared with untreated controls (mean Delta AD, 186% +/- 19%). Conclusion: Treatment with ACE inhibitors suppresses the development of elastase-induced AAAs in the rat. Although this is associated with the preservation of medial elastin, the mechanisms underlying these effects appear tobe distinct from hemodynamic alterations alone or events mediated solely by AT(1) receptors. Further studies are needed to elucidate how ACE inhibitors influence aortic wall matrix remodeling during aneurysmal degeneration.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 13:14:27