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 comparison has been made of some effects of a semi-synthetic heparin analogue, A73025, and heparin upon platelet function. In several of the in vitro tests performed, such as their potentiating effects on ADP and adrenaline induced aggregation and their effects on the aggregation of washed platelets by activated factor X, heparin proved to be more potent than A73025. Following intravenous injection of twice the quantity of A73025, an equivalent anti-factor Xa activity was obtained, in the agreement with our previous studies. However, it was found that PRP containing heparin and A73025 with comparable anti-Factor Xa acitvity responded differently to the addition of thrombin, as A73025 barely inhibited thrombin induced aggregation. Similarly, A73025 had little effect on the dilute thrombin clotting time of plasma, following intravenous injection. Heparin and A73025 were neutralized to approximately the same degree by a crude PF4 preparation.
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PMID:Comparison of heparin and a semi-synthetic heparin analogue, A73025. II. Some effects on platelet function. 60 58

HAL, a congener of clofibrate, has previously been shown to inhibit epinephrine- and ADP-induced platelet aggregation and 14C-serotonin release. We further investigated the site of action of HAL by examining platelet shape change, MDA production as a measure of prostaglandin synthesis, and platelet aggregation and MDA production induced by SA. At the usual maximal therapeutic concentration of HAL (0.96 mM), this drug did not affect the velocity of platelet shape change as measured by a spectrophotometric method. However, at a higher concentration (3.12 mM), HAL significantly inhibited shape change (p less than 0.01). When epinephrine was used to initiate aggregation of PRP, HAL (0.96 mM) was found to inhibit MDA production over a wide range of epinephrine concentrations (p less than 0.01). This was not due to a direct inhibition of prostaglandin formation, since HAL had no effect on SA-induced platelet aggregation or MDA production. Aspirin (4 mM), on the other hand, produced a marked inhibition of MDA production and of platelet aggregation after stimulation with SA. We conclude that HAL works to inhibit some step in the platelet reaction prior to the appearance of free arachidonic acid.
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PMID:The action of halofenate on platelet shape change and prostaglandin synthesis. 65 64

PCA was measured for human PRP by determining recalcification times assayed in a minimal-dilution, controlled PH/PCO2 system in a siliconized cuvette, with the use of light transmission measurements (aggregometry). Platelet shape, aggregation, and plasma clotting end points were assayed photometrically, with platelet morphology and aggregation studied in parallel by light microscopy. With varying concentrations of ADP preincubated with PRP initially containing essentially disc-shaped platelets, it was found that induced shape change in the absence of an aggregation is necessary and sufficient for the development of PCA. This was consistently measurable as a shortening of recalcification times by approximately 50% for suspensions of shape-changed platelets vs. disc-shaped platelets. The pharmacologic inhibition of the endoperoxide pathway-mediated platelet secondary aggregation and release by aspirin administered in vivo does not impair the ability of human platelets to develop this PCA. Inhibition of shape change with amounts of 5'-adenosine monophosphate insufficient to affect coagulation tests in the absence of platelets leads to 80% to 90% inhibition of the ADP-induced PCA. This PCA is shown to be fully reversible, with morphologic reversion of shape-changed platelets to the discoid form, and is shown to be distinct from other PCAs previously described for platelets activated in different ways, such as PF3 activity. It is suggested that the binding of coagulation factors to the platelet membrane may be regulated concomitantly with shape change.
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PMID:A platelet procoagulant activity associated with platelet shape change. 68 25

We have evaluated the effect on the response of citrated platelet-rich plasma to aggregating agents of storage at 4 degrees C versus room temperature (21 degrees C) for 2 and 4 h after venipuncture. While there were small decreases in some responses to epinephrine, ADP and collagen attributable to 21 degrees C storage, only in the case of ristocetin-induced aggregation was a profound difference noted. Platelets stored at 4 degrees C for 4 h showed no significant change in response to ristocetin. In contrast, those stored at room temperature showed a marked decrease. This change is not likely to be attributable to a change of pH, although pH rose less with storage at 4 degrees C than at 21 degrees C. It is recommended that PRP for in vitro testing be stored at 4 degrees C.
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PMID:Effect of temperature on short-term preservation of platelets for in vitro tests. 72 Sep 58

Studies with interference contrast microscopy reveal that platelets undergo a typical shape change within 30--60' after venepuncture, i.e. swelling, formation of large tentacles, tiny protrusions and vesicles at the platelet surface. This "shape change" can be observed in citrated blood and PRP, heparinized blood and EDTA-blood as well. It is enhanced by low incubation temperatures (4 degrees C, 10 degrees C) and delayed at 37 degrees C as compared with room temperature. An increased number of primarily shape changed platelets is found if platelets are strongly mechanically irritated at blood sampling. The shape change is partly reversible in vitro, it is completely or almost completely reversible in vivo. Some antiaggregating agents inhibit the in vitro shape change at varying degrees (Bencyclan, SH 869 greater than ASA greater than D-Propranolol). The shape change is partly inhibited after oral or i.v. administration of ASA. A typical transformation of platelets into "spheric" forms can be observed following the addition of Bencyclan, SH 869 and D-Propranolol to PRP in vitro. The spontaneous "primary shape change" which occurs in PRP or blood after blood sampling is probably different from the secondary ADP-induced shape change. The primary shape change may influence the results of different platelet function and aggregating tests. The shape change kinetics of "healthy" subjects and patients with Hodgkin's disease differ significantly. The described method may gain more clinical interest in the future.
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PMID:[Primary shape change of platelets in vitro (author's transl)]. 72 25

Geometries of platelets in citrated PRP obtained from normal donors (17) and donors (5) with a hereditary dominant giant platelet syndrome, herein referred to as "Montreal platelet syndrome" (MPS), are compared. The measured geometric axial ratio (rp = thickness/diameter) is used to classify platelet morphologies into three groups: discocytes (rp less than 0.5), disco-echinocytes (rp = 0.5 to 0.9), sphero-echinocytes (rp greater than 0.9). MPS discocytes are normal sized; however, MPS sphero-echinocytes and disco-echinocytes have mean volumes approximately two times larger than normal. It is demonstrated that these larger-than-normal sized MPS platelets can be produced directly from MPS discocytes by treatment with agents known to induce platelet shape change (adenosine diphosphate, thrombin, and incubation at 4 degrees C). Treatment of platelets obtained from normal donors which have been resuspended in MPS PPP and ADP or incubation at 4 degrees C causes the formation of normal-sized disco-echinocytes and sphero-echinocytes. The diameters of MPS disco-echinocytes are identical to the diameters of MPS platelets observed on peripheral blood smear, whereas those of MPS sphero-echinocytes are approximately 20% lower. It is suggested that the appearance of abnormally large platelets in MPS is related to a defect in the mechanism which regulates platelet size and shape during shape change.
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PMID:Shape-changing agents produce abnormally large platelets in a hereditary "giant platelets syndrome (MPS)". 75 24

We have determined the minimal concentrations of 4 aggregating agents that were required to cause a 65-75% increase in light transmission without disaggregation during the 5-min recording period in PRP samples of 14 neonates and 10 adults. We found, for example, that this degree of aggregation could be elicited in adult PRP by a mean value of 2.09 micronM ADP, whereas similar aggregation of neonatal PRP required 5.16 micronM ADP. Based on these figures, we observed that adult PRP was about 2.5 times more sensitive to ADP, at least 10 times to epinephrine and 2.3 times to collagen than neonatal PRP. However, neonatal PRP was approximately 20% more sensitive to ristocetin than adult PRP. By using concentrations of aggregating agents that caused comparable aggregation of neonatal and adult PRP, we noted comparable inhibition of aggregation in these samples by aspirin. While neonatal PRP was less sensitive than adult PRP to physiological aggregating agents, there was no evidence that the former was more susceptible to in vitro aspirin inhibition.
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PMID:Comparable inhibition of aggregation of PRP of neonates and adults by aspirin. 86 93

When gel filtration is used to transfer platelets from plasma into an established environment, alterations in platelet characteristics may result from the change in environment or from the effects of platelet contact with the gel matrix. To approach the problem of evaluating the relative contributions from these sources, a Sepharose 2B matrix was employed and platelets transferred from citrate anticoagulated PRP into autologous PPP to yield plasma-GFP. Platelet recoveries averaged 93%. PRP: plasma-GFP pairs were found to be indistinguishable with respect to: morphology; ADP, thrombin or collagen-induced aggregation response; uptake of 5-hydroxytryptamine (5-HT) or adenosine; and thrombin or collagen-induced release of accumulated 5-HT or adenosine. Pairs are distinguishable by prostaglandin E2 synthesis assayed immediately after filtration.
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PMID:Effects of matrix contact during gel filtration of human platelets in plasma. 103 35

C-PRP clotted by reptilase does not retract due to the lack of activation of platelets. In order to support retraction, the platelets must undergo membrane changes resulting in contractile system activation. Only in the presence of aggregating agents capable of eliciting these membrane changes in vitro (e.g. ADP, adrenaline and collagen but not bovine fibrinogen or ristocetin), strong reptilase clot retraction (RCR) occurs. During RCR an aggregating activity, platelet factor 4, and retraction stimulating factor (RSF) were released, but acid phosphatase was not available. Not only inhibitors of platelet adhesion-aggregation reaction (PAAR) but also specific blockers of release are capable of inhibiting RCR. In coagulation disorders RCR was normal in most cases, but in thrombopathies different abnormalities of RCR were found. The RCR defect may be associated not only with a defect in the initial stages of PAAR, but in some instances also with a specific defect in release reaction. Besides inducer--"activated" platelets and their adhesion to polymerizing fibrin, the presence of divalent cations and free thrombocytar--SH groups is necessary for the retraction of reptilase clots.
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PMID:Reptilase clot retraction test. (Its cofactors and relation to other platelet functions). 109 91

Platelets from nine patients with storage pool disease (SPD) and from ten control subjects were isolated by gel filtration into a suspension medium permitting the direct determination of platelet Mg-2+, Ca-2+, and K+ levels. The total intracellular levels of ATP and ADP, as well as the incorporation patterns of 14-C-adenine into the metabolic nucleotide pool, were also determined in these platelet suspensions. The gel-filtered platelets (GFP) from SPD patients exhibited slightly lowered levels of ATP and substantially reduced amounts of ADP, in agreement with previous studies using PRP suspensions. Diminished aggregation responses to ADP, epinephrine, and to collagen in particular, similar to those observed previously in PRP, were obtained in GFP from SPD patients. However, GFP from the patients exhibited more variable aggregation responses to addition of ADP and epinephrine than did GFP from the control subjects. Increases in the extent of radioactive hypoxanthine formation, observed previously in normal platelets as a result of isolation into the suspension medium used in these studies, were significantly reduced in the GFP from SPD patients. The levels of platelet Mg-2+ and K+ determined in GFP from the patients were not significantly different from the levels of these ions in GFP from control subjects. However, substantial reductions in platelet Ca-2+ were found in the SPD platelets. A strong correlation was obtained between this reduction in platelet Ca-2+ and the reduction in ADP in these platelets. No such correlation was apparent between the ATP and Ca-2+ deficiencies. These results suggest that a major portion of platelet Ca-2+ may be located in the dense granules and support previous hypotheses that granular ADP and/or Ca-2+ may play a role in the release reaction. The finding of normal levels of platelet Mg-2+ and K+ in SPD platelets, however, suggests that these latter ions are not located in the dense granules.
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PMID:Metal ion contents of gel-filtered platelets from patients with storage pool disease. 113 23


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