摘要:

The diameter, blood velocity, and blood flow of the brachial artery were evaluated with a pulsed-Doppler apparatus before and after wrist occlusion in 16 normocholesterolemic and 27 hypercholesterolemic male subjects of similar age and body mass index. Before occlusion, no hemodynamic differences were observed between the two groups. Occlusion significantly reduced blood velocity and blood flow in the two groups (p< 0.001), but such reductions were not different between hypercholesterolemic and normocholesterolemic groups. Occlusion decreased the arterial diameter in the hypercholesterolemic group only (p<0.001), and absolute diameter changes after occlusion were significantly different between the two groups (p< 0.001). No correlation was found between the change in arterial diameter after occlusion and the baseline diameter before occlusion in the normocholesterolemic and hypercholesterolemic population overall. Absolute and percent diameter changes after occlusion were correlated with total cholesterol (r=−0.73, r=−0.72; p<0.001) and with low density lipoprotein (LDL) cholesterol (r=−0.68, r=−0.69;p<0.001) in the normocholesterolemic and hypercholesterolemic population overall, respectively. These findings indicate that the low-flow state induces a reduction in large-artery diameter in the hypercholesterolemic but not in the normocholesterolemic state and is closely related to the degree of elevation of blood cholesterol and of its LDL fraction.

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Porcine aortic endothelial cells were cultured through four passages from primary cultures. The arachidonic acid content of individual phospholipid classes and the release of 6-keto-prostaglandin F1αand 15-hydroxyeicosatetraenoic acid in response to 1 μM ionophore A23187 were assayed at each passage. The content of arachidonic acid in phosphatidylinositol and diacyl phosphatidylethanolamine remained constant at passage 1 but declined at passage 2 by approximately 29% and at passage 4 by approximately 59%. The release of 6-keto-prostaglandin F1αwas also unchanged at passage 1 but decreased by 60% at passage 2 and by 82% from its original value at passage 4. In contrast, the arachidonic acid content of diacyl phosphatidylcholine and of alkenyl phosphatidylethanolamine decreased with each passage, by 34% at passage 1, 59% at passage 2, 71% at passage 3, and 76% of the original value at passage 4. Stimulation with arachidonic acid reversed the passage effect. The release of 15-hydroxyeicosatetraenoic acid decreased by 82% at passage 1 and diminished to a 97% decrement from the original value by passage 4. When stimulated with arachidonic acid, 15-hydroxyeicosatetraenoic acid steadily decreased by approximately 70% at passages 3 and 4. The data indicate that passage state strikingly and nonuniformly affects phospholipid class arachidonic acid content and eicosanoid release in response to agonist stimulation.

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The relations of high density lipoprotein (HDL) subclasses to severity and rate of progression of coronary atherosclerosis were investigated in 60 men who had survived a myocardial infarction before the age of 45 years and who had subsequently undergone two coronary angjographies, with an intervening time interval of 4–7 years between angiographies. Five HDL subclasses with different particle sizes were determined by gradient gel electrophoresis, and the major serum lipoprotein classes were separated by preparative ultracentrifugation in connection with the second angiography. Highly significant inverse correlations were found between the plasma levels of the largest HDL particles, the HDL2bsubclass, and both disease severity as observed on the second coronary angiogram (r=−0.53,p<0.001) and progression of coronary lesions between angiographies (r=−038,p<0.01). Grouping the patients according to the presence or absence of very low density lipoprotein (VLDL) triglyceride elevation revealed striking differences in the relations of HDL subspecies to coronary atherosclerosis between normotriglyceridemic and hvpertriglyceridemic subjects. There were strong inverse correlations between the plasma HDL2bconcentration and both severity of lesions (r=−0.72,p<0.001) and rate of lesion progression (r=−0.58,p<0.01) in the normotriglyceridemic patients, whereas this relation was absent in subjects with hypertriglyceridemia. Although it was retrospective in design, affected by an inherent selection bias due to unavoidable dropouts and exclusions, and limited to young, male, postinfarction patients, the study suggests that the inverse relation between HDL level and coronary heart disease or coronary atherosclerosis seen in previous epidemiological and angiographlc studies is accounted for by the largest HDL particles, the HDL2bsubclass. Furthermore, the hvpertriglyceridemic state appears to markedly influence the relations between plasma concentrations of HDL subclasses and coronary atherosclerosis. Prospective studies of unselected patients are needed to corroborate these findings.

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Plasminogen activator inhibitor-1 (PAI-1), a rapid inhibitor of tissue-type plasminogen activator, has been shown to be an independent risk factor for recurrent myocardial infarction (MI) at a young age. To investigate whether genetic variation in the PAI-1 gene is affecting plasma PAI-1 levels, a sample of 145 patients with an MI before the age of 45 years was genotyped for two polymorphisms at the PAI-1 locus, together with a sample of 95 healthy individuals of a similar age. All individuals were measured for plasma PAI-1 levels as well as for other fibrinolytic and metabolic risk indicators. A HindlU restriction fragment length polymorphism (RFLP) was used in this study in conjunction with a previously unreported eight-allele dinucleotide repeat polymorphism at the PAI-1 locus. The dinucleotide repeat polymorphism and HindIII RFLP were in strong linkage disequilibrium. There was no difference in the frequency of alleles of either polymorphism between patient and control groups. However, the smaller dinucleotide repeat alleles were significantly associated (p=0.03) with higher plasma PAI-1 levels in the patient sample. This association was also apparent in the control sample but not at significant levels. Differences in regression coefficients for the effect of triglycerides on plasma PAI-1 levels suggest that triglyceride regulation of PAI-1 is genotype specific Our data suggest that genetic variation at this locus contributes to between-individual differences in the level of plasma PAI-1, which is important in fibrinolysis and the pathogenesis of MI.

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

Proteoglycan metabolism was evaluated in megakaryocytes and platelets from guinea pigs fed a 1% cholesterol diet for 3 or 7 weeks. The animals were injected with a single dose of [35]sulfate at the end of the feeding period, and megakaryocytes and platelets were isolated after 3 hours and then daily for 4 days thereafter. Proteoglycans were extracted from the cells of each animal and analyzed by ion-exchange chromatography, gel filtration, and electrophoresis. The maximal labeling of platelets occurred 2 days after [35S]sulfate injection as compared with 3 days in controls. A proteoglycan that eluted at Kav 0.2 from the Sephorose CL-6B column appeared 1 day after labeling. Additional proteoglycans of Kav 0.15 appeared at subsequent time points. The labeling profile for cholesterol-fed animals was unchanged from 2 - 4 days, unlike profiles from controls, which had exhibited a gradual increase in mean proteoglycan size. Thus, the progressive change in size of proteoglycans synthesized during normal megakaryocyte maturation was altered. The mean chain length of the proteoghycanassociated glycosaminoglycans from cholesterol-fed animals was increased relative to that of controls. In conjunction with the twofold increase in mean megakaryocyte size induced by cholesterol feeding in guinea pigs, the changes in proteoglycan synthesis suggest a state of stimulated megakaryocytopoiesis.

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

摘要:

The Influence of native (N-) and oxidized (Ox-) low density lipoproteins (LDLs) on endothelium-dependent vasomotion is still controversial. We investigated the short-term effects of N-LDL and Ox-LDL on the formation of endotheliom-derived relaxing factor (EDRF) in native and cultured endothelial cells and on its inactivation after release from the cells. N-LDL was isolated from fresh human plasma via sequential ultracentrifugation and oxidized by incubation with Cu2+. EDRF released from cultured endothelial cells was inactivated by both N-LDL and Ox-LDL (1 mg/ml) as detected in a bioassay system. N-LDL reduced the EDRF-mediated vasodilations of the detector segments by 38.5 ±5.3%, and Ox-LDL, by 55.5 ±4.6%. The effects of lipoproteins on EDRF formation were studied in cultured endothelial cells preincubated with either N-LDL or Ox-LDL (1 mg/ml for 1 hour) and stimulated for EDRF release with bradykinin after washout of the lipoproteins. EDRF was assessed by measuring its stimulatory effect on the activity of a purified, soluble guanylate cyclase. Both N-LDL and Ox-LDL did not reduce the bradyldnin-induced EDRF formation. Consistent with this finding, acetylcholine-induced, EDRF-mediated dilations of intact rabbit femoral artery segments were not impaired by luminal exposure to N-LDL or Ox-LDL (1 mg/ml for 1 hour). However, these relaxations were significantly reduced by preincubation of aortic ring preparations with the same concentrations of the same charges of N-LDL and Ox-LDL. In conclusion, neither N-LDL nor Ox-LDL acutely impairs the formation of EDRF but does inactivate EDRF after its release from endothelial cells. This mechanism may be important in regions with accumulation of lipoproteins in the arterial wall and may favor the development of inappropriate vasoconstriction.

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID

ISSN:1049-8834    

出版商:OVID    

年代:1991

数据来源: OVID