TY - JOUR
T1 - Neointimal hyperplasia in balloon-injured rat carotid arteries
T2 - The influence of hyperhomocysteinemia
AU - Cook, Judith W.
AU - Malinow, M. Rene
AU - Moneta, Gregory L.
AU - Taylor, Lloyd M.
AU - Orloff, Susan L.
N1 - Funding Information:
Supported in part by a grant (No. RR00334) from the General Clinical Research Center Branches, Division of Resources, National Institutes of Health and a grant (No. RR00163) from the National Institutes of Health.
PY - 2002/1
Y1 - 2002/1
N2 - Purpose: Hyperhomocyst(e)inemia (hH[e]) is a risk factor for atherosclerosis. Neointimal hyperplasia (NH) after vessel injury can contribute to atherosclerosis. In this study, we investigated the effects of hH(e) on NH formation after arterial balloon injury in rats. Methods: Lewis rats that were given a hH(e)-inducing (high methionine, low folate) or normal diet for 150 days underwent common carotid artery (CCA) balloon injury. Two and 4 weeks after injury, CCAs were formalin perfusion-fixed, sectioned, and stained for elastin. Neointimal index (NI, percent lumen occlusion) and neointima (N) and media (M) area were measured by using computer-interfaced microscopy. Results: Plasma homocyst(e)ine (H[c]) levels were elevated in rats given the study diet compared with rats given the normal diet at days 40 and 90 (69 ± 8 and 73 ± 9 μmol/L vs 4 ± 0.4 and 4 ± 0.6 μmol/L, P < .001). After balloon injury, the CCA NI and N/M ratio, but not the M area, were increased by hH(e) compared with normal plasma H(e) (2 weeks [n = 6,7]: NI = 7.3 ± 1.7 vs 2.9 ± 0.7, P = .002, and N/M = 0.31 ± 0.08 vs 0.08 ± 0.02, P < .001; 4 weeks [n = 4,7]: NI = 13.1 ± 2.2 vs 6.3 ± 1.3, P = .002, and N/M = 0.36 ± 0.08 vs 0.17 ± 0.03, P < .001). Conclusion: hH(e) accelerates NH in a rat CCA balloon-injury model. The effect of hH(e) on NH may contribute to increased atherosclerosis in humans with hH(e).
AB - Purpose: Hyperhomocyst(e)inemia (hH[e]) is a risk factor for atherosclerosis. Neointimal hyperplasia (NH) after vessel injury can contribute to atherosclerosis. In this study, we investigated the effects of hH(e) on NH formation after arterial balloon injury in rats. Methods: Lewis rats that were given a hH(e)-inducing (high methionine, low folate) or normal diet for 150 days underwent common carotid artery (CCA) balloon injury. Two and 4 weeks after injury, CCAs were formalin perfusion-fixed, sectioned, and stained for elastin. Neointimal index (NI, percent lumen occlusion) and neointima (N) and media (M) area were measured by using computer-interfaced microscopy. Results: Plasma homocyst(e)ine (H[c]) levels were elevated in rats given the study diet compared with rats given the normal diet at days 40 and 90 (69 ± 8 and 73 ± 9 μmol/L vs 4 ± 0.4 and 4 ± 0.6 μmol/L, P < .001). After balloon injury, the CCA NI and N/M ratio, but not the M area, were increased by hH(e) compared with normal plasma H(e) (2 weeks [n = 6,7]: NI = 7.3 ± 1.7 vs 2.9 ± 0.7, P = .002, and N/M = 0.31 ± 0.08 vs 0.08 ± 0.02, P < .001; 4 weeks [n = 4,7]: NI = 13.1 ± 2.2 vs 6.3 ± 1.3, P = .002, and N/M = 0.36 ± 0.08 vs 0.17 ± 0.03, P < .001). Conclusion: hH(e) accelerates NH in a rat CCA balloon-injury model. The effect of hH(e) on NH may contribute to increased atherosclerosis in humans with hH(e).
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U2 - 10.1067/mva.2002.118819
DO - 10.1067/mva.2002.118819
M3 - Article
C2 - 11802148
AN - SCOPUS:0036363436
SN - 0741-5214
VL - 35
SP - 158
EP - 165
JO - Journal of vascular surgery
JF - Journal of vascular surgery
IS - 1
ER -