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At least 127 records · Page 7Linked to original sources
PubMed1985

Verapamil, an antagonist at 5-hydroxytryptamine receptors of human blood platelets.

In human blood platelets verapamil and D600 (2-methoxyverapamil) in therapeutic concentrations inhibited the shape change reaction induced by 5-hydroxytryptamine (5HT) but not that induced by ADP. The N-methylated derivatives (D575 and D890) had much less effect. The inhibitory action of verapamil was independent of external Ca2+. Nitrendipine and diltiazem (20 microM) had no effect on the 5HT- and the ADP-induced shape change reactions. Since both these shape change reactions are mediated by a rise in cytoplasmic free Ca2+, it is concluded that the inhibition of the 5HT effect by verapamil and D600 was not due to their interference with calcium channels but rather to an antagonistic action on 5HT2-receptors. This view is supported by the finding that verapamil but not D575 competed with [3H]ketanserin and [3H]spiroperidol for their specific binding sites on membranes of rat cerebral cortex.

Adenosine Diphosphate↗
PubMed1986

System for testing the phagocytic capacity of human blood platelets.

We have elaborated a system for testing the phagocytic activity of human blood platelets. Blood was sampled to heparin and ACD and centrifuged. This procedure yields platelet rich plasma (PRP). As a substrate for phagocytosis we used Staphylococcus aureus 209P. The ratio of platelets to bacteria is 1:1. Incubation of bacteria and platelets continued up to 10 minutes. Lysostaphine was introduced to the phagocytic system to destroy all bacteria outside the blood platelets. The maximal values for the percentage of phagocytizing blood platelets were 0.7% and the phagocytosis index of 1.0 was reached at 6 minutes with incubation of bacteria and platelets. The authors pay attention to the role of blood platelets in antibacterial mechanisms.

Blood Platelets↗
PubMed2000

[Use of platelet function analyzer PFA-100 and whole blood aggregometry to monitor blood platelet sensitivity to acetylsalicylic acid (aspirin). Is it possible to reliably monitor antiplatelet treatment using routine laboratory diagnostic methods?].

Introduction of the antiplatelet agents of new generations and the occurrence of the phenomenon of "aspirin-resistance" triggered the search for better, simpler and more reliable routine diagnostic methods to monitor platelet reactivity. Our objective was to evaluate the usefulness and reliability of two simple methods: platelet function analyzer (PFA-100) and whole blood platelet aggregometry for monitoring of platelet function in 18 healthy blood donors and 35 patients with ischaemic heart disease (IHD) subjected to small doses/75 mg and 150 mg a day) of acetylsalicylic acid (aspirin). In 50% of healthy blood donors the intake of 75 mg ASA a day resulted in the prolongation of PFA-100 collagen/epinephrine closure time (CEPI = (relevant to reduced platelet reactivity) of over 150 s, whereas 75% donors responded to 150 mg ASA-. Otherwise, the daily dose of 150 mg ASA resulted in a prolonged CEPI merely in 23% of in IHD patients. At both doses ASA completely inhibited the arachidonic acid-induced whole blood platelet aggregation in all healthy donors and in all but 3 IHD patients. Collagen-induced platelet aggregation was only negligibly affected by either dose of ASA. Our results point that the simultaneous monitoring of the PFA-100 collagen/epinephrine closure time and whole blood platelet aggregometry (Chrono-Log) enables to reliably evaluate the inhibition of platelet function by ASA and discriminate the partial or complete platelet insensitivity to aspirin. The phenomenon of more frequent platelet aspirin-resistance in IHD patients requires to be verified in randomised clinical prospective studies.

Adult↗
PubMed1988

[Specific antitumor cytotoxicity of blood platelets from the peripheral blood of patients with lung cancer].

The analysis of cytotoxic activity of platelets from patients with lung cancer is presented. It has been shown that these platelets lyse fresh isolated autological and allogenic tumor cells in 38.5% of cases and lyse the cells in the culture of lung adenocarcinoma cell line in 82.4% of cases, while platelets from healthy donors do not lyse fresh isolated and cultured cells of lung cancer. Cytotoxicity of platelets from patients and control subjects against HeLa and K 562 was identical and did not exceed 10%. The platelets from healthy controls, unlike platelets from patients with lung cancer, lysed tumor cells of melanoma cultured cell line Mel 1. Thus, it has been shown for the first time that platelets from the peripheral blood of patients with lung cancer have specific antitumor activity.

Adenocarcinoma↗
PubMed1993

Hyperaggregation of platelets detected by whole blood platelet aggregometry in newly diagnosed noninsulin-dependent diabetes mellitus.

Twenty-five newly diagnosed cases of noninsulin-dependent diabetes mellitus were studied at the time of diagnosis and again after metabolic control of diabetes was achieved (approximately 3 months later) for platelet aggregation abnormalities in whole blood by the impedance method. Adenosine diphosphate in 10 and 20 mumol/L final concentrations and arachidonic acid in 25 and 50 mmol/L final concentrations were used as agonists. Patients had a significant hyperaggregation of platelets (P < 0.01) at the time of diagnosis compared with age-matched healthy control subjects. After metabolic control of blood glucose was achieved using oral hypoglycemic agents (n = 20) and diet regulation alone (n = 5), there was a significant decrease in platelet aggregation (P < 0.01). There was a positive relationship between blood glucose levels and whole blood platelet aggregation with adenosine diphosphate (P < 0.02 and < 0.05, with 10 mumol/L and 20 mumol/L, respectively), but there was no relationship between aggregation and glycosylated hemoglobin levels. Thus, platelet hyperaggregation was present even at the time of diagnosis in patients with diabetes mellitus in the absence of any vascular complications, and there was significant improvement in platelet hyperaggregation after metabolic control of blood glucose levels was achieved.

Adult↗
PubMed1989

Anti-hypertensive drugs non-specifically reduce "spontaneous" activation of blood platelets.

Abnormal activation of blood platelets may be a contributory factor in the accelerated vascular disease which occurs in hypertension. We investigated the effects of lowering blood pressure in 12 patients with mild hypertension on several aspects of platelet function, initially in a placebo-controlled, double-blind, cross-over study with nisoldipine, and subsequently in the same patients comparing nisoldipine with the patients' usual anti-hypertensive therapy. Values were compared with those from an age, sex-matched control population. Seven hypertensive patients with renal failure were also studied. Administration of nisoldipine reduced ex vivo "spontaneous" aggregation of blood platelets significantly, and a similar significant effect was seen when blood pressure was lowered by the patients usual anti-hypertensive therapy. "Spontaneous" aggregation occurring in the control population was similar to that in the treated hypertensives. Blood platelet count, and aggregation in response to ADP and adrenalin were unaffected by treatment. Median plasma beta thromboglobulin levels were significantly higher in the untreated hypertensive patients (43 ng ml-1) than in the controls (30 ng ml-1), and there was a trend to reduced values for beta thromboglobulin on treatment of the hypertension. These results indicate that blood platelet activity is enhanced in hypertension and that function returns towards normal when blood pressure is lowered by treatment.

Adult↗
PubMed1983

Metabolism of platelet-activating factor by blood platelets and plasma.

High performance liquid chromatography in combination with a radioactivity detector was used to study the metabolism of platelet-activating factor (1-0-alkyl-2-acetyl-sn-glycero-3-phosphocholine) by washed platelets, platelet-free plasma and platelet-rich plasma obtained from rabbits and humans. Degradation of platelet-activating factor to its 2-lyso derivative was observed in rabbit and human plasma. This degradation of platelet-activating factor in plasma was completely inhibited by diisopropylfluorophosphate and was partially inhibited by ethylenediamine tetraacetic acid. Washed platelets metabolized platelet-activating factor not only to the 2-lyso compound but also, by reacylation of this lyso intermediate, to an analogue of platelet-activating factor probably containing a long-chain acyl group at the sn-2 position. These transformations occurred, but to a lesser extent, in platelet-rich plasma.

Animals↗
PubMedDate not supplied

UV-B-induced generation of free radicals in blood platelets.

UV-B irradiation of blood-platelet concentrates is used in transfusion practice to prevent the development of post-transfusion alloimmunization and inactivate viruses and bacteria in the concentrates. UV-B radiation may affect the blood-platelet metabolism and function; therefore we have investigated the effect of UV-B irradiation on free radical production in blood platelets. Our results show that exposure of pig blood platelets to UV-B radiation (0.36 and 1.08 J/cm2) induces the generation of free radicals measured by the chemiluminescence method (respectively 28 and 148.6% above the control). The superoxide radical level after UV-B irradiation measured by the cytochrome c reduction method shows only a slight increase (p > 0.05). Free radical generation induced by UV-B radiation is dependent partly on blood-platelet activation and enzymatic pathways, since we have shown that wortmannin, an inhibitor of phosphatidylinositide 3-kinase, reduces the level of radicals formed in blood platelets after UV-B irradiation. This indicates that free radicals generated in blood platelets after stimulation by UV-B radiation are involved in platelet activation and metabolism of platelet polyphosphoinositides.

Androstadienes↗
PubMed1983

Blood platelets in psychopharmacological research.

Blood platelets are a very good model for nerve endings, for study of serotonin uptake and imipramine binding. The efficiency of various drugs, mainly antidepressants, can be evaluated using blood platelets instead of synaptosomes. A few neuronal active compounds are effective in inducing platelet secretion and shape change reaction. Platelet MAO and c-AMP levels are not yet established as useful in psychopharmacological studies.

Autistic Disorder↗
PubMed1987

Biosynthesis of major platelet proteins in human blood platelets.

We studied de novo protein biosynthesis in platelets of normal adult donors and in newly formed platelets isolated from splenectomized patients with idiopathic thrombocytopenic purpura (ITP). After metabolic labelling of platelet proteins, performed with different radiolabelled amino acids or carbohydrates, a tenfold increase in incorporation of radioactivity into trichloroacetic-acid-precipitable material was obtained with ITP platelets compared to control platelets. Electron microscopic studies of ITP platelets revealed the presence of rough endoplasmic reticulum and polyribosomes, providing morphological evidence for protein synthesis. SDS-PAGE of radiolabelled ITP platelet proteins followed by autoradiography showed that [35S]methionine and [3H]leucine were incorporated into almost all Coomassie-blue-stained proteins whereas [3H]carbohydrates only labelled a few bands. Using crossed-immunoelectrophoresis we identified some of the labelled platelet compounds and demonstrated that major membrane glycoproteins (GPIb, IIb, IIIa) and alpha-granule proteins, such as fibrinogen, thrombospondin, albumin and von Willebrand factor, were synthesized in newly formed circulating platelets.

Adult↗
PubMed1989

Does acute experimental pancreatitis affect blood platelet function?

The role of blood platelets in the disturbed haemostasis in acute pancreatitis is not fully elucidated. The aim of this study was to evaluate the blood platelet function during the first hours of acute experimental pancreatitis (AEP) in dogs. AEP was induced by the retrograde injection of bile and trypsin into the main pancreatic duct. Platelet count, platelet aggregation induced with ADP, PAF, AA as well as plasma Beta-TG and TXB2 levels were determined. At 30 min after induction of AEP a significant decrease of platelet count was noted; these changes were observed until 4 th hr. At 30 min as well as at 60 min of AEP increased sensitivity of platelet aggregation to ADP was found. After that time evident decrease of platelet aggregation to ADP was shown. Platelets sensitivity to PAF was higher at 30 min of AEP whereas 60 min, 2 and 4 hrs after AEP normalization of platelet aggregation by PAF was observed. The significant increase of plasma Beta-TG and TXB2 concentrations corresponded well to changes of platelet aggregation. These results indicate that AEP affects blood platelet function with the drop of their count.

Acute Disease↗
PubMed1975

Blood platelet monoamine oxidase activity in anergic schizophrenics.

Blood platelet monoamine oxidase (MAO) activity was evaluated in twenty-four anergic, schizophrenic outpatients during a double-blind study comparing a chlorpromazine-imipramine combination to thio-thixeneplacebo. Platelet MAO activity was determined on blood samples drawn after a two-week drug-free washout and once weekly over a four-week on-drug period. Schizophrenic patients could be classified according to their blood platelet MAO activity into either a low-MAO or a high-MAO group. In neither group of this population of schizophrenics did blood platelet MAO activity correlate with any of the primary or secondary symptoms of schizophrenia. Ten alcoholics and seven volunteer non-patients could similarly be divided into low- and high-MAO groups. Mean blood platelet MAO activity for these groups was not significantly different from the mean values of the low and high-MAO groups of the schizophrenics. These findings do not support published reports of low blood platelet activity as a genetic marker for schizophrenia. Discriminate function analysis of symptomatology ratings at baseline was used to characterize the low- and high-MAO schizophrenic patient groups. Individuals in the low-MAO group were distinguished by hyperactivity, anergia and sleep disturbance.

Alcoholism↗
PubMed1989

[3H]SCH 23390 labels a novel 5-hydroxytryptamine binding site in human blood platelet membranes.

In human blood platelet membranes, 5-HT displaced the binding of the putative selective D-1 dopamine receptor antagonist [3H]SCH 23390 in a competitive manner with a Ki value of 5.7 +/- 0.8 nM, which was about 1000-fold lower than the Ki value for dopamine (Ki = 4400 +/- 150 nM). Thus the 'D-1 dopamine-like' site in human blood platelet membranes described previously corresponds to a 5-HT1-type site. [3H]SCH 23390 competition experiments with a number of serotonergic drugs disclosed a pharmacological profile that was distinct from the four 5-HT1 site subtypes reported previously. We therefore propose that this novel 5-HT site be designated the 5-HT1E site. Binding of [3H]SCH 23390 to 5-HT1-type sites could not be detected in several regions of the human brain. In some regions, however, 5-HT displaced part of the [3H]SCH 23390 binding with a K1 value of 320-380 nM. These sites correspond to 5-HT2 receptors.

Antipsychotic Agents↗