ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundPrevious findings concerning the serum levels of fish-derived (n-3) fatty acids and coronary heart disease are inconsistent. The purpose of this study was to investigate the association between the serum n-3 end-product fatty acids docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and eicosapentaenoic acid and the risk of acute coronary events in middle-aged men.Methods and ResultsWe studied this association in the Kuopio Ischaemic Heart Disease Risk Factor Study, a prospective population study in Eastern Finland. Subjects were randomly selected and included 1871 men aged 42 to 60 years who had no clinical coronary heart disease at baseline examination. A total of 194 men had a fatal or nonfatal acute coronary event during follow-up. In a Cox proportional hazards’ model adjusting for other risk factors, men in the highest fifth of the proportion of serum DHA+DPA in all fatty acids had a 44% reduced risk (P=0.014) of acute coronary events compared with men in the lowest fifth. Men in the highest fifth of DHA+DPA who had a low hair content of mercury (≤2.0 &mgr;g/g) had a 67% reduced risk (P=0.016) of acute coronary events compared with men in the lowest fifth who had a high hair content of mercury (>2.0 &mgr;g/g). There was no association between proportion of eicosapentaenoic acid and the risk of acute coronary events.ConclusionsOur data provide further confirmation for the concept that fish oil–derived fatty acids reduce the risk of acute coronary events. However, a high mercury content in fish could attenuate this protective effect.

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundCytotoxic oxidized LDL (oxLDL) has been shown to promote apoptosis in cultured vascular smooth muscle cells (VSMCs). We investigated the localization of oxLDL and its association with apoptosis and the expression of apoptosis-related proteins in early and advanced atherosclerotic lesions.Methods and ResultsAtherosclerotic plaques (n=23) from patients undergoing aortic, carotid, or femoral arterial surgery were studied. In early lesions, oxLDL was located predominantly in the superficial intima and in the media just beneath the internal elastic lamina. Medial VSMCs staining positive for oxLDL showed expression of BAX, a proapoptotic protein of the BCL-2 family. Apoptosis, as detected by DNA in situ terminal deoxynucleotidyl transferase end-labeling (TUNEL), was not present in these early lesions. In advanced plaques, areas of the intima positive for oxLDL showed lower &agr;-smooth muscle actin immunoreactivity (P<0.01) and higher BAX immunoreactivity (P<0.05). Furthermore, these areas showed an increased number of apoptotic VSMCs (P<0.01). Western blot analysis revealed that oxLDL increases BAX expression in cultured human coronary VSMCs.ConclusionsWe conclude that in early atherosclerotic lesions, oxLDL-positive VSMCs express BAX, which increases the susceptibility of these cells to undergo apoptosis. This could be important in our understanding of the transition of early lesions into advanced atherosclerotic plaques, which are characterized by regions of cell death. In advanced plaques, oxLDL-positive areas of the intima show higher BAX immunoreactivity and TUNEL-positive VSMCs, and this may contribute to plaque instability and rupture.

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundWe determined whether the vascular effects of estradiol depend on the route of administration by comparing the effects of oral estradiol and transdermal placebo, transdermal estradiol and oral placebo, and transdermal placebo and oral placebo on in vivo endothelial function in 27 postmenopausal women.Methods and ResultsEndothelial function was assessed from blood flow responses to intrabrachial artery infusions of endothelium-dependent (7.5 and 15 &mgr;g/min acetylcholine) and endothelium-independent (3 and 10 &mgr;g/min of sodium nitroprusside) vasodilators at 0, 2, and 12 weeks. In the oral estradiol group, the increase in flow above basal during infusion of the low dose of acetylcholine at 0, 2, and 12 weeks averaged 6.0±0.8, 6.9±0.8, and 11.3±1.2 (P<0.01 versus 0 and 2 weeks) mL · dL−1· min−1at 0, 2, and 12 weeks. The percentage increases versus 0 weeks averaged 21±14% at 2 and 120±34% at 12 weeks. During the high-dose acetylcholine infusion, the increase in flow above basal averaged 8.6±1.3, 10.2±1.5, and 15.1±1.8 (P<0.05 versus 0 weeks) mL · dL−1· min−1, respectively. The percentage increases versus 0 weeks averaged 22±10% at 2 weeks and 119±46% at 12 weeks. In the oral estradiol group, endothelium-independent vasodilatation also improved significantly, but less markedly than endothelium-dependent responses. In the transdermal and placebo groups, all vascular responses remained unchanged. Oral but not transdermal estradiol also induced significant decreases in LDL cholesterol and Lp(a) concentrations and an increase in HDL cholesterol within 2 weeks.ConclusionsWe conclude that oral but not transdermal estradiol induces potentially antiatherogenic changes in in vivo endothelium-dependent vasodilatation and lipid concentrations.

ISSN:0009-7322    

出版商:OVID    

年代:2000

数据来源: OVID