[Preliminary results of transfusions of blood platelets in gynecology].
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Blood Platelets↗
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[Effects of L-carnitine on erythropoiesis and blood platelet aggregation in patients with chronic renal failure treated with hemodialysis].
The aim of the work has to assess the effects of L-carnitine therapy on erythropoiesis and whole blood platelet aggregation. The studies were performed in 28 patients divided into 3 groups: I-group was given erythropoietin, II-group was given erythropoietin and L-carnitine, III-group was given L-carnitine. After 22 month of the therapy a statistically significant rise in hematocrit was observed in group III, improvement in muscle strength, a rise in free and total carnitine concentration was found in group II and III. There were no significant changes in urea concentration, platelet count and iron metabolism. Whole blood platelet aggregation induced by ADP, collagen and ristocetin was impaired relative to healthy volunteers. After 2 month of L-carnitine treatment of significant rise in collagen induced platelet aggregation was observed in group II.
Adult↗
Inhibition of platelet aggregation by S-nitroso-cysteine via cGMP-independent mechanisms: evidence of inhibition of thromboxane A2 synthesis in human blood platelets.
S-Nitroso-cysteine (SNC), a putative endothelium-derived relaxing factor, potently inhibited collagen- and arachidonic acid-induced platelet aggregation (IC50=100 nM) and thromboxane A2 (TxA2) synthesis of human blood platelets. ODQ, a selective inhibitor of the soluble guanylyl cyclase, inhibited SNC-induced formation of cGMP but did not reverse inhibition by SNC of collagen- and arachidonic acid-induced platelet aggregation. Combination of ODQ with SQ-29548, a specific platelet TxA2 receptor antagonist, did not modify the antiaggregatory action of SNC. Our study shows that SNC inhibits platelet aggregation by cGMP-independent mechanisms that may involve inhibition of TxA2 synthesis in human platelets.
Arachidonic Acid↗
Antioxidants with carcinostatic activity (resveratrol, vitamin E and selenium) in modulation of blood platelet adhesion.
Compounds with potential antiplatelet activity can be used in the therapy of cardiovascular disorders. We investigated the effects of three different antioxidants with carcinostatic property: trans-resveratrol, Trolox a water-soluble analog of vitamin E, and inorganic selenocompounds (sodium selenite and selenate) on blood platelet adhesion to fibrinogen (Fg). Adhesion, the initial step of platelet activation, was estimated by the colorimetric method with BCA (bicinchoninic acid) solution in 96-well Fg-coated microtiter dishes. It was shown that resveratrol significantly inhibited adhesion of both thrombin- and ADP-activated platelets to Fg. After incubation of platelets for 30 min. at 37 degrees C with resveratrol at the concentration of 100 microg/ml above 40% inhibition of adhesion was achieved. The inhibition of platelet adhesion of Fg caused by Trolox was lower than by resveratrol and at higher concentration (1 mM) reached maximum 12%. We also demonstrated that neither sodium selenite nor selenate significantly altered platelet adhesion to Fg. We conclude that changed adhesion of blood platelets to Fg in the presence of resveratrol and Trolox, but not selenium may be the result of different antioxidative activities of tested compounds.
Animals↗
Serum albumin stimulates serotonin uptake into human blood platelets.
Active uptake of serotonin (5-hydroxytryptamine, 5-HT) into blood platelets from healthy donors exhibited a lower Vmax value in buffer media than in plasma. Also in plasma ultrafiltrate Vmax was reduced, but it returned to the level measured in plasma upon addition of human serum albumin (40 milligrams) containing fatty acids. Fatty-acid-free albumin was even more stimulatory and when added to platelets in a phosphate-buffered medium, it increased Vmax beyond the value observed in plasma. Km values calculated on the basis of unbound 5-HT were not affected by the media except for a slight decrease in ultrafiltrate as compared to plasma. The fraction of 5-HT (0.5 mumol/l) bound to 40 milligrams albumin was 17% with the preparation containing fatty acids and 22% with fatty-acid-free albumin, while total plasma proteins dissolved in phosphate buffer bound 24%. The uptake of 1 mumol/l 5-HT was enhanced by both albumin preparations already at 1 milligram and near-maximal effects occurred at 10 milligrams.
Adult↗
Human blood platelet alpha adrenoceptor in view of the effects of various imidazol(in)e drugs on aggregation.
1. Sixteen imidazol(in)e derivative drugs were tested with regards to their aggregatory and antiaggregatory effects on human blood platelets. 2. Platelet aggregation in response to fixed concentrations of the agents was quantified by the turbidimetric method of Born. 3. Inhibitory effects of the imidazol(in)es against the epinephrine (10(-5) M) induced aggregation was related to concentration of the agents. Of the compounds studied, UK 14,304 elicited an aggregatory effect of a magnitude similar to epinephrine. 4. A strong aggregatory agent appeared also moxonidine. 5. Small aggregation was observed in response to clonidine, antazoline and tetryzoline. 6. For all the group of imidazol(in)e drugs, excepting UK 14,304 and moxonidine, a significant inhibition of the epinephrine induced aggregation was noted. 7. Analysing inhibitory activity of imidazol(in)es one notes the drugs commonly assumed to interact with alpha 2 adrenoceptor among the most potent inhibitors, and those classified as alpha 1 adrenoceptor agonists among the less active agents. 8. The results here obtained suggest some similarity between the platelet adrenoceptor and the alpha 2 subtype of adrenoceptor identified in human circulatory system. 9. Differences appear between the two types of receptors and the existence of a separate alpha 3 class of adrenoceptors in human blood platelets should be considered.
Blood Platelets↗
Receptors for ADP on human blood platelets.
It is well established that ADP causes aggregation of human blood platelets, and indeed it was the first aggregating agent to be studied, but the ways in which platelets respond to ADP are still relatively obscure. Although it is apparent that increases in intracellular Ca2+ concentrations are of major importance in activating platelets, it is not clearly understood how ADP causes these increases and what other signal transduction mechanisms it uses. It is not even clear whether ADP causes its effects by interacting with only one receptor, or whether multiple receptors for ADP exist on platelets. In this review, Susanna Hourani and David Hall examine some of the conflicting evidence in this field, and draw some tentative conclusions about the number and nature of receptors for ADP on human platelets.
Adenosine Diphosphate↗
Nature of lowered 5-hydroxytryptamine uptake by blood platelets of patients with Down's syndrome.
Disturbance of central serotoninergic system has been suggested in Down's syndrome (DS). In this syndrome the 5-HT concentration in blood platelets is below normal, but the mechanism behind this has been controversial. Recently, evidence has accumulated indicating a decreased active transport of 5-HT possibly due to lowered activity of Mg++-dependent Na+-K+-stimulated adenosine triphosphatase. In the present study the kinetic analysis of 5-HT uptake by blood platelets from DS patients revealed a decreased Vmax, suggesting decreased transport function but an unchanged affinity to the uptake receptors, as indicated by normal Km values. The controls were mentally retarded patients from the same institute. The uptake continued in a linear fashion up to 20 min., suggesting an unchanged storage of 5-HT. Also the effect of zinc on the 5-HT uptake was studied; plasma zinc levels have been noted to be lowered in DS infants. In vitro zinc caused a dose-dependent inhibition of uptake at 10(-5) and 10(-4) M. In vivo, after 2 weeks treatment 135 mg/day orally no significant effect was noted.
Adolescent↗
Isolation of palmitoyl-CoA hydrolases from human blood platelets.
The palmitoyl-CoA hydrolase activity, which in human blood platelets is mainly localized in the cytosol fraction [Berge, Vollset & Farstad (1980) Scand. J. Clin. Lab. Invest. 40, 271--279], was found to be extremely labile. Inclusion of glycerol or palmitoyl-CoA stabilized the activity during preparation. Gel-filtration studies revealed multiple forms of the enzyme with molecular weights corresponding to about 70 000, 40 000 and 24 000. The relative recovery of the mol.wt.-70 000 form was increased by the presence of 20% (v/v) glycerol or 10 microM-palmitoyl-CoA. The three enzyme forms are probably unrelated, since they were not interconvertible. The three different species of palmitoyl-CoA hydrolase were purified by DEAE-cellulose and hydroxyapatite chromatography, isoelectric focusing and high-pressure liquid chromatography (h.p.l.c.) to apparent homogeneity. The three enzymes had isoelectric points (pI) of 7.0, 6.1 and 4.9. The corresponding molecular weights were 27 000--33 000, 66 000--72 000 and 45 000--49 000, calculated from h.p.l.c. and Ultrogel AcA-44 chromatography. The apparently purified enzymes were unstable, as most of the activity was lost during purification. The enzyme with an apparent molecular weight of 45 000--49 000 was split into fractions with molecular weights of less than 10 000 by re-chromatography on h.p.l.c. concomitantly with a loss of activity. The stimulation of the activity by the presence of serum albumin seems to depend on the availability of palmitoyl-CoA, as has been reported for other palmitoyl-CoA hydrolases. [Berge & Farstad (1979) Eur. J. Biochem. 96, 393--401].
Blood Platelets↗
(2-Piperidine)- and (2-pyrrolidine)ethanones and -ethanols as inhibitors of blood platelet aggregation.
(E)-4-[4-(Methylthio)phenyl]-1-(2-piperidinyl)-3-buten-2-one hydrochloride (44, RMI 14 133A) was found to inhibit ADP-induced aggregation of blood platelets. It was selected from a large series of (2-piperidinyl)- and (2-pyrrolidinyl)ethanones synthesized by a modified Schopf reaction from enolate magnesium salts of beta-keto acids and 2,3,4,5-tetrahydropyridine trimer or 3,4-dihydro-2H-pyrrole trimer, respectively. Evaluation of the compounds was carried out in vitro on human blood platelets. Structure-activity relationships are discussed. 44 also inhibited platelet aggregation ex vivo in guinea pigs. Subacute toxicity evaluation in dogs and guinea pigs showed it to have an unfavorable therapeutic ratio. 1-[4'-Chloro(1,1'-biphenyl)-4-yl-a1-2-(2-piperdinyl)ethanone hydrochloride (18, RMI 12436A) was found to lower serum cholesterol levles in rats with concurrent accumulation of (3beta)-cholesta-5,7-dien-3-ol, suggesting inhibition of 7-dehydrocholesterol delta7-reductase.
Adenosine Diphosphate↗
The 5-hydroxytryptamine system of blood platelets: physiology and pathophysiology.
The 5-hydroxytryptamine (5HT)-system of human blood platelets consists of a relatively specific uptake mechanism for 5HT at the plasma membrane, intracellular storage organelles (dense bodies), a metabolizing enzyme (monoaminoxidase B) and a 5HT2-receptor whose stimulation leads to activation of the phosphatidylinositide turnover, a rise in free cytoplasmic Ca2+, phosphorylation of proteins and a shape change reaction. There is neither a relevant 5HT-biosynthesis nor a marked physiological 5HT-turnover in platelets. Under physiological conditions the platelet 5HT-system may have a role as a scavenger for free extracellular 5HT and in hemostasis. Disturbances which have been described in pathophysiological states include impairment of 5HT-uptake (hypertension, migraine), impairment of 5HT-storage (storage pool deficiencies, thromboembolic disorders, hypertension) and increased sensitivity to activating agents like 5HT (cardiovascular disorders, diabetes). Besides their role in physiology and pathophysiology platelets may be useful partial models for vascular smooth muscle cells.
Blood Platelets↗
Effects of Yunnan Bai Yao on blood platelets: an ultrastructural study.
The effects of Yunnan Bai Yao on blood platelets were studied at an ultrastructural level. This herbal drug is found to cause the release of platelet constituents which accounts for its hemostatic effects. The fine structural changes of platelets in response to this drug are also described.
Animals↗
Uncoupling of muscle and blood platelets Ca2+ transport ATPases by heparin. Regulation by K+.
Heparin (1-10 micrograms/ml) inhibits the Ca2+ transport ATPases found in the sarcoplasmic reticulum of skeletal muscle, the plasma membrane of red cells, and the dense tubular system of blood platelets, but not the (Na+ + K+)-ATPase or the mitochondrial F1-ATPase. In the reversal of the Ca2+ pump, heparin uncouples the synthesis of ATP from Ca2+ efflux and inhibits the phosphorylation of the sarcoplasmic reticulum Ca(2+)-ATPase by Pi, but has no effect the phosphorylation by ATP. The effect of heparin on the muscle Ca(2+)-ATPase is abolished by KCl and NaCl (100 mM) and to a lesser extent by LiCl. These monovalent cations are not effective as antagonists of heparin on the platelet Ca(2+)-ATPase. The effects of heparin are antagonized by the polyamines spermine, spermidine, and ruthenium red. Unlike KCl, polyamines are equally effective in counteracting the effects of heparin in both muscle and platelet Ca(2+)-ATPases. In addition to heparin, the Ca(2+)-ATPases of muscle and blood platelets are also inhibited by dextran sulfate and fucose-branched chondroitin sulfate. The inhibition promoted by these glycosaminoglycans is antagonized by monovalent cations and polyamines in the same manner as heparin. Heparan sulfate, chondroitin sulfate, and hyaluronic acid have not effect on the Ca(2+)-ATPases studied.
Animals↗
Phospholipase A-1 of human blood platelets.
Substantial phospholipase A(1) activity has been demonstrated in human blood platelets, and a rapid method for its measurement is described. The enzyme requires taurocholate for full activity and in these conditions the pH optimum is 4.8. The phospholipase activity is released from platelets by incubation with thrombin.
Blood Platelets↗
Thrombosis and bleeding in myeloproliferative disorders: identification of at-risk patients with whole blood platelet aggregation studies.
Seventy-five patients with chronic myeloproliferative disorders were studied to investigate platelet function by simultaneous measurement of platelet aggregation by the impedance method and ATP dense granule release using a whole blood platelet lumi-aggregometer, in an attempt to identify patients at risk for thrombosis and bleeding. Thirty-nine patients had at least one abnormal result indicating platelet hyperactivity (i.e. impedance or release with one agonist being above the reference range); 16 patients had platelet hypoactivity (i.e. at least one result was below the reference range), whilst 14 had co-existence of hyper- and hypoactivity. Six patients had normal results. 20/53 patients with platelet hyperactivity (alone or mixed) had a positive history of venous and/or arterial thrombosis; in comparison, only two of the other 22 patients had a positive history. During a median follow-up of 33 months, nine patients with and one patient without platelet hyperactivity respectively developed new thrombotic events before the addition of specific therapy. A total of 50 patients with and eight patients without platelet hyperactivity respectively received specific treatment including aspirin and/or cytotoxic therapy. All but one elderly patient with platelet hyperactivity have remained free of new thrombotic events on specific therapy. Two of the 17 patients with platelet hypoactivity had major clinical bleeding. These observations highlight the need to test platelets for hyper- as well as hypo-function and suggest a useful role for routine whole blood platelet aggregation studies to identify the patients at risk for thrombosis or bleeding.
Aged↗
[Comparison of the number of dense bodies in blood platelets in patients with myocardial infarction].
Dense bodies present in blood platelets contain also serotonin, which together with other factors stimulates vasoconstriction. This paper presents an investigation of possible differences in the number of dense bodies in platelets of patient R.T., affected by two myocardial infarctions resulted in death, with the number of dense bodies in platelets of patient L.T., affected by the same type of myocardial infarct, however, without complications. Dense bodies were labelled with mepacrin and viewed and counted under the fluorescence microscope. Score for each type of platelet (containing 1-6 dense bodies) as well as a total score for each of 3 blood samples collected during acute phase of the infarct and then after 5 and 10 consecutive days were calculated. Increased number of dense bodies (6 per platelet) was seen in patient R.T. Also the total score was the highest. For comparison total score was calculated in an healthy person.
Blood Platelets↗
Demonstration of labile platelet desaggregation-promoting substance(s) in human blood, using the donor's own blood platelets ("DOP assay") as indicator cells, with special reference to the possibility of measuring diet-induced alterations.
A method is described for the semi-quantitative biological determination of labile platelet desaggregation-promoting substance(s) in human platelet suspensions and in platelet-free fresh plasma by using the donor's own platelets ("DOP assay"). Using the donor as his own control it is possible to demonstrate a dose-related increase of the platelet desaggregation-promoting potency in response to cod-liver oil. The labile platelet desaggregation-promoting activity can also be observed in fresh platelet-free plasma. Circumstantial evidence is presented for the prostaglandin-like nature of these labile platelet desaggregation-promoting substance(s).
Adenosine Diphosphate↗
Blood platelets stimulate the expression of chondroitin sulfate proteoglycan in human monocytes.
Mononuclear phagocytes synthesize chondroitin sulfate proteoglycan (CSPG), which is constitutively secreted. Because mononuclear phagocytes are known to interact with blood platelets, the effect of platelets on the release of CSPG in cultured human monocytes was investigated. After 6 days in vitro, the monocytes were supplied with fresh medium with different additions and subsequently exposed to [35S]sulfate for 24 hours before the medium fractions were harvested and analyzed for content of [35S]CSPG. Indirect evidence for the release of stimulatory factors from blood platelets was found when the addition of medium containing 50% serum made from platelet-rich plasma increased the expression of [35S]CSPG almost sevenfold compared with serum-free medium, whereas medium containing 50% serum made from platelet-depleted plasma increased the expression of [35S]CSPG about fourfold. Further, direct evidence for the stimulatory effect of platelets was found as the addition of autologous platelets to serum-free medium increased the expression of [35S]CSPG about threefold, and addition of supernatant from a corresponding number of thrombin-stimulated platelets was almost as efficient. The effect of five different platelet-derived factors (which are all present in serum) was investigated. Both platelet-derived growth factor (PDGF), platelet factor 4 (PF 4), and prostaglandin E2 (PGE2) used in physiologic concentrations were found to stimulate the expression of [35S]CSPG twofold to threefold, whereas transforming growth factor-beta had a slight inhibitory effect. 12-Hydroxyeicosatetraenoic acid had no significant effect on the expression of [35S]CSPG. Further evidence for the stimulatory effect of PDGF, PF 4, and PGE2 was found as serum depleted of these factors had significantly less stimulatory effect than control serum. The increased incorporation of [35S]sulfate into [35S]CSPG in cultures stimulated with serum or platelet-derived factors was not due to differences in molecular size or extent of sulfation of the proteoglycan molecules.
Aspirin↗