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At least 217 records · Page 12Linked to original sources
PubMed1983

Life span and tissue distribution of 111indium-labeled blood platelets in hypomagnesemic lambs.

Circulating platelets may be activated by exposed triple-helical collagen in atherosclerotic lesions in Mg-deficient ruminants. Autologous platelets, labeled in vitro with 111In and determined to be active, were injected into 5 hypomagnesemic and 3 control lambs fed semipurified diets with 100 or 2,000 mg of Mg/kg of feed for 3 months. During the first 68 hours, 111In concentrations were 11 times higher in packed cells than in plasma. Packed-cell 111In increased 60% during the first 2 hours, probably due to initial tissue sequestration and later release of labeled platelets. Thereafter, platelet half-life span averaged 60 and 63 hours for hypomagnesemic and control lambs. After 68 hours, lambs were injected with native vascular collagen fibrils at 500 micrograms/kg of body weight to initiate reversible platelet aggregation. Within 1 minute, 83% of packed-cell 111In disappeared from circulation. Thirty minutes later, the lambs were euthanatized and necropsied and in the lungs, liver, and spleen, 111In averaged 24%, 19%, and 9%, respectively, of 111In injected 68 hours earlier. Organ deposits were not affected by Mg intake, but 111In in the lungs was somewhat lower in 2 lambs injected with inactivated collagen. Pathologic changes induced by reversible platelet aggregation were compatible with right ventricular failure complicated by pulmonary edema, similar to changes in hypomagnesemic lambs that died spontaneously. Platelets in blood exposed to vascular lesions in hypomagnesemic ruminants could be a major mortality risk factor in grass tetany disease.

Animals↗
PubMed1993

[Immunology of blood platelets].

Platelet specific antigen systems, their molecular structure and localization in cell membrane is presented. New techniques for the detection of platelet antibodies are discussed.

Antibodies↗
PubMed1980

An evaluation of a whole-blood platelet counter.

The performance of the platelet count in the hematology laboratory remains a laborious, time-consuming technic requiring separation of platelet-rich plasma, correction for leukocyte counts, lysis of erythrocytes, etc. The availability of an instrument that would count platelets in whole blood would appear to be a distinct advantage. One such instrument has been recently evaluated. The Ultra-Flo 100 Whole Blood Platelet Counter was found to be a reliable instrument for performing platelet counts on microspecimens of untreated whole blood. Counts were both accurate and precise, with no carry-over from specimen to specimen. The major advantage of the system is the speed with which platelet counts may be performed (25 sec) and results produced, a distinct advantage in those laboratories serving large outpatient hematology/oncology clinics. Six months of day-to-day experience in the laboratory has shown a favorable frequency-of-repair record, with little downtime.

Evaluation Studies as Topic↗
PubMed1996

Blood platelet responses to laboratory stress in young men. The effect of awareness of high blood pressure.

Healthy 19-year old males from the 95th percentile of mean arterial screening blood pressure were randomized to prolonged mental stress by receiving a letter informing of a high screening blood pressure (n = 13), or a neutral letter (n = 13). Blood platelet function in vivo was assessed by measurements of plasma concentrations of the platelet-specific protein beta-thromboglobulin, platelet counts, and mean platelet volumes before and during two laboratory stress tests (hand cold pressor test and arithmetic challenge). The cold pressor test caused a significant increase in beta-thromboglobulin concentrations in both groups, and significantly more in the uniformed group. Platelet count increased significantly in both groups during mental arithmetic with significantly higher counts in the uninformed group. Overall plasma beta-thromboglobulin responses were significantly larger in the uninformed group. This study demonstrates that laboratory stress is associated with blood platelet activation and that awareness of high blood pressure attenuates the platelet responses to such stress tests.

Adult↗
PubMed1972

Exocytosis of secretory organelles from blood platelets incubated with cationic polypeptides.

The blood platelet release reaction involves the secretion, in parallel, of specific chemical constituents stored in intracellular organelles to the plasma without loss of substances suggestive of cell damage. The present investigation has employed an unusual effect of cationic polypeptides to follow the platelet secretory process. When platelets were incubated with polybrene and polylysine, the agents were taken up and deposited in cytoplasmic organelles. The matrix of granules developed a lattice-like substructure not produced by other chemical agents, and dark zones of granules and dense bodies became more electron opaque. Subsequently, the platelets exposed to cationic polypeptides underwent the shape change and internal transformation similar to that produced by potent aggregating agents. Granules and dense bodies appeared in the open canalicular system and were extruded in a relatively intact state from the altered platelets. No differences were observed in the response of normal, afibrinogenemic or thrombasthenic platelets to incubation with polybrene and polylysine. The results indicate that cationic polypeptides can stimulate the extrusion of secretory organelles, and support the previous reports suggesting that channels of the open canalicular system serve as conduits for discharging the products of the release reaction.

Afibrinogenemia↗
PubMed1989

Blood platelet uptake of serotonin in episodic aggression.

Blood platelet uptake of 3H-serotonin (5HT uptake), a potential marker of serotonergic function, was determined in male outpatients with episodic aggression (n = 15) and in age- and sex-matched nonaggressive controls (n = 15). Correlations with rating scales of "impulsivity" (Barratt Impulsivity Scale, 10th revision) and "anger" (Spielberger Anger Expression Scale) were performed. Mean 5HT uptake was 18% lower in patients with episodic aggression. A significant negative correlation between % difference in platelet 5HT uptake and impulsivity score was observed, but the correlation between 5HT uptake and anger was not significant. These results support the hypothesis of disturbed serotonergic function in aggression and suggest that the primary relationship is in the "control" of aggression. The blood platelet may be useful in identifying impulsive subtypes.

Adolescent↗
PubMed1996

[Effect of acute hypoxia on blood catecholamine and whole blood platelet aggregation].

Experiments were performed on 250-300 g male Sprague-Dawley rats under urethane (700 mg/kg) and alpha-chloralose (35 mg/kg) anesthesia. Plasma catecholamine concentration and the whole blood platelet aggregation were measured during normoxia, acute hypoxia, reoxygenation, acute hypoxia immediately after bilateral adrenalectomy and acute hypoxia at the end of 15 and 30 min after bilateral adrenalectomy. The plasma adrenaline concentration and the whole blood platelet aggregation increased markedly (P < 0.01), while the plasma noradrenaline concentration tended to increase (P > 0.05) during acute hypoxia. The plasma adrenaline concentration and the whole blood platelet aggregation are capable of restoring to the normal level during reoxygenation. The plasma noradrenaline concentration did not change, while the plasma adrenaline concentration and the whole blood platelet aggregation decreased significantly (P < 0.001 or 0.05) during acute hypoxia for 15 min immediately after bilateral adrenalectomy. On the other hand, plasma adrenaline and noradrenaline were not detectable during acute hypoxia 30 min after bilateral adrenalectomy while the whole blood platelet aggregation deceased markedly (P < 0.01). When adrenaline (1 ng/ml) was added to the blood (in vitro), the whole blood platelet aggregation increased significantly (P < 0.01). All the above results indicate that acute hypoxia leads to increament of whole blood platelet aggregation and plasma adrenaline concentration due to release from the adrenal gland and the increament of the whole blood platelet aggregation may be partly mediated by increased plasma adrenaline.

Acute Disease↗
PubMed1996

Effects of thimerosal, an organic sulfhydryl modifying agent, on serotonin transport activity into rabbit blood platelets.

The effects of the sulfhydryl group inhibitor thimerosal on serotonin (5-HT) transport activity into rabbit blood platelets were investigated, along with its effects on the intracellular concentration of Ca2+ ([Ca2+]i). 3H-5-HT transport activity into rabbit blood platelets was inhibited by treatment with 10(-5) M thimerosal for 30 min, which did not cause 5-HT release from platelets. The thimerosal-induced inhibition of 5-HT transport was antagonized by dithiotheritol. It was suggested that the thimerosal acts as a sulfhydryl inhibitor and inhibits 5-HT transport activity independently of the 5-HT release reaction in our experiment using rabbit blood platelets. As aspirin did not affect thimerosal-induced 5-HT transport inhibition, it was suggested that the thromboxane A2-generating system does not operate in the effect of thimerosal on 5-HT transport into blood platelets. Furthermore, thimerosal induced a transient elevation of [Ca2+]i, which was followed by a sustained increase. In the absence of extracellular Ca2+, thimerosal caused only a transient increase in [Ca2+]i. It was suggested that the elevation of [Ca2+]i consisted of two phases, e.g. a transient phase induced by Ca2+ mobilization from the intracellular store sites and a sustained phase which might be explained by Ca2+ influx from the extracellular environment. In conclusion, thimerosal inhibited 5-HT transport into blood platelets at a concentration which did not induce 5-HT release, and intracellular Ca2+ mobilization might mediate the inhibitory effect of thimerosal on 5-HT transport.

Animals↗
PubMed1974

Transport of taurine by normal human blood platelets.

1 Because normal human blood platelets contain higher concentrations of taurine than any other amino acid, and have a platelet: plasma concentration gradient exceeding 400: 1, we isolated the cells in vitro and incubated them with radioactively labelled taurine in order to investigate the existence of a metabolically-dependent accumulation process.2 Platelets incubated with taurine (1 to 100 nmol/ml) in autologous plasma or Krebs solution accumulated [(14)C]-taurine against the concentration gradient.3 The transport process was saturable at high concentrations, showed a requirement for sodium ions, and was temperature-dependent.4 The kinetics of transport fulfilled the criteria of Michaelis & Menten for saturable enzyme/substrate interactions, but the kinetic constants were influenced by the incubation medium.5 The metabolic inhibitors 2,4-dinitrophenol and iodoacetic acid in combination inhibited taurine transport in Krebs solution, but stimulated transport in autologous plasma. The latter result suggested the involvement of a sodium-dependent ATPase in taurine transport.6 We conclude that platelets actively transport taurine in vitro under experimental conditions closely resembling those likely to occur in vivo, and that this taurine transport process may be involved in the maintenance of the platelet: plasma concentration gradient.

Amino Acids↗
PubMed1986

Blood platelets in human essential hypertension.

Blood platelets of patients with essential hypertension display signs of both increased sensitivity in vitro to aggregating stimuli believed to contribute to thrombosis and of activation in vivo possibly expressing the release of vasoactive products. The mean features of the modified platelet profile in hypertension include an increased alpha 2-adrenergic receptor density, an enhanced rate of adhesion/aggregation in particular in response to ADP and arachidonic acid, a greater sensitivity for thrombin and adrenaline to stimulate increases in cytoplasmic-free Ca2+, increased resting levels of cytoplasmatic-free Ca2+, a reduced content of serotonin often combined with a defective uptake mechanism, a facilitated efflux rate of noradrenaline, an exaggerated release reaction in vivo as indicated by the increased plasma levels of Beta-thromboglobulin and a shortened platelet life span. These changes occur to various extents in some, but not all, hypertensive patients and are not always strictly related to the degree of blood pressure increase. On the contrary, platelet cyclooxygenase and thromboxane synthetase activity are in the normal range.

Blood Platelets↗
PubMed1986

Uptake of 3H-dopamine in megakaryocytes and blood platelets measured by quantitative electron-microscope autoradiography.

We studied the uptake of dopamine by mature megakaryocytes and blood platelets in mouse spleen after a single intraperitoneal injection of 3H-dopamine. In order to compare the uptake of 3H-dopamine in mature megakaryocytes and blood platelets, we used quantitative autoradiography at the electron-microscope level. Dense accumulations of silver grains were observed on both mature megakaryocytes and blood platelets; all other tissue elements of the spleen exhibited considerably less dense labeling. No significant differences with regard to dopamine uptake were observed in megakaryocytes and blood platelets. This is in contrast to the previous finding of very different patterns of 3H-5-hydroxytryptamine labeling in mature megakaryocytes and blood platelets (Daimon and Uchida 1985). The results of the present study provide new evidence in favor of the hypothesis that the active uptake mechanism of dopamine through the plasma membrane is different from the uptake mechanism of 5-hydroxytryptamine.

Animals↗
PubMed1977

Factors which influence blood platelet migration.

Migration of human blood platelets in vitro was investigated by a modification of the capillary-tube migration chamber technique used to study the migration inhibition factor of macrophages. Platelets were packed in capillary tubes and incubated in autologous platelet-free plasma (PFP). The extent of migration was quantified by planimetry (measurement of the area of platelet migration visible by stereomicroscopy). Among the various anticoagulants employed, sodium citrate was most suitable for studying platelet migration. Optimal migration occured at 22 degrees to 37 degrees C and pH 7.2 to 7.4. Migration was inhibited by metabolic inhibitors such as iodoacetic acid, sodium fluoride, and 2,4-dinitrophenol, and inhibition was proportional to the dose of the agent added to the incubation medium. Mobility was also inhibited by cytochalasin B, which disrupts cellular microfilaments, at 1 microgram/ml PFP, but not by colchicine, a microtubule inhibitor, even at 40 microgram/ml of PFP. Light and electron microscopy showed that this inhibition was not ascribable to platelet clumping. These observations suggest that platelet mobility is an active process. The possible significance of platelet migration in hemostasis is discussed.

Anticoagulants↗