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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 6 healthy adults the effect of essential oil of garlic on platelet aggregation was studied in vitro with an aggreganometer. The blood was collected in a siliconized centrifuge tube containing sodium citrate. The aggregating agents used were ADP, epinephrine and collagen. In each subject aggregation was studied 3 times: (i) initial fasting control; (ii) immediately after (i) but with essential oil of garlic drawn into the syringe together with the sodium citrate; (iii) 5 days after feeding 0.5 mg of essential oil of garlic daily. Addition of essential oil of garlic inhibited in-vitro platelet aggregation induced by ADP, epinephrine or collagen; the effect was dose-related. Oral administration of garlic also decreased platelet aggregation. Thus, garlic seems to inhibit some aspects of thrombus formation.
Atherosclerosis 1978 Aug
PMID:Effect of garlic on human platelet aggregation in vitro. 70 92

This review has highlighted some of the factors which influence the formation and fate of thrombi. Rheology and flow, the coagulation mechanism, the fibrinolytic enzyme system, and the properties of platelets to adhere and aggregate all play a significant role. Of paramount importance to neurosurgeons is the role of the vascular wall in thrombogenesis. The ulcerated atherosclerotic plaque demonstrates this point. Factors contributing to thromboembolism in this setting include stenosis and reduced flow, turbulence, and the elements in the lesion with which blood interacts. These are principally collagen, ADP, fatty acids, and the thromboplastic activity of vascular subendothelial tissue. Current concepts of the etiologies of atherosclerosis were discussed. Along with other predisposing factors, platelets may play a significant role in the initiation of the process. The current status of clinical trials with inhibitors of platelet function in the treatment of cerebrovascular disorders was reviewed. In vascular reconstructive surgery, the principles which underlie good technique are those which best insure against thrombosis. The briefest possible period of stasis during surgery should be maintained. The reconstruction should result in a smooth blood flow pattern with rapid runoff and minimal stenosis or gaps between apposed endothelial surfaces.
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PMID:Hematological and vascular concepts in relation to stroke. 97 74

In 120 patients with atherosclerosis, complicated in 43 patients by a haemorrhagic, in 47 patients by an ischaemic, and in 30 patients by a transient cerebral insult, phase analysis of platelet aggregation was performed by the turbidimetric method according to Born with graphic recording according to O'Brien. An increase in the platelet activity was found in ischaemic insult, manifesting itself by the occurrence of spontaneous aggregationin 60% of the cases, an acceleration of ADP-induced aggregation, and the second aggregation phase in all patients examined. A direct correlation was revealed between the secondary aggregation and the intensity of spontaneous and of ADP-induced aggregation, and the possibility of a transformation of the spontaneous into the secondary aggregation of platelets was demonstrated. Haemorrhagic insults were characterized by the absence of spontaneous and secondary aggregation and by the suppression of ADP-induced aggregation. In a transient insult, the mean values of the aggregatogram items did differ from normal. In vitro, the role of increased permeability of platelet membranes in the mechanism triggering off spontaneous aggregation and the second phase of ADP-induced aggregation was documented.
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PMID:Phase analysis of platelet aggregation in acute disturbances of cerebral circulation. 115 98

The effect of dietary fatty acids on the formation and growth of intra-arterial occlusive thrombi in rats was investigated. It appeared that fats containing a large amount of saturated fatty acids promote arterial thrombus formation, whereas dietary linoleic acid has a specific anti-thrombotic effect. Oleic acid on its own does not seem to act as an anti-thrombotic substance. However, the replacement of thrombogenic fatty acids by oleic acid results in a decrease of the dietary thrombogenic potency. Moreover, the results indicated that the thrombogenicity of the saturated fatty acids increases with their chain length. As for the anti-thrombotic effect of cis fatty acids and their trans isomers, no obvious differences have been observed. Almost identical results were obtained when thrombogenicity was related to either absorption or to composition of the dietary fatty acids. Further research can therefore be restricted to this latter criterion. For the majority of the fats tested, thrombosis tendency and ADP-induced platelet aggregation were closely associated. It is therefore highly probable that platelet aggregation is involved in the mechanism by which dietary fats affect arterial thrombus formation.
Atherosclerosis
PMID:Relationship between the type of dietary fatty acid and arterial thrombosis tendency in rats. 120 Nov 49

Twenty necroptic atherosclerotic aortas were studied using a modified en face Hautchen preparation method. Endothelium of 1 x 1 cm pieces of aortas was frozen onto slides with the help of dry ice. Endothelial cells on atherosclerotic lesions were irregularly oriented, had ununiform shape and giant multinucleated endothelial cells were present. The endothelial pavement on atheromatous lesions was usually defective. There was increased activity of ATPase and 5'Nase in endothelial cells on atherosclerotic lesions and on their borders. It is suggested that the high activity of ectonucleotidases of the endothelium on atherosclerotic lesions results in rapid dephosphorylation of ATP and ADP released by platelets aggregating to adenosine. Adenosine accumulated in the unstirred layer of plasma in the macrovasculature can effectively inhibit platelet aggregation and subsequent thrombosis on pathologically changed vascular pavement in atherosclerosis.
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PMID:Activity of ATPase and 5'nucleotidase in endothelium of human atherosclerotic aortas. 130 20

Hypercholesterolemia and hypertension are two of the major risk factors associated with increased atherosclerotic vascular disease. An abnormal platelet function is one of the mechanisms proposed to participate in atherogenesis. This study was undertaken to find out whether hypercholesterolemia in hypertensive patients can change platelet lipid composition and reactivity. Twenty-nine untreated hypertensive patients were distributed into 3 age, body mass index and blood pressure-matched groups according to their plasma cholesterol levels (normal, borderline or elevated, group NC, BC and HC respectively). Their platelet lipid composition, cytosolic Ca2+ concentration, cyclic AMP content and aggregating response to ADP and collagen were determined. Platelet from group HC patients were characterized by reduced cyclic AMP content (evaluated in the presence and absence of a platelet phosphodiesterase inhibitor) and aggregating responses to ADP and collagen, increased palmitic acid content and decreased arachidonic, eicosapentaenoic and docosatetraenoic and pentaenoic acid content, resulting in a lowered polyunsaturated to saturated fatty acid ratio (P less than 0.001). In contrast, platelet cytosolic Ca2+ concentration, DPH steady-state anisotropy and cholesterol to phospholipid molar ratio were not significantly changed. This indicates that hypercholesterolemia is accompanied in hypertensive patients by marked changes in platelet fatty acid composition, cyclic AMP content and response to aggregating agents. These changes, which clearly differ from those induced by in vitro cholesterol loading, could reflect not only the balance between LDL and HDL stimulation but also an adaptation to hemodynamic perturbations.
Atherosclerosis 1992 Jun
PMID:Biochemical and functional alterations associated with hypercholesterolemia in platelets from hypertensive patients. 132 32

The coagulative system has an important role on haemodialysis and on atherosclerosis genesis; in particular the platelets are key elements of the coagulation and of atherosclerosis phenomena. Alterations of the coagulative system and increase risk of developing atherosclerosis are reported in the aging. We in this paper, report the results obtained studying the influence of the interaction between the elderly and dyslipidemia on the coagulative system in haemodialyzed patients. The obtained data showed that the hypertriglyceridaemia in interaction with the elderly accelerates and increases platelet aggregation after stimulation by ADP, Epinephrine and Collagen. So, it is important to consider hypertriglyceridaemia and age as thrombogenic factors and atherosclerosis accelerating factors in haemodialyzed patients.
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PMID:The coagulative system in haemodialyzed patients: the relationship between the elderly and hypertrygliceridaemia. 138 42

Vascular responses to intraluminal and abluminal activation of human platelets were examined in carotid arteries from normal and atherosclerotic rabbits. The carotid artery was perfused in vitro, platelets were activated with thrombin (0.1 unit/ml), and changes in diameter were measured. In vessels from normal animals, intraluminal activation of platelets produced dilatation of preconstricted arteries. The dilator response was attenuated by N omega-nitro-L-arginine (10(-5) M), an inhibitor of synthesis of endothelium-derived relaxing factor-nitric oxide (EDRF-NO), and augmented by LY53,857 (10(-5) M), a 5-HT2-serotonergic antagonist. Abluminal activation of platelets produced modest constriction in quiescent arteries, which was inhibited by LY53,857. Intraluminal but not abluminal ADP produced pronounced dilatation of preconstricted arteries. In vessels from atherosclerotic animals, endothelium-dependent dilatation to intraluminal activation of platelets and to ADP was impaired and dilator responses to sodium nitroprusside were normal. These experiments indicate that 1) intraluminal activation of human platelets produces endothelium-dependent dilatation in perfused carotid arteries, whereas abluminal activation of human platelets produces vasoconstriction, which is mediated primarily by serotonin, and 2) atherosclerosis markedly impairs vasodilator responses to activation of human platelets, probably because vasodilatation to ADP released from platelets is impaired.
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PMID:Effect of atherosclerosis on responses of the perfused rabbit carotid artery to human platelets. 139 May 92

In the present study performed on rats, we investigated the influence of an in vivo acute iron load on several platelet parameters and their modification after vitamin E supplementation. Iron load was achieved by injecting iron dextran corresponding to 0.1 mg Fe3+ per kg in the gluteus muscles. Control rats were injected with an equal amount of a dextran solution. Analyses were performed 18 h after injection. By comparison with controls, in iron-injected animals, we found significant increases of: (1) serum total iron (by 110%); (2) aggregation of isolated platelets induced by low concentration of thrombin and ADP (by 350% and 120%, respectively); (3) thrombin-induced endogenous serotonin secretion (by 94%). We also studied the mobilization of radiolabeled arachidonate preincorporated into platelet phospholipids. The results indicated that the thrombin-stimulated release of arachidonate and formation of cyclooxygenase and lipoxygenase products (particularly thromboxane B2), were significantly increased. We also found in plasma an increase (by 67%) of malondialdehyde (MDA) as well as a decrease of vitamin E (by 60%). When vitamin E was injected the day before iron injection, platelet hyperactivity and thromboxane biosynthesis were reduced as well as the plasma MDA concentration. Consequently, given the key role of calcium flux in the activation processes in platelets, we also investigated the thrombin-induced Ca2+ uptake by means of radiocalcium. We found that in platelets from iron-treated rats the Ca2+ uptake amounted to 3670 +/- 201 pmol/10(9) platelets (plt) and was significantly different from controls (1680 +/- 192 pmol/10(9) plt, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1992 Oct
PMID:Effect of vitamin E on acute iron load-potentiated aggregation, secretion, calcium uptake and thromboxane biosynthesis in rat platelets. 146 49

This study was conducted to investigate acute effects of smoking on platelet function, endothelial cells and plasma lipids and to follow these parameters after Aspirin ingestion. Twelve fasting smokers each inhaled the smoke of one cigarette. Blood was drawn before and 10 min after smoking. Plasma nicotine, measured by gas chromatography, increased from 13.48 before smoking to 78.41 nM after smoking. Platelet aggregation to thrombin and ADP increased significantly (P less than 0.001). The platelet aggregate ratio decreased from 0.95 to 0.75 (P less than 0.005). Plasma beta-thromboglobulin also increased in post-smoking samples as measured using radioimmunoassay. 'Circulating endothelial cells' increased significantly after smoking (P less than 0.005). Triglycerides decreased (P less than 0.005) in plasma and in the VLDL fraction (P less than 0.05). Both post-smoking plasma free fatty acids and free glycerol increased, respectively, as compared with respective values. Lipase activity ascribable to lipoprotein lipase and hepatic lipase, absent in pre-smoking plasma samples, could be detected in post-smoking plasma without heparin injection. At least 1 week later, the subjects returned to follow an identical protocol except that they had ingested Aspirin (650 mg) 10-14 h before blood sampling. The same parameters were measured before and after smoking the same cigarette. Except for plasma nicotine, all the smoking-induced changes were abolished by ingestion of Aspirin. The results of this study indicate an interrelationship between platelet hyperactivity, endothelial injury and plasma lipids. They also demonstrate an inhibition of the major smoking-induced changes by Aspirin in the presence of high plasma nicotine levels. It is concluded that Aspirin may offset several of the deleterious acute effects of smoking. However, our conclusions cannot be, in any way, extended for long-term effects of both smoking and Aspirin treatment. Based on these data, it is suggested that there may be some links between platelet hyperactivity, endothelium injury and plasma lipids.
Atherosclerosis 1992 Apr
PMID:Acute influence of smoking on platelet behaviour, endothelium and plasma lipids and normalization by aspirin. 146 56


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