Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:001400 (PRP)
 1,320 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new method has been developed to investigate the direct effect of endothelial cells on platelet aggregation in the presence of cultured confluent human EC monolayers. The inside of the disk shaped cuvettes are covered by human umbilical vein ECs. The cuvettes rotate in the light beam of a photometer. In these cuvettes the effect of different aggregation inducers was inhibited in a concentration-dependent manner, e. g. for collagen at 0.5 microgram/ml, ADP at 5 x 10(-7) M, epinephrine at 5 x 10(-7) M and thrombin at 0.05 U/ml final concentration. (Platelet count 5 x 10(5)/microliters). Higher concentrations of the inducers led to irreversible platelet aggregation and were used for testing of antiplatelet drugs. In this system we detected a synergism between the antiaggregatory effect of the EC monolayer and that of SIN 1 (Cassella, Frankfurt/Main) the main metabolite of Molsidomine. 10 micrograms/ml PRP of SIN 1 alone partially inhibited platelet aggregation induced by 1 microgram/ml collagen and 10(-6) M ADP respectively in uncovered aggregation cuvettes. In the presence of an EC monolayer complete inhibition of platelet aggregation was obtained at a 5-fold final concentration of both inducers. After pretreatment of ECs with 1 mmol ASA over 30 min. the antiaggregatory effect of SIN 1 decreased, but was more pronounced (50%) than in uncovered cuvettes (25%).
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PMID:[Effect of SIN 1 on the interactions of endothelial cells and thrombocytes]. 177 29

The present in vitro study of the effects of iron on the blood coagulation mechanism in rats showed that addition of ferrous sulphate to pooled rat plasma resulted in inhibition of blood coagulation, as shown by prolongation of the clotting parameters tested, an effect which was dose-dependent. In vitro addition of ferrous sulphate to rat PRP in doses of 2-5 mg/ml significantly decreased platelet aggregation in response to ADP, while collagen-induced aggregation was significantly diminished in presence of the higher doses of ferrous sulphate (4-5 mg/ml). Also, preincubation of ferrous sulphate with thrombin or with pure fibrinogen indicated that iron could produce decrease of thrombin activity as well as impairment of fibrinogen clottability. In vitro addition of copper sulphate (300-1000 micrograms/ml) elicited an anticoagulant effect, though thrombin time was markedly shortened with all tested concentrations of copper sulphate. Addition of copper sulphate to PRP produced inhibition of platelet aggregation in response to PRP produced inhibition of platelet aggregation in response to ADP and to collagen. Preincubation of copper sulphate with thrombin resulted in slight enhancement of thrombin activity followed by inhibition, while preincubation of copper sulphate with pure fibrinogen caused only minimal impairment of fibrinogen clottability. Also, addition of gold chloride in doses of 50-500 micrograms/ml to plasma in vitro produced a dose-dependent progressive prolongation of all clotting parameters tested, the effects reaching a maximum after 30 min. incubation. Further the in vitro addition of gold chloride to rat PRP resulted in marked inhibition of platelet aggregation in response to both ADP and collagen. In addition, preincubation of gold chloride with thrombin or with pure fibrinogen showed that gold exerted an antithrombin action and prolonged the fibrinogen clotting time indicating impaired fibrinogen clottability.
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PMID:In vitro effects of trace elements on blood clotting and platelet function. A--Iron, copper, and gold. 180 Jun 20

The in vitro effects of zinc and magnesium salts on blood coagulation mechanism and platelet aggregation were studied on rat plasma. Addition of zinc sulphate to pooled rat plasma in a range of concentrations (0.3-1 mg/ml) caused a dose dependent significant prolongation of recalcification, prothrombin and partial thromboplastin times. These effects reached a peak after 30 minutes while the thrombin clotting time was not significantly altered and was even shortened in the presence of highest concentration of zinc tested (1 mg/ml). Incubation of thrombin with zinc sulphate (150 micrograms/ml) for up to 30 minutes did not affect significantly the action of thrombin. Incubation of the same concentrations of zinc sulphate with fibrinogen produced non clotting of fibrinogen after 0-minutes. Addition of rising concentrations of zinc sulphate to rat PRP produced inhibition of ADP-induced platelet aggregation. On the other hand, collagen-induced aggregation was insignificantly inhibited in the presence of zinc. In contrast, in vitro additions of rising concentrations of magnesium sulphate (2-5 mg/ml) to pooled rat plasma exerted no effect on recalcification time immediately after addition (0-minutes), but after 5 minutes following incubation it produced significant shortening of recalcification time in all the doses tested. The prothrombin time showed a general trend of shortening, maximal after 5-minutes incubation. The results of partial thromboplastin times revealed clotting before addition of calcium chloride. The thromboplastin time also showed progressive shortening with rising concentrations of magnesium sulphate. When thrombin solution was exposed to magnesium sulphate (2.5 mg/ml) no effect on the activity of thrombin was seen for up to 30 minutes. Fibrinogen solution similarly exposed to the same concentration of magnesium sulphate did not show any significant effect on its clottability with thrombin for up to 30 minutes. Magnesium sulphate in the range of doses tested significantly enhanced platelet aggregation of PRP in response to both ADP and collagen, and the responses observed were not dose dependent. The mechanisms underlying the effects of these two metals on blood clotting and platelet aggregation are discussed.
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PMID:In vitro effects of trace elements on blood clotting and platelet function. B--Zinc and magnesium. 180 Jun 25

Functional and metabolic response of an isovolumically perfused heart of a rat to isoproterenol (0.1 microM) has been studied. A heart with the normal content of adenine nucleotides (AN) and phosphocreatine (PCr) as well as that with the 5-fold reduced AN content (with 2-deoxyglucose treatment) significantly increased cardiac work index (PRP), maximal contraction rate (MCR) and maximal relaxation rate (MRR) (by 50, 30-40 and 100-150%, respectively). The effect was preserved for all the period of the hormone action (30 min) and was followed by a temporary decrease in the PCr content. The heart with an inhibited unidirectional flux of metabolites through creative kinase (CK) and normal level of AN responded to the hormone by the slower and decelerated growth of the function and in the heart with almost completely iodoacetamide (IAAm)-blocked CK the functional response was minimal and transient. In the latter a significant and irreversible decline in PCr and ATP content and a concomitant rise of inorganic phosphate took place. Both basal and isoproterenol-stimulated adenylate cyclase activity remained unchanged after IAAm treatment. An increase in PRP correlated with the elevation of the cytosolic ADP concentration, however, correlation was not uniform for different experimental groups. These data show significance of the creatine kinase system not only for maintenance of maximal work but also for a rapid functional response to the catecholamine stimulation.
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PMID:[Adrenergic stimulation of the heart during inhibition of phosphocreatine or adenylate pathways of energy transfer in cardiomyocytes]. 182 Sep 58

In part 1, we reported that human (H) platelets, activated with high concentrations (10 microM) of adenosine diphosphate, aggregate under Brownian diffusion (nonstirred, platelet-rich plasma) with an apparent efficiency of collision (alpha B) approximately 4 times and 8 times larger than observed, respectively, for canine (C) and rabbit (R) platelets. Further evaluations of parallel inhibition of alpha B and shape change suggested a central role for platelet pseudopods in mediating the long-range interactions associated with the elevated alpha B values. We found that greater than 90% of all platelet contacts in the doublets and triplets formed were via at least one pseudopod. We therefore compared pseudopod number and length per platelet generated by approximately 30 s post ADP activation in nonstirred PRP from human, canine, and rabbit donors, using phase-contrast, video-enhanced microscopy of fixed platelets. Theoretical calculations assessing the effects of pseudopod length and number on the collision frequency enhanced by an increased radius of a collision sphere supported the experimental observations that approximately 3 or 4 pseudopods per human or canine platelet, and approximately 5 or 6 pseudopods per rabbit platelet yield optimal alpha B values, with the average pseudopod length: approximately 3:2:1 for H/C/R, paralleling the alpha B differences. After correcting for effects of pseudopods and platelet size on platelet diffusion and sedimentation, it still appeared that the small number of long pseudopods formed on human platelets could largely explain the unusually large alpha B values. The quantitative discrepancies between theory and experiment do not appear related to time-dependent refractoriness within the less than 60 s of observation, but may be related to biochemical differences in dynamics and surface density of adhesive (sticky sites) present on the pseudopod surface.
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PMID:Long-range interactions in mammalian platelet aggregation. II. The role of platelet pseudopod number and length. 220 39

In vitro, the oxacyclic epoprostenol (prostacyclin) analogue taprostene like the native epoprostenol inhibited platelet aggregation and adhesion and induced deaggregation. Antiaggregatory action of taprostene was demonstrated towards arachidonic acid-, ADP-, thrombin- and norepinephrine-induced aggregations of human platelet rich plasma with IC50 values between 17 and 34 nmol/l. ADP-induced aggregations of human, dog or rabbit platelets were inhibited with an equivalent efficacy. Under the present conditions taprostene was about 3fold less active than epoprostenol. The deaggregatory effect, measured in arachidonic acid-induced aggregates of human PRP, could be detected only in concentrations from 1 mumol/l taprostene. The adhesion-inhibiting effect towards glass beads, measured in whole blood, appeared at comparable high concentrations (IC50 value: 2.4 mumol/l) and likewise the antihaemolytic effect on rat erythrocytes, which was exerted with a threshold concentration of 10 mumol/l. Heparin in a concentration range of 0.1-1000 micrograms/ml increased thrombocyte adhesion and this effect was prevented by 1 mumol/l taprostene.
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PMID:In vitro studies with the stabilized epoprostenol analogue taprostene. Effect on platelets and erythrocytes. 222 58

It has been shown in Poiseuille flow, that the ADP-induced aggregation of human platelets in citrated plasma from female donors is significantly greater than from male donors over a range of mean tube shear rate, G, from 41.9 s-1 to 1920 s-1 and mean transit time, t, from 0.2 to 86 s. The present work verifies the sex difference at G = 335 s-1 and t = 43 s and deals with the effect of free Ca2+ on it. An inverse correlation between the extent of single platelet aggregation and donor hematocrit, and between hematocrit and the plasma ionized calcium concentration, [Ca2+], as well as a positive correlation between the extent of single platelet aggregation and [Ca2+] was found. This indicated that the sex difference is due to hematocrit-dependent differences in the [Ca2+] that result when a fixed volume of the chelating agent citrate is used to anticoagulate blood. When the initial citrate concentration was adjusted to compensate for the variable volume dilution of citrate in plasma among donors and the [Ca2+] of males raised above that of females, the sex difference was reversed. Again, aggregation correlated with [Ca2+]. At the physiological [Ca2+] in both heparinized PRP and hirudinized PRP, the rate of aggregation and aggregate size were much greater than in citrated plasma but no sex difference was detected.
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PMID:Extracellular-free Ca++ accounts for the sex difference in the aggregation of human platelets in citrated platelet-rich plasma. 234 44

1. Dopexamine is a novel analogue of dopamine which is free of alpha-adrenoceptor activity and is of therapeutic value in chronic heart failure. The effects of dopexamine on the in vitro function of platelets from 10 healthy subjects at rest, after exercise and after in vitro addition of adrenaline and noradrenaline were investigated. 2. Dopexamine in a wide range of concentrations (10(-9)M-10(-3)M) did not appear to function as an agonist on platelets either in whole blood or in PRP preparations. 3. Dopexamine caused a dose-dependent inhibition of agonist-induced platelet aggregation in both whole blood and PRP. The inhibitory effect of dopexamine was significantly greater in PRP than in whole blood, and significantly greater to adrenaline than to collagen or ADP as agonists in whole blood. 4. After exercise or after in vitro addition of adrenaline and noradrenaline at concentrations commonly seen in myocardial infarction, dopexamine produced similar levels of inhibition seen with platelets from resting subjects. 5. Dopexamine did not affect plasma catecholamine levels but caused an increase in intraplatelet noradrenaline levels. 6. This study suggests that dopexamine is unlikely adversely to affect the hyperaggregable state found in patients with cardiogenic shock after myocardial infarction.
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PMID:The effects of dopexamine, a new dopamine analogue, on platelet function in stress. 239 Apr 35

We have investigated in vitro platelet aggregation in platelet rich plasma from Trypanosoma vivax infected and control sheep using the dual channel Payton Aggregometer. Final concentrations of the following inducing agents were used: 1.2 um ADP, 6.2 ug collagen, 1.2 ug ristocetin and 1 u thrombin. These showed that there was a significantly reduced aggregation of platelets from infected sheep (13.4 +/- 1.1 pc at week 3 post infection when compared with control sheep PRP 95.0 +/- 1.0pc; P less than 0.001) using ADP. Similar differences were also obtained with other inducing agents. Preliminary 14C-5HT uptake and release studies showed that there was difference in the uptake of label between platelets from infected (18.6pc) and control (28.4pc) sheep. However, when release was inducted, comparable results were obtained for both infected and control sheep platelets. It is concluded that the degree of aggregation inhibiting varies directly with the level of parasitaemia.
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PMID:Platelet aggregation inhibition in Trypanosoma vivax infection of sheep. 239 92

The authors tested the influence of gentamicin, spectinomycin dihydrostreptomycin on the ADP and epinephrine in vitro induced platelet aggregation. Our aim was to demonstrate if platelet aggregation in vitro had some influences by antibiotics. A reduction in platelet aggregability, strictly dependent from the used antibiotic dose was observed. We have studied platelet function thanks to Born's method, adding to PRP gradual therapeutics doses of antibiotics. The results showed a reduction of platelet function which was dose-depended, and, particularly, gentamicin seemed to be the most effective among aminoglycosides. An interference between these drugs and the ADP and epinephrine binding to specific platelet receptor sites is proposed.
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PMID:[Action of aminoglycosides on platelet aggregation in vitro]. 241 Dec 77


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