PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Blood Platelets”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources
PubMed1969

Microfibrils of blood platelets: their relationship TO MICROTUBULES AND THE CONTRACTILE PROTEIN.

Human blood platelets were subjected to osmotic shock, brief sonication, pressure homogenization, or treatment with adenosine diphosphate (ADP). These procedures demonstrated an abundance of cytoplasmic microfibrils. The fibrils resembled those found on electron microscopy of partially purified thrombosthenin, the actomyosin-like protein isolated from platelets, and they also appeared to resemble the myofilaments of smooth muscle. Similar fibrils were not found in leukocytes studied under identical conditions. Treatment with colchicine (2 x 10(-5) mole/liter) resulted in the disappearance of microtubules but did not affect the morphology of the microfibrils or interfere with platelet-dependent clot retraction. Thus, microfibrils rather than microtubules may represent the morphologic counterpart of the contractile protein. Brief osmotic shock at low temperature or treatment with 10(-4) M ADP caused the marginal band of microtubules to be replaced by a bundle of intertwining microfibrils. The apparent inter-conversion of microtubules and microfibrils under a variety of conditions led to the hypothesis that fibrils and tubules consist of similar subunits whose degree of polymerization might be dependent on local cytoplasmic forces. Furthermore, on the basis of these observations, it is postulated that the contractile properties of the cells may be vested in the microfibrils, whereas the tubules may serve to maintain the highly asymmetric shape characteristic of circulating and irreversibly aggregated platelets.

Adenine Nucleotides↗
PubMed2005

Effect of L-carnitine on acetyl-CoA content and activity of blood platelets in healthy and diabetic persons.

BACKGROUND: Excessive blood platelet activity contributes to vascular complications in diabetic persons. Increased acetyl-CoA in platelets from diabetic persons has been suggested to be a cause of this hyperactivity. We therefore investigated whether L-carnitine, which up-regulates metabolism of acetyl-CoA in muscles and brain, may affect platelet function in healthy and diabetic individuals. METHODS: We obtained platelets from healthy and diabetic persons and measured acetyl-CoA concentrations, malonyl dialdehyde (MDA) synthesis, and platelet aggregation in the absence and presence of L-carnitine. Activities of selected enzymes involved in glucose and acetyl-CoA metabolism were also assessed. RESULTS: Fasting glucose, fructosamine, and hemoglobin A1c were present in significantly higher amounts in the blood of diabetic patients than in healthy individuals. Activities of carnitine acetyltransferase, glucose-6-phosphate dehydrogenase, oxoglutarate dehydrogenase, and fatty acid synthase were 17%-62% higher in platelets from diabetic patients. Mitochondrial acetyl-CoA was increased by 98% in platelets from diabetic patients, MDA synthesis was increased by 73%, and platelet aggregation by 60%. L-Carnitine had no or only a slight effect on these indices in platelets from healthy individuals, but in platelets from diabetic patients, L-carnitine caused a 99% increase in acetyl-CoA in the cytoplasmic compartment along with increases in MDA synthesis and platelet aggregation. CONCLUSIONS: Excessive platelet activity in persons with diabetes may result from increased acetyl-CoA, which apparently increases synthesis of lipid activators of platelet function. L-Carnitine may aggravate platelet hyperactivity in diabetic persons by increasing the provision of surplus acetyl-CoA to the cytoplasmic compartment.

Acetyl Coenzyme A↗
PubMed1985

Liquid chromatography of serotonin and adenine nucleotides in blood platelets, illustrated by evaluation of functional integrity of platelet preparations.

In this relatively rapid liquid-chromatographic procedure the endogenous serotonin in blood platelets is quantified by fluorometry. We used this experimental procedure to estimate the platelet-release reaction as an indicator of the functional integrity of stored platelets. a decrease in the platelet-release reaction more sensitively indicates platelet changes during storage than do alterations in total ATP concentration or adenylate energy charge. The described method for quantifying serotonin is convenient enough for routine use in blood banks.

Adenine Nucleotides↗
PubMed1986

Blood platelet adrenoceptor: aggregatory and antiaggregatory activity of imidazoline drugs.

The effects of seven commonly used imidazoline drugs on human blood platelet aggregation and their inhibitory activity against the adrenaline-induced process were studied. The alpha-adrenoceptor reacting drugs, prazosin and yohimbine, were used as the standards. Low agonistic properties were found in the case of antazoline, clonidine and tetryzoline, whereas those three drugs along with naphazoline, phentolamine, tolazoline and xylometazoline exhibited marked antagonistic activity against the adrenaline-induced aggregation. The results are discussed from the point of view of the existing classification of the alpha-receptors. The conclusion is that the human blood platelet alpha-adrenoceptors, although resembling the properties of the alpha 2-subtype, form either a separate subclass of the receptors or a heterogeneous population of the alpha 2-subtype and an adrenergic receptor different from both alpha 1- and alpha 2-subclasses.

Adult↗
PubMed1997

Comparative effects of selenite and selenite on the glutathione-related enzymes activity in pig blood platelets.

The effects of inorganic selenium (Se) compounds (sodium selenite and selenate) on the activities of glutathione-related enzymes (glutathione peroxidase, glutathione-S-transferase [GST] and glutathione reductase [GR]) in pig blood platelets were investigated in vitro. GST activity in blood platelets treated with 10(-4)M of selenite was reduced to 50%, whereas no decrease GST activity was observed after the treatment of platelets with the same dose of selenate. In platelets incubated with physiological doses (10(-7) and 10(-6)M) of Se compounds, the activity of glutathione peroxidase (GSH-Px) was enhanced (about 20%). GR activity after the exposure of platelets to tested Se compounds was unaffected.

Animals↗
PubMed2004

The role of adenosine triphosphate citrate lyase in the metabolism of acetyl coenzyme a and function of blood platelets in diabetes mellitus.

Diabetes is known to increase blood platelet activity. Activities of pyruvate dehydrogenase (PDH), adenosine triphosphate (ATP)-citrate lyase (ATPCL), acetyl-coenzyme A (acetyl-CoA) content, malonyl dialdehyde (MDA), synthesis, and platelet aggregation in resting conditions and after activation with thrombin were measured in diabetic subjects and in age- and sex-matched healthy subjects. Activities of ATPCL and PDH, acetyl-CoA content, and thrombin-evoked MDA synthesis as well as platelet aggregation in diabetes were 31%, 51%, 62%, 35%, and 21%, respectively, higher than in healthy subjects. In addition, activation of diabetic platelets caused 2 times greater release of acetyl-CoA from their mitochondria than in controls. Both 1.0 mmol/L (-)hydroxycitrate and 0.1 mmol/L SB-204490 decreased acetyl-CoA content in platelet cytoplasm along with suppression of MDA synthesis and platelet aggregation. These inhibitory effects were about 2 times greater in diabetic than in control platelets. The data presented indicate that the ATPCL pathway is operative in human platelets and may be responsible for provision of about 50% of acetyl units from their mitochondrial to cytoplasmic compartment. Increased acetyl-CoA synthesis in diabetic platelets may be the cause of their excessive activity in the course of the disease. ATPCL may be a target for its specific inhibitors as factors decreasing platelet activity.

ATP Citrate (pro-S)-Lyase↗
PubMed1986

Phagocytic activity of human blood platelets examined by electron microscopy.

On the basis of a previously elaborated system for testing the phagocytic ability of the human blood platelets we have undertaken studies of testing the interaction between platelet and bacteria during phagocytosis examined by the electron microscope. We have found that during phagocytosis platelets lose their discoid shape and demonstrate numerous pseudopods. During 2 min a complete engulfment of the bacterium could be observed. 10 min after starting phagocytosis it is possible to note partially destroyed bacteria. The role of human blood platelets in the antibacterial mechanisms is briefly discussed.

Blood Platelets↗
PubMed1990

Protective effect of ceruloplasmin against lipid peroxidation in blood platelets.

The effect of ceruloplasmin on the peroxidation of blood platelet lipids was tested. Using thiobarbituric acid reactivity for measuring lipid peroxidation it was shown that ceruloplasmin inhibited peroxidation of pig platelet lipids induced by UV-irradiation, and much less when enzymatic peroxidation was stimulated by thrombin.

Animals↗
PubMed1995

Effects of submaximal physical exercise and immobilization in bed on the adenine nucleotides concentration in human blood platelets.

The effects of submaximal physical exercise (75% VO2max) and one month immobilization in bed on the adenine nucleotides concentration in human blood platelets were studied and compared. We have shown that after submaximal exercise and after immobilization in bed the concentrations of adenine nucleotides in blood platelets mainly ATP and ADP were decreased and probably caused by the stimulation of platelet secretory process. Thrombin which stimulated the release of 58.2% +/- 1.5% of total adenine nucleotides from control platelets, liberated decreased amounts of nucleotides from platelets after physical exercise and after immobilization in bed (39.9 +/- 2.1% and 23.6 +/- 2.03% of total, respectively).

Adenine Nucleotides↗
PubMed1999

The effect of cis-diamminedichloroplatinum, selenite and a conjugate of cisplatin with selenite [(NH3)2Pt(SeO3)] on oxidative stress in blood platelets measured by chemiluminescence method.

The effects of cisplatin, sodium selenite and a conjugate of these compounds [(NH3)2Pt(SeO3)] on the generation of free radicals in blood platelets measured by chemiluminescence method were investigated in vitro. In platelets incubated with cisplatin (20 microM, 5 min) a dose-dependent increase of chemiluminescence was observed (p < 0.05). Contrary to the stimulatory action of cisplatin (20 microM) on the production of free radicals, selenite (1 microM) and its conjugate with cisplatin (20 microM) had only slight effects on the oxidative stress in platelets (p < 0.05). The observed increase of chemiluminescence after cisplatin action correlated with a decrease of platelet free thiols present in reduced glutathione. Pre-treatment of blood platelets with buthionine sulfoximine (50 microM, 1 h, 37 degrees C) leading to a decrease of glutathione reduced the cisplatin-induced generation of free radicals in these cells (p < 0.05).

Animals↗
PubMed1997

Aluminum induces lipid peroxidation and aggregation of human blood platelets.

Aluminum (Al3+) intoxication is thought to play a major role in the development of Alzheimer's disease and in certain pathologic manifestations arising from long-term hemodialysis. Although the metal does not present redox capacity, it can stimulate tissue lipid peroxidation in animal models. Furthermore, in vitro studies have revealed that the fluoroaluminate complex induces diacylglycerol formation, 43-kDa protein phosphorylation and aggregation. Based on these observations, we postulated that Al(3+) -induced blood platelet aggregation was mediated by lipid peroxidation. Using chemiluminescence (CL) of luminol as an index of total lipid peroxidation capacity, we established a correlation between lipid peroxidation capacity and platelet aggregation. Al3+ (20-100 microM) stimulated CL production by human blood platelets as well as their aggregation. Incubation of the platelets with the antioxidants nor-dihydroguaiaretic acid (NDGA) (100 microM) and n-propyl gallate (NPG) (100 microM), inhibitors of the lipoxygenase pathway, completely prevented CL and platelet aggregation. Acetyl salicylic acid (ASA) (100 microM), an inhibitor of the cyclooxygenase pathway, was a weaker inhibitor of both events. These findings suggest that Al3+ stimulates lipid peroxidation and the lipoxygenase pathway in human blood platelets thereby causing their aggregation.

Adult↗
PubMed1979

Tryptophan accumulation by blood platelets of depressed patients.

The accumulation of tryptophan by blood platelets has been investigated in depressive patients and controls using short incubation times and low substrate concentrations. The accumulation of tryptophan by the platelet is significantly greater in the acutely depressed patients than the control group. The results are discussed with reference to tryptophan transport in depression and also to the regulation of plasma levels of tryptophan.

Biological Transport, Active↗
PubMed1987

Serotonin efflux-inducing effects on human blood platelets by carbamoylpiperidine and nipecotoylpiperazine aggregation inhibitors.

The serotonin efflux-inducing potency of carbamoylpiperidine and nipecotoylpiperazine aggregation inhibitors was evaluated in human blood platelets. Findings were interpreted in terms of structure-activity relationships, and related to actions exerted by the compounds on other human blood platelet functions. Termination of the active efflux period in the presence and absence of acetylsalicylic acid allowed assessment of the influence of aspirin on the quenching process.

Blood Platelets↗
PubMed1991

Effect of skim milk on cholesterol induced blood platelet hyperaggregability in rabbit.

Effect of high cholesterol diet on blood platelet aggregation, and the influence of skim milk on cholesterol induced platelet hyperaggregability were studied in rabbits. The level of aggregated platelets (AP) increased to 19900/mm3 and that of plasma cholesterol to 1605mg/dl, while platelet aggregate ratio (PAR) decreased to 0.32 in rabbits fed high cholesterol diet (0.5% cholesterol) for 12 wk. The levels of AP (12500/mm3) and plasma cholesterol (1196mg/dl) were lower, and the PAR (0.46) was higher in rabbits which received the cholesterol diet supplemented with 16 per cent skim milk powder. In the second experiment, hypercholesterolaemia and platelet aggregation were induced in rabbits by high cholesterol diet given for 6 wk. The animals then received cholesterol-free diets for 8 wk, one group receiving the diet supplemented with 16 per cent skim milk powder and the other without milk served as the control group. The mean PAR in the milk powder supplemented group was restored to normal at 6 wk, while in the control group the level continued to be lower even up to 8 wk. The results thus demonstrate that the milk can prevent the process of cholesterol induced platelet aggregation.

Animals↗
PubMed1980

Anticoagulant-free prepared blood platelets and the effect of calcium on their aggregation behaviour.

Human blood platelets were prepared by gel filtration of native blood and subsequent centrifugation in a Ficoll density gradient avoiding any anticoagulant during the preparation. In ADP, ionophore A 23 187 and thrombin induced aggregation an increase in extracellular Ca++ enhanced the velocity of aggregation. From a defined Ca++ concentration threshold on there was a shift from monophasic to biphasic aggregation.

Adenosine Diphosphate↗
PubMed1999

Inhibitory effect of resveratrol on free radical generation in blood platelets.

Resveratrol (3,4',5-trihydroxystilbene), a compound found in many plants, has been shown to prevent coronary heart diseases and to exert a variety of antiinflammatory and anticancerogenic effects. It is effective in lowering the level of serum lipids and in inhibiting platelet aggregation. We evaluated the effect of trans-resveratrol on the production of free radicals in pig blood platelets and showed that resveratrol inhibited the production of different reactive oxygen species (O2*-, H2O2, singlet oxygen and organic radicals) measured by the luminol-dependent chemiluminescence in resting platelets (P < 0.05). Resveratrol inhibited also the generation of radicals in platelets activated by thrombin (P < 0.05). Treatment of platelets with resveratrol at concentrations of 6.25 and 12.5 microg/ml caused a statistically insignificant increase in the production of O2*- in these cells, as measured by reduction of cytochrome c; however, at higher doses (25, 50 and 100 microg/ml) resveratrol distinctly reduced the generation of O2*- in platelets (P < 0.05). We suggest that free radicals play an important role in the reduced reactivity of blood platelets induced by resveratrol.

Animals↗