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)

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

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

A comparison is made between the shape of human platelets obtained from nine normal donors and two BSS donors. Sizes are evaluated from a cinematographic analysis of freely rotating, unfixed, and glutaraldehyde-hardened platelets in citrated PRP and of platelets on blood smear. On blood smeae, the mean diameters of BSS platelets are 1.7 to 1.8 times larger than those of normal platelets, with a major fraction having a diameter greater than 2.5 micrometer. As for normal donors, 80% to 90% BSS platelets in PRP are in the disc form (discocyte). In addition, they are essentially indistinguishable from a normal discocyte. Echinocytes (spherical forms with pseudopods) for BSS have a main body diameter (i.e., excluding pseudopods) 1.6 times larger than normal and in addition a reduced number of pseudopods. The results demonstrate that the giant size of BSS platelets results from abnormal behavior of these platelets during the preparation of the blood smear. It is suggested that this disorder is associated with a defect in the mechanism of platelet shape change.
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PMID:Platelets from "giant platelet syndrome (BSS)" are discocytes and normal sized. 61 83

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

The results presented in the paper showed that PRP increased permeability of skin vessels in guinea pigs and that PRP stimulates or suppresses the immunological response in mice, depending on the magnitude of the response.
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PMID:Immunological activity of a proline-rich polypeptide from ovine colostrum. 74 75

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

Sulfinpyrazone added to PRP inhibited the release of serotonin induced by collagen. The inhibitory effect depended strongly on the strength of the collagen stimulus. Serotonin release was also inhibited (up to 73%) in PRP prepared from subjects who had ingested the drug. This is the first demonstration of a direct effect of a sulfinpyrazone in vivo on in vitro tests of platelet function. Prostaglandin synthesis was studied with lysates of washed platelets, arachidonic acid-14C, and silicic acid chromatography to isolate a reaction product which was tentatively identified as thromboxane B2. Platelet prostaglandin synthesis was shown to be strongly inhibited by sulfinpyrazone. Inhibition was competitive with respect to substrate. It is proposed that effects of sulfinpyrazone on platelet function may be due to inhibition of prostaglandin synthesis. The competitive nature of sulfinpyrazone inhibition may explain why sulfinpyrazone is a strong inhibitor of the release reaction under conditions of dilute collagent stimulation but is weak in the presence of stronger stimuli. In comparing the potency of inhibitors of platelet prostaglandin synthesis the nature of inhibition must be considered. Competitive inhibitors may be incorrectly regarded as weak if studied only at high substrate concentration.
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PMID:Effects of sulfinpyrazone on platelet prostaglandin synthesis and platelet release of serotonin. 84 86


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