Platelet-collagen interaction: adhesion of human blood platelets to purified (CB4) peptide from type III collagen.
Explore the source record for details and available documents.
Animals↗
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.
Establishing a practical blood platelet threshold to avoid reporting spurious potassium results due to thrombocytosis.
BACKGROUND: Thrombocytosis is one of several pre-analytical factors which contribute to spuriously high serum potassium concentrations, yet there is little published data to guide analysts in the selection of a specific platelet count threshold above which serum potassium results become unreliable. We have studied the sensitivity and specificity of blood platelet count as a predictor of false elevations in potassium. METHODS: Paired serum and plasma potassium measurements together with full blood count were performed for 300 patients. All samples were stored at room temperature and analysed within 4 h of collection. The difference between serum and plasma potassium was plotted against blood platelet count. RESULTS: When the difference (serum-plasma) in potassium concentration was plotted against platelet count, there was a direct linear relationship. Blood platelet counts of >500 x 10(9)/L will detect elevations in serum relative to plasma potassium of >0.5 mmol/L, with a sensitivity of 71% and a specificity of 89%. CONCLUSION: It is recommended that where blood platelet count is above 500 x 10(9)/L, potassium measurements should be repeated using lithium heparin plasma. When serum potassium results of >5.4 mmol/L are obtained, it is our policy to check the platelet count if a sample is available before reporting results. If available and above 500 x 10(9)/L, potassium results are withheld and plasma requested.
Adult↗
Whole blood platelet aggregation in dogs with liver disease.
Whole blood platelet aggregation was determined in response to collagen, arachidonic acid, and adenosine diphosphate in 20 dogs with liver disease and in 20 control dogs. Platelet aggregation in response to collagen and arachidonic acid was reduced in dogs with liver disease, compared with control dogs (P less than 0.05), whereas there was no significant difference in platelet response to adenosine diphosphate between the 2 groups of dogs. Adenosine diphosphate was found not to be a reliable aggregation agent for determination of whole blood platelet aggregation in dogs. Dogs whose platelets did not aggregate in response to collagen and/or arachidonic acid manifested bleeding tendencies that could be attributed to platelet dysfunction.
Adenosine Diphosphate↗
1H-NMR lipid profiles of human blood platelets; links with coronary artery disease.
Blood platelets are closely involved in the early development of atherosclerosis and in the events that lead to thrombosis, both of which are dominating factors in coronary artery disease (CAD). The aim of the present study was to evaluate the platelet lipid profiles of patients suffering from CAD and explore the possibility of a link between platelet lipids and CAD, using high-resolution high-field proton nuclear magnetic resonance spectroscopy as the analytical tool. The total platelet lipid profiles of healthy volunteers were compared with those of patients presenting with chest pain requiring coronary angiography. Two lipid groups changed significantly: cholesterol increased by 16.5% and total diacylglycerophospholipids decreased by 15.7%. There was also a significant decrease of the ethanolamine-containing phospholipids, by 4.7%; the extent of unsaturation of the fatty acid chains, by 0.2, and increase of the linoleate content of the fatty acid chains, by 1.9%. Our results suggest that platelet lipid abnormalities occur in patients with CAD and these changes may predate the development of overt atherosclerosis.
Blood Platelets↗
Effect of physical exercise on antioxidative enzymatic defense in blood platelets from healthy men.
Our investigations were carried out on blood platelets obtained from 41 healthy men subjected to submaximal physical exercise. Physical exercise was found to induce a significant increase of superoxide dismutase, catalase and glutathione peroxidase activities in blood platelets accompanied by a decrease of platelet malonyldialdehyde and thromboxane A2 concentration.
Adult↗
Inhibition of cyclic AMP phosphodiesterase activity of human blood platelet membrane by ADP.
Purified human blood platelet membrane showed the presence of one low Km (1.1 microM) and one high Km (5.0 microM) cyclic AMP phosphodiesterase(s). Incubation of platelet-rich plasma or gel-filtered platelets with ADP (4.0 microM), a well-known platelet aggregating agent, resulted in the inhibition of phosphodiesterase activity of the isolated membrane by 25% in 5 min at 23 degrees C. A Lineweaver-Burk plot of the enzymic activity of the membrane preparation showed that ADP specifically inhibited the low Km (1.1 microM) phosphodiesterase by reducing the Vmax from 241 to 176 pmol/mg per min with concomitant lowering of Km to 0.5 microM. In contrast, neither the high Km (5.0 microM) enzymic activity of the membrane preparation nor the phosphodiesterase activities of the cytosolic fraction of the ADP-treated platelets was affected. This effect of ADP, which was independent of platelet aggregation, reached maximal level within 5 min of incubation. When platelet-rich plasma was incubated longer in the presence of nucleotide, the inhibition of phosphodiesterase activity began to decrease, and after 20 min of incubation approx. 90% of the original enzymic activity was regained. The incubation of platelet-rich plasma with 4.0 microM ADP also increased the cyclic AMP level to twice the basal level. The effect of ADP on the phosphodiesterase activity could be demonstrated only by incubating the intact platelets with the nucleotide. The treatment of isolated membrane from platelets, previously unexposed to ADP, with the nucleotide did not inhibit the enzymic activity. The inhibition of phosphodiesterase by the nucleotide in the absence of stirring, as expected, resulted in the inhibition of platelet aggregation when these cells were subsequently stirred with 1-epinephrine or an increased concentration of ADP.
3',5'-Cyclic-AMP Phosphodiesterases↗
[Effect of thrombin stimulated blood platelets on plasma fibrinolytic activity].
The influence of thrombin stimulated-blood platelets on plasma fibrinolytic activity was evaluated. Thrombin-activated blood platelets have been shown to significantly inhibit plasma fibrinolytic activity before and after venous stasis. This was expressed by a reduction of the digestion area of fibrin dish from 10.3 +/- 3.3 cm2 to 3.7 +/- 1.5 cm2 and from 15.6 +/- 6.8 cm2 to 3.7 +/- 1.7 cm2, respectively.
Adult↗
Vitamin E consumption by human blood platelets activated by latex particles.
Human blood platelet activation elicited by latex particles is associated to a 30% decrease in the cellular content of vitamin E. The vitamin E consumption is inhibited by the addition of catalase (500 U/ml) and azide (1 mM), but it is not affected by potassium cyanide (1 mM). It may be proposed that the challenge of platelets with particulate stimuli causes generation of oxygen reduction products, which leads to vitamin E depletion.
Azides↗
Cooperation of chloroquine and blood platelets in inhibition of polymorphonuclear leukocyte chemiluminescence.
Effect of activated blood platelets and chloroquine on concentration of reactive oxygen species produced by polymorphonuclear leukocytes (PMNL) stimulated with Ca(2+)-ionophore A23187 was investigated. Oxygen metabolites localized outside PMNL were visualized by isoluminol enhanced chemiluminescence, whereas chemiluminescence, enhanced with luminol and measured in the presence of the extracellular scavengers superoxide dismutase and catalase, was used for the detection of radicals originated intracellularly. Significant reduction of chemiluminescence was observed in the presence of platelets (added to PMNL in the physiological cell ratio 50:1) and of chloroquine (10 and 100 micromol/L). Although chloroquine decreased effectively both the extra- as well as the intracellular part of the chemiluminescence signal, the activity of platelets occurred largely outside PMNL. Serotonin liberated from platelets by A23187 appeared to be involved in inhibition of chemiluminescence; its concentrations achieved in platelet supernatants were found to be sufficient for elimination of PMNL-derived oxygen metabolites. The presented results indicated that chloroquine and blood platelets cooperate in inhibition of chemiluminescence because their common effect was found to be much more extensive than reduction induced by these inhibitors separately. Therefore, for accurate prediction of drug effect in the whole organism, the use of multicellular test systems seems to be pertinent.
Blood Platelets↗
Bovine fibrinogen-induced 14C-serotonin and other compounds release from human blood platelets.
Bovine fibrinogen can aggregate human blood platelets by a direct mechanism (first wave) and also indirectly by releasing endogenous ADP (second wave). A primarily non-altered surface structure of the thrombocytes is important for the induction of the first wave. Under certain conditions a second aggregation wave, concomitant with the release and the availability reaction is elicited. Besides the cell's contact, the presence of ADP and calcium ions are necessary for the induction of the release reaction in human platelet rich plasma. The changes induced by bovine fibrinogen thus follows the same pattern as the irreversible phase of aggregation, linked to release as induced by ADP.
Acid Phosphatase↗
Abnormalities of 5-hydroxytryptamine uptake and binding by blood platelets from children with Down's syndrome.
1. Blood platelets from normal children and children with the trisomy 21 form of Down's syndrome (mongolism) were studied to determine the cause of the well established reduction in platelet 5-HT in the disease.2. Concentrations of endogenous 5-HT in the platelets from mongols were 25.3% of the concentrations found in normal children.3. The net accumulation of 5-HT in the mongol cells was decreased to 52.7% of normal. This reduction was probably due, in part, to a defect in 5-HT transport, because the initial rates of 5-HT uptake at plasma concentrations of 10(-6) and 10(-5)M were significantly slower.4. Experiments on the efflux of 5-HT from mongol platelets loaded with amine showed that the rate of loss was initially 2.6 and later 7.8 times faster than normal.5. Platelet ATP in mongol cells was 26% of normal, and the reduction of ATP and 5-HT was in the molar ratio of 3:1.6. It is considered that the low platelet 5-HT in Down's syndrome is due to a defective 5-HT transport mechanism and impaired 5-HT binding, resulting from a reduction in the essential binding substance, ATP.
Adenosine Triphosphate↗
Blood platelet behaviour in mothers and neonates.
Blood platelet behaviour was compared in mothers at birth and their babies, and in non-pregnant, female controls. Platelet responses to arachidonic acid (AA) and to adrenaline were measured in platelet-rich plasma and the inhibitory effects of prostacyclin (PGI2) were determined. Platelets from the mothers differed from those from the neonates and controls in that lower concentrations of AA were needed to induce platelet aggregation and a release reaction. In addition, more PGI2 was needed to inhibit AA-induced platelet aggregation. Platelets from the neonates differed from the mothers and controls in that they were almost completely insensitive to adrenaline. They did not differ from the controls in their sensitivity to AA or PGI2 but the extent of the release reaction induced by AA was significantly reduced.
Arachidonic Acid↗
Early changes in the substructure of the marginal bundle in human blood platelets responding to adenosine diphosphate.
Human blood platelets were exposed to 10 microM adenosine diphosphate in order to induce shape changes and their ultrastructure was examined in preparations fixed with a glutaraldehyde-tannic acid mixture. Within 5 sec after the addition of ADP the marginal bundle along the perimeter of the platelet had undergone profound changes. The intertubular filaments of the marginal bundle were lost and, probably as a consequence, the microtubules were dispersed. The microtubules also had fragmented and appeared as straight rods rather than smoothly curved coils. Profiles with 14 or 15 protofilaments rather than the common 13-unit pattern were seen in 16% of the cross-sectioned microtubules. The proportion of incomplete (C-shaped) microtubules or of microtubules with an electron-dense interior also had increased and were interpreted as sections near the terminal ends of a microtubule. We interpret the C-shaped and the "filled" microtubules as signs of a disassembled microtubule and the 14- and 15-protofilament profiles as probably representing new (ends of) microtubules reassembled with a defective control of the proper structure.
Adenosine Diphosphate↗
Effect of flunarizine and calcium on serotonin uptake in human and rat blood platelets and rat synaptosomes.
Calcium and the calcium overload blocker flunarizine exert profound effects on mood. We therefore studied the effect of calcium and flunarizine on serotonin uptake in human and rat blood platelets and in rat synaptosomes. Calcium (1.3 mmol/L) had a weak inhibiting effect on serotonin uptake in blood platelets, whereas no effect was observed in synaptosomes. Flunarizine inhibited serotonin uptake in a concentration dependent manner with an IC50 value of 1 mumol/L in blood platelets and 5 mumol/L in synaptosomes. The inhibition did not depend on the presence of extracellular calcium indicating that the effect is not coupled to a blockade of cellular calcium influx. In human blood platelets, the inhibition was of the noncompetitive type. These results indicate that flunarizine interacts directly with the 5-HT uptake site. The relatively high concentration of flunarizine required to inhibit 5-HT uptake may question the clinical importance of this effect.
Animals↗
Effect of heparin on in vitro platelet reactivity in cardiac surgical patients--a comparative assessment by whole blood platelet aggregometry and haemostatometry.
The in vitro effect of heparin on platelet reactivity was assessed simultaneously by haemostatometry (response to shear stress) and whole blood platelet aggregometry response to collagen (WBPA). From each blood sample a ratio (HR for haemostatometry and MR and IR for WBPA) showing platelet reactivity in the presence or absence of heparin (5 U/ml) was calculated. A value less than 1 represented a proaggregatory effect and greater than 1 an inhibitory effect. Non-anticoagulated blood samples obtained from 290 cardiac surgical patients were tested by haemostatometry and citrated whole blood samples from 100 patients with aggregometry. Haemostatometry demonstrated a proaggregatory effect of heparin in 8.6% (25) and an inhibitory effect in 91.4% (265). Assessed by WBPA, heparin was proaggregatory in 41-46% and inhibitory in 54-59%. In the 100 patients tested by both methods there was a significant correlation between the findings with the two techniques (r = 0.46, p less than 0.0001). A wide individual variation in the platelet effect of heparin was demonstrated. This variation appeared greater and a higher proportion showed inhibition when blood was tested by haemostatometry.
Blood Platelets↗
Does the liquid method of electret forming influence the adhesion of blood platelets?
This work presents the results of the effect of the electric charge on the adhesion of blood platelets. All experiments were carried out on polyethylene foil. The liquid method was used to form electrets. The evaluation of the electret effect influence on the adhesion of blood platelets was made on the basis of the observation of the electret surface after the contact with fresh citrate human blood group O Rh+ in an electron scanning microscope. Experimental results confirmed the essential influence of the electric charge on the process of adhesion of blood platelets. It was noticed that the preliminary aging of electrets decreases the density of the surface charge and improves the athrombogenic characteristics of polyethylene foil.
Biocompatible Materials↗
Effect of adrenalectomy and corticosterone on [3H]imipramine binding in rat blood platelets and brain.
The effect of adrenalectomy and administration of glucocorticoids on [3H]imipramine binding (IB) of rat blood platelets and brain was investigated. Adrenalectomy significantly increased both Kd and Bmax of IB in the blood platelets but not the brain of male Sprague-Dawley rats. Administration of corticosterone acetate, 1 mg/kg i.p. for 7 days, decreased both Kd and Bmax in the blood platelets of sham-operated rats, but only Bmax in adrenalectomized rats. Corticosterone administration also decreased Bmax in frontal cortex and hypothalamus of sham and adrenalectomized rats but had no effect on Kd. These results suggest that glucocorticoids may modulate imipramine binding.
Adrenalectomy↗
Ultrastructural characteristics of freeze-dried human blood platelets.
Ultrastructural characteristics of freeze-dried human blood platelets were investigated. Extensive ice crystal formation was found in platelets frozen in the absence of cryoprotective agents. Platelet preservation was much improved by the addition of dimethyl sulfoxide, or dimethyl acetamide, with glucose or 0.25 M sodium glycerophosphate, to platelet-rich plasma prior to the freeze drying process. Platelet membranes and organelles were generally well preserved, and many granules demonstrated eccentric areas of electron density. Microtubules were not clearly identified, but some platelets showed tubule-like structures within platelet hyaloplasm. Pseudopods were often observed at the platelet surface, and often contained membrane-bound granule-like structures. Some pseudopods contained electrondense material which extended between adjacent platelets in interplatelet bridges and which was released to the surrounding medium. Interplatelet bridge formation was not prevented by chelation of calcium by ethylenediamine tetraacetic acid. The observations were consistent with the suggestion that contractile protein is present in interplatelet bridges and serves as a basis for clot retraction.
Acetamides↗