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Query: HUMANGGP:001400 (PRP)
 1,320 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of divalent cations on ADP-induced aggregation response were examined. Bovine platelets were transferred by Sepharose 2B gel filtration from citrate-PRP into citrate free buffer (buffer-GFP). Response increases, reaches a maximum and decreases with increasing calcium and/or magnesium concentration. For either calcium or magnesium alone, increasing response is proportional to a rate coefficient and, through an apparent ion-platelet association constant, to the fraction of platelet critical sites bound to cation. With both ions present, bound magnesium appears to inhibit bound calcium in excess of that accounted for by competition and a lower rate coefficient for bound magnesium. With citrate present in buffer-GFP, apparent association constants increase, excess magnesium inhibition is present, but systems are path dependent. Initial conditions appear to establish a response which is thereafter immutable to environmental magnesium alteration. Citrate-PRP resembles buffer-GFP: response is sensitive to the selective removal of calcium and excess magnesium inhibition is present. With heparin-PRP, response is immutable to the selective removal of approximately 90% of initial calcium. The dependency of response inhibition observed at high divalent cation concentrations indicates that aggregation is not due to interplatelet cross linking by ions. Ion effects are similar for bovine and human platelets.
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PMID:Effects of ions on ADP-induced aggregation of bovine or human platelets. 1 94

The ADP- and collagen-induced aggregation of platelets in PRP of healthy probands was tested in vitro in the presence of 4 heparin preparations (Novo, Vitrum, Liquemin, Haemoderivate) and of a heparinoid (Eleparon). None of the preparations caused a significant direct aggregation. The collagen-induced aggregation was inhibited by all mentioned preparations; thereby the heparins proved to be effective approx. to the same degree whereas the heparinoid proved to be significantly less effective. The ADP-induced aggregation was potentiated by all preparations. A considerably different sensitivity to heparin could be observed in the single PRP's. A special method was found out to exclude the influence of the heparin-sensitivity of the PRP's to compare the special effects of the heparins.
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PMID:[Influence of five commercial heparin preparations on the collagen induced platelet aggregation (author's transl)]. 7 75

1) On log-log-coordiantes a direct correlation has bee shown to exist between plasma cyclic AMP and plasma Cr levels. 2) hemodialysis results in a significant reduction in the arterial plasma cyclic AMP levels, but a return of plasma cyclic AMP to pre-dialysis levels is seen within 30 mins post-dialysis. 3) the dialyzer clearance of cyclic AMP, both in vitro and vivo, is commensurate with its M.W. 4) In vitro platelet aggregation responses, to ADP, EPI, and COLL are not influenced by PRP cell counts between 150,000 and 300,000/mm3. 5) the BT of NC and CHDP are not significantly different, indicating that the in vivo hemostatic properties of the CHDP are otherwise intact. 6)the CHDP have PVPC significantly lower than the NC, a finding commensurate with the usual mold thrombocytopenia of renal failure. 7)the aggreation responses of the CHDP to COLL and to both Lo and Hi concentrations of ADP and EPI are significantly less than those of the NC. 8)A statistically significant inverse correlation between aggregation response and plasma cyclic AMP is observed.
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PMID:Depressed in vitro aggregation of platelets of chronic hemodialysis patients (CHDP): a role for cyclic AMP. 16 91

102 sera from polytransfused patients have been screened in platelet aggregometry. Anti-human platelet isoantibodies, tested against 'responsive' human platelets in PRP, give in the aggregometer a decrease in optical density recorded as a sigmoidal curve. In the first step of reaction PF3 availability suggests that the primary action of antibody is to damage the platelet membrane. The second step might be a true aggregation (an ADP-mediated platelet clumping) or a platelet lysis, depending on the type and the potency of antibody, on the type of platelets (normal or thrombasthenic) and on some experimental conditions. These conclusions, confirmed by electron microscopy findings, suggest that aggregometry is a very rapid and simple method of detecting platelet antibodies.
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PMID:Platelet aggregometry and anti-platelet isoantibodies. 17 12

The potencies of prostaglandins (PG) I2, PGD2 and PGE1 as inhibitors of human platelet aggregation induced by threshold concentrations of four aggregating agents were determined in platelet-rich plasma from normal individuals who had not ingested aspirin. The order of activity against ADP, adrenaline and collagen was always PGI2 greater than PGD2 greater than PGE1. However, PGD2 and PGE1 were almost equipotent with PGI2 when tested against arachidonic acid (AA). The threshold inhibitory effects of PGD2, PGE1 and PGI2 could be over come by increasing the concentrations of the aggregating agents AA, collagen or ADP. Adrenaline was found to be different from the other aggregating agents. It could overcome inhibition of platelet aggregation by PGD2 but could not overcome inhibition by PGI2 or PGE1. These facts support the hypothesis that platelet receptors for PGI2 and PGE1 are similar to each other and different from the receptor(s) for PGD2. PRP obtained from normal subjects after the ingestion of aspirin exhibited only one wave of aggregation in response to ADP, adrenaline or collagen, PGI2, PGD2 and PGE1 were all powerful inhibitors of this single wave of aggregation. The inhibitory activity of all three prostaglandins at threshold concentrations was overcome by increasing the concentration of ADP or collagen but not by increasing the concentration of adrenaline.
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PMID:Prostaglandins as inhibitors of human platelet aggregation. 39 96

The individual and combined effects of PGD2, PGI2 and an aortic proteoglycan on human platelet aggregation and plasma clotting were studied. PGI2 was at least 10 times more potent than PGD2 in inhibiting platelet aggregation. Small doses of prostaglandins inhibited ADP- and thrombin-induced aggregation, but only prolonged aggregation time without affecting the extent of arachidonic acid (AA)-induced aggregation. Small doses of prostaglandins did not affect thrombin-induced clotting of PRP. Large doses of prostaglandins abolished platelet aggregation and prolonged the onset of thrombin-induced clotting. The aortic proteoglycan (APG) had no appreciable effect on ADP- or AA-induced aggregation. Small doses of APG abolished thrombin-induced clotting, while large doses of APG suppressed both clotting and aggregation induced by thrombin. PGI2 and PGD2 showed additive inhibition of platelet aggregation regardless how the aggregation was induced. APG and prostaglandins showed additive inhibition of only thrombin-induced aggregation. APG, but not any of the prostaglandins, prolonged clotting time of PPP. This prolongation was not potentiated by PGI2 or PGD2.
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PMID:Combined effect of prostaglandins and an aortic proteoglycan on platelet aggregation and plasma clotting. 39 32

Employing the Haemonetics Blood Processor (IFC), a relatively pure platelet concentrate can be prepared by collecting only the first portion of the PRP leaving the centrifuge bowl (Fraction I). A subsequent fraction containing RBC and WBC contaminants (Fraction II) can be purified by means of a second centrifugation, using a conventional blood bank centrifuge (Fraction II), if transfusion of these contaminants would be detrimental to the recipient. Utilising the new 1.4% Na3-citrate anticoagulant, platelet metabolic parameters (ATP, ADP, AMP, lactate and pyruvate) as well as O2-uptake, were determined in Fraction I and II prepared from 10 normal healthy subjects. In contrast to previous studies reporting marked dysfunction in platelets contained in Fraction II when standard ACD-A was used during IFC, we observed no significant difference (Student's t test) in the present study between Fractions I and II, in regard to platelet metabolism, when using the new anticoagulant. It is further concluded that the second centrifugal manipulation does not exert a detrimental effect on platelet metabolism.
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PMID:The utilisation of a new strength citrate anticoagulant during centrifugal plateletpheresis. III. Assessment of in vitro platelet metabolism. 49 71

The hypothesis that platelet ADP is responsible for collagen-induced aggregation has been re-examined. It was found that the concentration of ADP obtaining in human PRP at the onset of aggregation was not sufficient to account for that aggregation. Furthermore, the time-course of collagen-induced release in human PRP was the same as that in sheep PRP where ADP does not cause release. These findings are not consistent with claims that ADP alone perpetuates a collagen-initiated release-aggregation-release sequence. The effects of high doses of collagen, which released 4-5 microM ADP, were not inhibited by 500 microM adenosine, a concentration that greatly reduced the effect of 300 microM ADP. Collagen caused aggregation in ADP-refractory PRP and in platelet suspensions unresponsive to 1 mM ADP. Thus human platelets can aggregate in response to collagen under circumstances in which they cannot respond to ADP. Apyrase inhibited aggregation and ATP release in platelet suspensions but not in human PRP. Evidence is presented that the means currently used to examine the role of ADP in aggregation require investigation.
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PMID:Collagen-induced platelet aggregation:--evidence against the essential role of platelet adenosine diphosphate. 54 29

Changes in platelets in 48 patients with uterine myoma before and after hysterectomy with and without ovariectomy were examined. Bilateral ovariectomy in 25 cases (ovariectomized group) and unilateral or non-ovariectomy in 23 cases (control group) were performed at the hysterectomy. Platelet count and an appearance rate of secondary aggregation decreased at one day after and increased at one week after the operation, similarly in both the ovariectomized and the control group. The appearance rate of secondary aggregation was reflected in an intensity of aggregation at 5 min after the addition of reagent to PRP. At one month after the operation, the appearance rate of secondary aggregation induced by 3 microM ADP showed a statistically significant decrease in comparison with the preoperation value (P less than 0.05) and the enhancement of 5-min aggregation was still observed in the control group, while ceased in the ovariectomized group. The difference between the two groups was significant (P less than 0.05). There was almost no change in the speed and intensity of primary and secondary aggregation during the observation period. No significant differences in collagen-induced aggregation were noted between the two groups. The results suggest that ovarian hormones, mainly estrogen, facilitate platelet activation which is mediated by the so-called secondary aggregation.
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PMID:Changes in platelet aggregability after ovariectomy. 54 38

Oral administration of onion and garlic reportedly decreases platelet aggregation in both human and animal subjects. An oily chloroform extract of onion (Allium Cepa) was prepared and separated by column chromatography on silicic acid into six fractions by elution with solvents of increasing polarity. The least polar fraction contained most of the inhibitory activity towards platelet aggregation induced by either ADP or arachidonic acid. Further purification was afforded by thin-layer chromatography. The specific activity of this major active fraction (I50 per ml of PRP) was approximately 7 units per milligram. Platelets incubated in the presence of onion inhibitor and (1-14C)-arachidonic acid showed striking changes in the pattern of arachidonic acid metabolites formed. Thromboxane B2 synthesis was almost completely suppressed without significant decreases in total hydroxy fatty acid formation. It was concluded that the observed antiplatelet activity of onion relates to the presence of a non-polar, heat stable inhibitor of thromboxane synthesis. This appears to be the first demonstration of this type of inhibitor present in significant quantities in a common foodstuff.
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PMID:Effects of onion (Allium cepa) extract on platelet aggregation and thromboxane synthesis. 55 92


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