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Titolo:
Hyperhomocysteinemia impairs angiogenesis in response to hindlimb ischemia
Autore:
Duan, JL; Murohara, T; Ikeda, H; Sasaki, K; Shintani, S; Akita, T; Shimada, T; Imaizumi, T;
Indirizzi:
Kurume Univ, Sch Med, Inst Cardiovasc Res, Kurume, Fukuoka 8300011, Japan Kurume Univ Kurume Fukuoka Japan 8300011 , Kurume, Fukuoka 8300011, Japan Kurume Univ, Sch Med, Dept Internal Med 3, Kurume, Fukuoka 8300011, Japan Kurume Univ Kurume Fukuoka Japan 8300011 , Kurume, Fukuoka 8300011, Japan
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 12, volume: 20, anno: 2000,
pagine: 2579 - 2585
SICI:
1079-5642(200012)20:12<2579:HIAIRT>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL GROWTH-FACTOR; NITRIC-OXIDE SYNTHASE; PERFORMANCE LIQUID-CHROMATOGRAPHY; RISK FACTOR; FOLIC-ACID; INDUCED ARTERIOSCLEROSIS; DEPENDENT VASODILATION; PLASMA HOMOCYSTEINE; CEREBROSPINAL-FLUID; VASCULAR-DISEASE;
Keywords:
endothelium; homocysteine; nitric oxide; peripheral artery disease; risk factors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Murohara, T Kurume Univ, Sch Med, Inst Cardiovasc Res, 67 Asahi Machi, Kurume, Fukuoka8300011, Japan Kurume Univ 67 Asahi Machi Kurume Fukuoka Japan 8300011 Japan
Citazione:
J.L. Duan et al., "Hyperhomocysteinemia impairs angiogenesis in response to hindlimb ischemia", ART THROM V, 20(12), 2000, pp. 2579-2585

Abstract

Hyperhomocysteinemia (HH) is an independent risk factor for atherosclerosis, including peripheral arterial occlusive disease (PAOD). Because angiogenesis and collateral vessel formation are important self-salvage mechanisms for ischemic PAOD, we examined whether HH modulates angiogenesis in vivo ina rat model of hindlimb ischemia. Rats were divided into 3 groups: the control group was given tap water, the HH group was given water containing L-methionine (1 g.kg(-1).d(-1)), and the HH+L-arg group was given water containing methionine (1 g.kg(-1).d(-1)) and L-arginine (2.25 vol%). At day 14 ofthe dietary modifications, the left femoral artery and vein were excised, and the extent of angiogenesis and collateral vessels in the ischemic limb were examined for 4 weeks. Plasma homocysteine levels significantly increased (P<0.001), and plasma and tissue contents of nitrite+nitrate as well as tissue cGMP levels significantly decreased in the HH group compared with the control group (P<0.01). Laser Doppler blood flowmetry (LDBF) revealed a significant decrease in the ischemic/normal limb LDBF ratio in the HH group at days 7, 14, 21, and 28 (P<0.01 versus control). Angiography revealed a significant decrease in the angiographic score in the HH group at day 14 (P<0.001 versus control). Immunohistochemistry of ischemic tissue sections showed a significant reduction in the capillary density in the HH group (P<0.001 versus control). Oral L-arginine supplementation in rats with HH (HH+L-arg) restored the decreased plasma and tissue nitrite+nitrate and cGMP contents (P<0.05) as well as angiogenesis, as assessed by LDBF (P<0.05 versus HH), angiographic score (P<0.01 versus HH), and capillary density (P<0.001 versus HH). In summary, HH impaired ischemia-induced angiogenesis and collateral vessel formation in a rat model of hindlimb ischemia in vivo. The mechanism of the HH-induced impairment of angiogenesis might be mediated in partby a reduced bioactivity of endogenous NO in the I-III state.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 14:16:31