e0302 Effects of xuezhikang on blood lipids and the levels of plasma endothelins, thromboxane B2, 6-keto-PGF--1a in Patients with primary hyperlipidaemia

Background: Previous studies showed an anti-atherosclerotic effect of PADMA 28, an herbal formula based on Tibetan medicine. As the mechanisms of action are not fully understood, we investigated whether PADMA 28 may lower blood lipids and lipid oxidisability, and affect early endothelial dysfunction. Patients and methods: Sixty otherwise healthy subjects with total cholesterol ≥5.2 mmol/l and < 8.0 mmol/l were randomly assigned to placebo or PADMA 28, 3 x 2 capsules daily, for 4 weeks (double-blind). Blood lipids (total, LDL-, and HDL-cholesterol, triglycerides, Apo-lipoprotein A1 and B) and ex vivo lipid oxidisability were measured before and after treatment. In a subset of 24 subjects, endothelial function was assessed using venous occlusion plethysmography with intraarterial infusion of acetylcholine. Isolated LDL and plasma both untreated and pre-treated with PADMA 28 extract were oxidised by the radical generator AAPH. Conjugated diene formation was measured at 245 nm. Results: Blood lipids did not change during the study in both groups. In contrast to previous reports in mild hypercholesterolaemia, no endothelial dysfunction was seen and, consequently, was not influenced by therapy. Ex vivo blood lipid oxidisability was significantly reduced with PADMA 28 (area under curve: 5.29 ± 1.62 to 4.99 ± 1.46, p = 0.01), and remained unchanged in the placebo group (5.33 ± 1.88 to 5.18 ± 1.78, p > 0.1). This effect persisted one week after cessation of medication. In vitro experiments confirmed the prevention of lipid peroxidation in the presence of PADMA 28 extracts. Persistent protection was also seen for LDL isolated from PADMA 28-pretreated blood after being subjected to rigorous purification. Conclusions: This study suggests that the inhibition of blood lipid oxidisability by PADMA 28 may play a role in its anti-atherosclerotic effect.

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Type A behavior in healthy males and females as related to physiological reactivity and blood lipids

PsycEXTRA Dataset ◽

10.1037/e576092009-001 ◽

1987 ◽

Cited By ~ 1

Author(s):

Ulf Lundberg ◽

Monica Hedman ◽

Bo Melin ◽

Marianne Frankenhaeuser

Keyword(s):

Blood Lipids ◽

Type A ◽

Type A Behavior ◽

Physiological Reactivity ◽

Males And Females ◽

Healthy Males

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The Interrelationship between Thromboxane Biosynthesis, Aggregation and 5-Hydroxytryptamine Secretion in Human Platelets in Vitro

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650007 ◽

1980 ◽

Vol 43 (01) ◽

pp. 038-040 ◽

Cited By ~ 55

Author(s):

L C Best ◽

T K Holland ◽

P B B Jones ◽

R G G Russell

Keyword(s):

Human Platelet ◽

Human Platelets ◽

Dense Granule ◽

Thromboxane B2 ◽

Essential Requirement ◽

Direct Mechanism ◽

Thromboxane Synthetase ◽

Thromboxane Production ◽

Higher Doses

SummaryPlatelet aggregation, secretion of 5-hydroxy tryptamine and production of thromboxane B2 were monitored simultaneously in human platelet suspensions in the absence and presence of cyclooxygenase or thromboxane synthetase inhibitors. Aggregation, secretion and thromboxane B2 formation in response to either sodium arachidonate or epinephrine were blocked by aspirin or by 1-N-butyl imidazole suggesting that thromboxane biosynthesis was an essential requirement for platelet activation by these agents. In contrast, thrombin and collagen could apparently induce aggregation and secretion via two pathways: at low doses involving thromboxane production, but at higher doses by a direct mechanism independent of thromboxane biosynthesis. In the case of ADP, inhibition of thromboxane production blocked secretion but had little effect on aggregation, indicating that secretion was probably dependent on thromboxane biosynthesis which probably occurred as a result of aggregation. Thus it appears that although the processes of thromboxane production, release of dense granule constituents and aggregation may often be intimately linked, each process can occur independently of the other, depending upon the stimulus used.

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Stimulated Platelet Aggregation, Thromboxane B2 Formation and Platelet Sensitivity to Prostacyclin - A Critical Evaluation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650170 ◽

1981 ◽

Vol 45 (03) ◽

pp. 204-207 ◽

Cited By ~ 42

Author(s):

Wolfgang Siess ◽

Peter Roth ◽

Peter C Weber

Keyword(s):

Arachidonic Acid ◽

Platelet Count ◽

Platelet Aggregation ◽

Reliable Method ◽

Platelet Rich Plasma ◽

Critical Evaluation ◽

Vascular Diseases ◽

Thromboxane B2 ◽

Test Time ◽

Stimulation Of

SummaryPlatelets have been implicated in the development of atherosclerotic and thrombotic vascular diseases. Evaluation of platelet aggregation in relation to endogenously formed compounds which affect platelet function may provide information of clinical and pharmacological relevance. We describe a method in which thromboxane B2 (TXB2) formation was analyzed following stimulation of platelet-rich plasma (PRP) with ADP, 1-epinephrine, collagen, and arachidonic acid. In addition, we determined platelet sensitivity to prostacyclin following ADP- and collagen-induced platelet aggregation. The parameters under study were found to depend on the platelet count in PRP, on the type and dose of the aggregating agent used, and on the test time after blood sampling. By standardization of these variables, a reliable method was established which can be used in clinical and pharmacological trials.

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Trimucytin: A Collagen-Like Aggregating Inducer Isolated from Trimeresurus mucrosquamatus Snake Venom

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651597 ◽

1993 ◽

Vol 69 (03) ◽

pp. 286-292 ◽

Cited By ~ 13

Author(s):

Che-Ming Teng ◽

Feng-Nien Ko ◽

Inn-Ho Tsai ◽

Man-Ling Hung ◽

Tur-Fu Huang

Keyword(s):

Platelet Aggregation ◽

Snake Venom ◽

Inositol Phosphate ◽

Shape Change ◽

Platelet Activating Factor ◽

Atp Release ◽

Platelet Membrane ◽

Thromboxane B2 ◽

Dependent Manner ◽

Concentration Dependent Manner

SummaryTrimucytin is a potent platelet aggregation inducer isolated from Trimeresurus mucrosquamatus snake venom. Similar to collagen, trimucytin has a run of (Gly-Pro-X) repeats at the N-terminal amino acids sequence. It induced platelet aggregation, ATP release and thromboxane formation in rabbit platelets in a concentration-dependent manner. The aggregation was not due to released ADP since it was not suppressed by creatine phosphate/creatine phosphokinase. It was not either due to thromboxane A2 formation because indomethacin and BW755C did not have any effect on the aggregation even thromboxane B2 formation was completely abolished by indomethacin. Platelet-activating factor (PAF) was not involved in the aggregation since a PAF antagonist, kadsurenone, did not affect. However, RGD-containing peptide triflavin inhibited the aggregation, but not the release of ATP, of platelets induced by trimucytin. Indomethacin, mepacrine, prostaglandin E1 and tetracaine inhibited the thromboxane B2 formation of platelets caused by collagen and trimucytin. Forskolin and sodium nitroprusside inhibited both platelet aggregation and ATP release, but not the shape change induced by trimucytin. In quin-2 loaded platelets, the rise of intracellular calcium concentration caused by trimucytin was decreased by 12-O-tetradecanoyl phorbol-13 acetate, imipramine, TMB-8 and indomethacin. In the absence of extracellular calcium, both collagen and trimucytin caused no thromboxane B2 formation, but still induced ATP release which was completely blocked by R 59022. Inositol phosphate formation in platelets was markedly enhanced by trimucytin and collagen. MAB1988, an antibody against platelet membrane glycoprotein Ia, inhibited trimucytinand collagen-induced platelet aggregation and ATP release. However, trimucytin did not replace the binding of 125I-labeled MAB1988 to platelets. Platelets pre-exposed to trimucytin were resistant to the second challenge with trimucytin itself or collagen. It is concluded that trimucytin may activate collagen receptors on platelet membrane, and cause aggregation and release mainly through phospholipase C-phosphoinositide pathway.

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Coagulation Factor VII, Dietary Fat and Blood Lipids: A Review

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650609 ◽

1996 ◽

Vol 76 (04) ◽

pp. 492-499 ◽

Cited By ~ 50

Author(s):

L I Mennen ◽

E G Schouten ◽

D E Grobbee ◽

C Kluft

Keyword(s):

Dietary Fat ◽

Blood Lipids ◽

Coagulation Factor ◽

Factor Vii ◽

Coagulation Factor Vii

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Haematocrit: Relationships with Blood Lipids, Blood Pressure and other Cardiovascular Risk Factors

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648811 ◽

1994 ◽

Vol 72 (01) ◽

pp. 058-064 ◽

Cited By ~ 14

Author(s):

Goya Wannamethee ◽

A Gerald Shaper

Keyword(s):

Physical Activity ◽

Risk Factors ◽

Blood Pressure ◽

Body Mass Index ◽

Cardiovascular Risk ◽

Cardiovascular Risk Factors ◽

Alcohol Intake ◽

Blood Lipids ◽

The Other ◽

The Relationship

SummaryThe relationship between haematocrit and cardiovascular risk factors, particularly blood pressure and blood lipids, has been examined in detail in a large prospective study of 7735 middle-aged men drawn from general practices in 24 British towns. The analyses are restricted to the 5494 men free of any evidence of ischaemic heart disease at screening.Smoking, body mass index, physical activity, alcohol intake and lung function (FEV1) were factors strongly associated with haematocrit levels independent of each other. Age showed a significant but small independent association with haematocrit. Non-manual workers had slightly higher haematocrit levels than manual workers; this difference increased considerably and became significant after adjustment for the other risk factors. Diabetics showed significantly lower levels of haematocrit than non-diabetics. In the univariate analysis, haematocrit was significantly associated with total serum protein (r = 0*18), cholesterol (r = 0.16), triglyceride (r = 0.15), diastolic blood pressure (r = 0.17) and heart rate (r = 0.14); all at p <0.0001. A weaker but significant association was seen with systolic blood pressure (r = 0.09, p <0.001). These relationships remained significant even after adjustment for age, smoking, body mass index, physical activity, alcohol intake, lung function, presence of diabetes, social class and for each of the other biological variables; the relationship with systolic blood pressure was considerably weakened. No association was seen with blood glucose and HDL-cholesterol. This study has shown significant associations between several lifestyle characteristics and the haematocrit and supports the findings of a significant relationship between the haematocrit and blood lipids and blood pressure. It emphasises the role of the haematocrit in assessing the risk of ischaemic heart disease and stroke in individuals, and the need to take haematocrit levels into account in determining the importance of other cardiovascular risk factors.

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Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate

Thrombosis and Haemostasis ◽

10.1055/s-0038-1660081 ◽

1985 ◽

Vol 54 (03) ◽

pp. 612-616 ◽

Cited By ~ 17

Author(s):

A J Carter ◽

S Heptinstall

Keyword(s):

Platelet Aggregation ◽

Whole Blood ◽

Adenosine Diphosphate ◽

Blood Platelet ◽

Thromboxane B2 ◽

Lipoxygenase Inhibitor ◽

Thromboxane Synthase Inhibitor ◽

Synthase Inhibitor

SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature and concentration of the aggregating agent used. The various inhibitors of thromboxane synthesis - aspirin and flurbiprofen (cyclo-oxygenase inhibitors), BW755C (a cyclo-oxygenase and lipoxygenase inhibitor) and dazoxiben (a selective thromboxane synthase inhibitor) - did not markedly inhibit aggregation. Results obtained using apyrase showed that adenosine diphosphate contributed to the aggregation process, and that its role must be acknowledged when devising means of inhibiting platelet aggregation in vivo.

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