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PubMed1997

Comparative cytotoxicity of cisplatin, sodium selenite and selenium-cisplatin conjugate [(NH3)2Pt(SeO3)]; changes of blood platelet activation.

The cytotoxic effects of a novel compound, conjugate Se-Pt [(NH3)2Pt (SeO3)] on blood platelet function (aggregation, release of adenine nucleotides) were studied. Contrary to the action of cisplatin or selenite alone, [(NH3)2Pt(SeO3)] did not inhibit ADP-induced platelet aggregation, thrombin-induced release of adenine nucleotides from platelets, and had no effect on the metabolism of platelet arachidonate. The tested compound seems to be less toxic than cisplatin alone, and has no effect on blood platelet activation.

Adenine Nucleotides↗
PubMed1995

Whole-blood platelet aggregation predicts in vitro and in vivo primary hemostatic function in the elderly.

Increased platelet aggregation is associated with higher coronary artery disease mortality. Enhanced platelet aggregation in platelet-rich plasma has also been described in the elderly. To define age-related changes in primary hemostasis, we studied 37 elderly and 31 young blood donors. There were no significant age-related differences in whole-blood platelet aggregation, platelet adherence and thrombus formation on human umbilical artery segments, or bleeding time. Plasma fibrinogen was significantly higher in elderly men and women, whereas activated factor VII was elevated only in elderly women. Collagen-induced platelet aggregation was significantly correlated with platelet adherence to the subendothelium in elderly (r = .488, P = .002) but not in young donors. Accordingly, collagen-induced platelet aggregation showed a significant inverse correlation with bleeding time only in the elderly (r = -.401, P = .014). Arachidonic acid-induced platelet aggregation was significantly associated with platelet adherence to the subendothelium (r = .658, P = .003) and bleeding time (r = -.540, P = .021) only in elderly men. In young donors, ADP-induced platelet aggregation was significantly correlated with platelet adherence to the thrombogenic adventitial surface (r = .395, P = .031); in the elderly this association only approached significance (r = .315, P = .058). Whole-blood platelet aggregation in response to collagen and arachidonic acid may be more useful in predicting primary hemostatic function in the elderly than in the young. Furthermore, in the elderly, the correlation between platelet aggregation in whole blood and platelet-arterial wall interactions in vitro and in vivo may contribute to the ability of this test to predict coronary risk.

Adenosine Diphosphate↗
PubMed1984

Acquisition and aggregation of canine blood platelets: basic mechanisms of function and differences because of breed origin.

A method for obtaining reliable blood platelet yields in canine platelet-rich plasma, using increased sodium citrate concentration, is presented. Maintaining a quiet environment or anesthetizing the animals with thiamylal sodium aids in collection of platelets. Aggregation of platelets from 60 dogs of various breeds in response to arachidonic acid, collagen, adenosine diphosphate, epinephrine, and serotonin was monitored. Canine platelets reversibly or irreversibly aggregated to arachidonic acid. The percentage of arachidonate-irreversible platelets varied from 0% to 100% depending upon the breed of dogs examined. Arachidonate-irreversible platelets also aggregated irreversibly at lower concentrations of collagen and exhibited biphasic irreversible aggregation to adenosine diphosphate and serotonin. Serotonin-induced irreversible aggregation was dependent upon receptor activation and upon arachidonic acid metabolism. Irreversible aggregation to serotonin was associated with release of 3H-serotonin and thromboxane B2 formation, indicating that a couple between the serotonergic receptor and arachidonic acid metabolism may exist.

Adenosine Diphosphate↗
PubMed2003

The clearance mechanism of chilled blood platelets.

Platelet transfusion is a very common lifesaving medical procedure. Not widely known is the fact that platelets, unlike other blood cells, rapidly leave the circulation if refrigerated prior to transfusion. This peculiarity requires blood services to store platelets at room temperature, limiting platelet supplies for clinical needs. Here, we describe the mechanism of this clearance system, a longstanding mystery. Chilling platelets clusters their von Willebrand (vWf) receptors, eliciting recognition of mouse and human platelets by hepatic macrophage complement type 3 (CR3) receptors. CR3-expressing but not CR3-deficient mice exposed to cold rapidly decrease platelet counts. Cooling primes platelets for activation. We propose that platelets are thermosensors, primed at peripheral sites where most injuries occurred throughout evolution. Clearance prevents pathologic thrombosis by primed platelets. Chilled platelets bind vWf and function normally in vitro and ex vivo after transfusion into CR3-deficient mice. Therefore, GPIb modification might permit cold platelet storage.

Animals↗
PubMed1987

Succinic semialdehyde dehydrogenase activity in bovine adrenal medulla and blood platelets: a comparative study with the brain enzyme.

In the present paper we report the presence of succinic semialdehyde dehydrogenase (SSADH) in bovine adrenal medulla and blood platelets. Both enzymes present some analogies with the brain enzyme in terms of cofactor requirements, optimal pH, mitochondrial localizaton and inhibition by AMP. However, the activity of the platelet enzyme is 100 times lower than that of the brain and affinities of both enzymes for their specific substrate succinic semialdehyde and NAD are different. The presence of SSADH in adrenal medulla and blood platelets allows us to confirm the presence of a complete GABA bypass in these tissues, where the neurotransmitter could have important regulator functions.

Adrenal Medulla↗
PubMedDate not supplied

Blood platelet responsivity to acute mental stress.

To evaluate the effects of mental stress on blood platelet activity, platelet secretion and aggregation were measured in 40 healthy young men, assigned in a 3:1 ratio to an experimental and control condition. After a baseline period, experimental subjects participated in a 21-minute, frustrating computer task (the Stroop test), while control subjects remained seated quietly for the same duration. Blood was drawn from all subjects immediately before and after the task period for assessment of platelet activity (secretion of ATP and aggregation in response to 5 and 20 microM ADP). Heart rate and blood pressure were also assessed at baseline and throughout the task period. Results indicated that measures of platelet secretion, heart rate, and blood pressure rose significantly from baseline to posttask assessments in subjects exposed to the experimental stressor (p < .05), but not among controls. These findings are consistent with the hypothesis that stress may potentiate coronary disease pathogenesis, in part, via activation of blood platelets and their associated effects on coronary artery occlusion and/or constriction.

Adenosine Triphosphate↗
PubMed1986

[Immunologic aggregation of human blood platelets and its inhibition in vitro].

Unwashed human thrombocytes are best suitable for the immunological activation in PBS-glucose solution. The immunological aggregability of the blood platelets increases in this solution up to more than 1 hour. Rabbit-anti-human-Ig-L-chain (chi) or -anti-human-C1q serum aggregate once washed thrombocytes. The combined application of both antisera has a potencive effect. Soluble human-IgG-rabbit-anti-human-IgG-antibody-F(ab')2-complexes produce a strong thrombocyte aggregation in an intermediate human IgG excess. 4 minutes past heating of human IgG at 63 degrees C a mixture of IgG aggregates (AHGG) arises which activates blood platelets maximally. The AHGG can be stored at -20 degrees C up to at least 4 weeks. Therapeutical aspirin concentrations inhibit the AHGG induced thrombocyte aggregation. Plasma from patients with idiopathic thrombocytopenia inhibits the AHGG mediated platelet aggregation less than plasma from healthy persons.

Animals↗
PubMed1977

Binding of collagen by canine blood platelets.

The binding of 125I-collagen (tropocollagen) by canine blood platelets occurred in a concentration-dependent manner but no saturation effect could be observed. The binding of collagen was not entirely specific for platelets since various eucaryotic and procaryotic cells quantitatively bound collagen as well or better. The temporal response to added collagen appeared to be binding, 3H-serotonin release, and finally platelet aggregation. Non-polymerizing salt-soluble tropocollagen was bound as well as acid-soluble tropocollagen, however neither 3H-serotonin release nor platelet aggregation occurred. Furthermore, the binding activity was not destroyed by treatment with collagenase, galactose oxidase and glucose oxidase, nor by periodate oxidation. Platelet aggregation closely paralleled acid soluble collagen polymerization and both events were equally inhibited by arginine; however, arginine did not interfere with collagen binding. Scanning electron microscopy revealed an unusual morphological platelet response to collagen and platelets appeared to be nucleation sites for collagen polymerization.

Animals↗
PubMed1979

Shape change of blood platelets--a model for cerebral 5-hydroxytryptamine receptors?

1. In blood platelets of rabbits isolated by a stractan gradient and incubated in a protein-poor medium, tryptamine, 5-hydroxytryptamine (5-HT) and derivatives, quipazine and mescaline caused a shape change. This shape change was inhibited by low concentrations of methysergide. 2. The most potent antagonists of the 5-HT-induced shape change included ergoline derivatives and neuroleptic drugs, which showed high stereoselectivity. 3. (+)-Lysergic acid diethylamide ((+)-LSD), psilocine and some N',N'-dimethylated tryptamines acted as mixed agonist-antagonists. 4. The compounds found to be agonists or mixed agonist-antagonists on platelets have previously been shown to act also as 5-HT agonists in the central nervous system (CNS). 5. With regard to 5-HT antagonists, the 5-HT receptors of platelets reacted differently from those described earlier in brain areas with dense 5-hydroxytryptaminergic innervation, but showed similarities to 5-HT receptors investigated previously in spinal cord, cerebral cortex and possibly reticular formation. 6. It is concluded that platelets may be considered with caution as models for some, but not for all, 5-HT receptors in the CNS.

Adenosine Diphosphate↗
PubMed2003

[Morphologic parameters of blood platelets and activity NA+/H+ (NHE-1) exchanger in normal pregnancy and pregnancy complicated with preeclampsia].

UNLABELLED: The aim of the study was the evaluation of number and morphologic parameters of blood platelets and sodium-proton platelet exchangers in pregnant women in the 3rd trimester of pregnancy, healthy (155) and with preeclampsia (40). RESULTS: Blood platelet number was significantly lower in patients with preeclampsia than in healthy subjects (195,000 vs 222,000). Mean platelet volume was significantly higher in patients with preeclampsia (9.5 fl vs 8.6 fl). The activity of Na+/H+ was slightly higher in pregnants with preeclampsia.

Adult↗
PubMed1994

On the inhibitory effect of chloroquine on blood platelet aggregation.

Chloroquine inhibited aggregation of rat blood platelets in a dose-dependent way. The inhibitory effect decreased, depending on the aggregation stimulus used, in the rank order of potency: ADP > thrombin > A23187. Effect of 1 millimolar chloroquine on A23187-stimulated aggregation was significantly decreased or completely abolished by addition of Ca2+ ions in the concentration of 0.1 or 1 mmol/l, respectively. For thrombin-stimulated aggregation the effect of chloroquine was partially decreased by corresponding isomolar calcium; platelet aggregation induced by ADP was not changed in the presence of extracellular Ca2+ ions. Addition of chloroquine during aggregation resulted in disaggregation of ADP-stimulated platelets and inhibition of thrombin- and A23187-induced aggregation.

Animals↗
PubMed1975

Blood platelet aggregation and personality traits.

Changes in blood platelet aggregation may precipitate episodes of arterial occlusive diseases. Little is known, however, regarding the influence of psychological traits, emotional states and other behavioral stressors on platelet aggregation phenomena. This study examined 46 healthy college men at rest and after submaximal treadmill exercise. Associations were found between the duration of platelet aggregation and a number of scores from the California Psychological Inventory and self-administered anxiety scales. The more socially adequate, poised and dominant persons--those with more mature ego development and less overt anxiety--had platelets with more prolonged aggregation reactions to the in vitro introduction of noradrenalin. Irreversible aggregation of platelets occurred more regularly to lower in vitro concentrations of noradrenalin in platelet samples drawn from subjects who were less anxious and tended to be more rigidly defensive. It is premature to attempt to derive clinical implications from this exploratory work, but some implications for the design of future research are discussed.

Adult↗
PubMed1977

Solubilization and resolution of thromboxane synthesizing system from microsomes of bovine blood platelets.

The thromboxane synthetase system of the microsomes of bovine blood platelets was solubilized by the treatment with Triton X-100. The solubilized preparation was separated into two enzyme fractions by DEAE-cellulose chromatography. One catalyzed the formation of prostaglandin H2 from arachidonic acid in the presence of heme and tryptophan. The other fraction converted prostaglandin H2 to thromboxane B2 and 12L-hydroxy-5,8,10-heptadecatrienoic acid. However, incubation of the latter fraction with prostaglandin H2 at lower temperature produced an unstable compound with platelet-aggregating activity, which was presumably thromboxane A2 and which decomposed readily to thromboxane B2 and 12L-hydroxy-5,8,10-heptadecatrienoic acid.

Animals↗