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At least 37 records · Page 2Linked to original sources
PubMed1975

The effect of ADP, calcium and some inhibitors of platelet aggregation on protein phosphokinases from human blood platelets.

A protein phosphokinase (ATP: protein phosphotransferase EC 2.7.1.37) which is stimulated by 3',5'-cyclic adenosine monophosphate (cyclic AMP) has been partially purified from both the cytoplasmic and membrane fractions of human platelets. The kinetics of both enzymes preparations are similar in respect to cyclic AMP, ATP, ADP and AMP. 5-10-minus 7 M cyclic AMP stimulated both preparations by approximately 100%. Both ADP and AMP at a concentration of 5-10-minus 5 M inhibited protein phosphokinase activity of the soluble and membrane preparation by between 50% and 70%. The response of the two enzyme preparations to calcium differed. 10 mM Ca-2+ inhibited soluble protein phosphokinase activity approximately 80% both in the presence and absence of 5-10 minus 7 M cyclic AMP whereas the same concentrations of Ca-2+ inhibited the membrane-bound enzyme by approximately 60% in the presence of 5-10-minus 7 M cyclic AMP and 40% in the absence of cyclic AMP. This observation may be of importance in understanding the mechanism of platelet aggregation.

Adenosine↗
PubMed1978

Ionophore A-23187- and thrombin-induced platelet aggregation: independence from cycloxygenase products.

Stimulation of platelets labeled with [14C]-arachidonate by ionophore A23187 or thrombin produces rapid degradation of specific membrane phospholipids. This is also reflected by the release of [14C]archidonate, which is immediately transformed into products of the cycloxygenase and lipoxygenase enzyme systems, and by increased labeling of phosphatidic acid. Arachidonate metabolism can be effectively prevented by preincubation with indomethacin and eicosatetraynoic acid, but platelet aggregation induced by ionophore A23187 or trombin is not blocked under these conditions. Nevertheless, in the virtually total absence of metabolism of arachidonate, platelet aggregation still occurs concomitantly with phospholipid breakdown and with increased labeling of phosphatidic acid. Increased levels of cyclic AMP block both phospholipase activation and aggregation induced by ionophore A23187 and trombin. These data suggest that some early consequence of phospholipase activation, independent of a metabolic product of arachidonate but possibly related to the production of phosphatidic acid, may play a central, causative role in mediating platelet aggregation.

Animals↗
PubMed1978

Prostaglandin E1 inhibitis platelet aggregation by a pathway independent of adenosine 3',5'-monophosphate.

Aggregation of human blood platelets induced by adenosine diphosphate or 1-epinephrine was inhibited when the platelets were suspended in plasma which had been previously exposed to an insolubilized omega-aminohexylagarose derivative of prostaglandin E1. This decrease of platelet aggregation was not accompanied by a change in the concentration of adenosine 3',5'-monophosphate (cyclic AMP) in platelets. The results demonstrate the existence of an alternative pathway independent of cyclic AMP for the inhibition of platelet aggregation by plasma.

Adenosine Diphosphate↗
PubMed1979

Effect of vitamin E on platelet aggregation in diabetic retinopathy.

The effect of vitamin E on platelet aggregation was investigated in a group of 10 patients with diabetic retinopathy. Adenosine diphosphate induced platelet aggregation was inhibited in the patients' group as well as in the controls in the presence of vitamin E. An increased platelet aggregation was obtained with arachidonic acid in both groups when platelet-rich plasma was incubated prior with vitamin E. The clot retraction inhibition test parallels the findings of aggregation obtained with the platelet aggregation meter.

Adenosine Diphosphate↗
PubMed1979

Effect of a single oral dose of aspirin on the platelet aggregation response to arachidonic acid.

1 The platelet aggregation response to arachidonic acid ex vivo was measured in six volunteers daily before and for 10 days after a single oral dose of 600 mg aspirin. 2 Arachidonic acid induced aggregation of platelets from all subjects before aspirin and aggregation occurred after an interval which varied inversely with the concentration of arachidonic acid. No aggregation occurred for 4 days after aspirin; a reduced response, compared with pre-aspirin values, was obtained on the 5th, 6th and 8th day. The values on days 7, 9 and 10 were not consistently different from the pre-aspirin values. In 6 subjects 24 h after aspirin ingestion the addition of 10--25% v/v normal platelets restored the aggregation response. 3 It is concluded that aspirin has an effect on the platelet precursors in the marrow in addition to its effect on circulating platelets.

Adult↗
PubMed1976

The pH dependence of quantitative ristocetin-induced platelet aggregation: theoretical and practical implications-a new device for maintenance of platelet-rich plasma pH.

Quantitative ristocetin-induced platelet aggregation of normal platelet-rich plasma (PRP) decreased with time after PRP preparation. An increase in p H of the PRP with time proved to be responsible for this finding. Diffusion of CO2from the plasma is the prime determinant of the change in pH. Since a complex combination of factors influences CO2 diffusion (surface area-to-volume relationship, capping, mixing, etc.) The change in pH is variable with time. Thus, quantitative ristocetin aggregation should be pH controlled. A simple device for maintaining PRP pH constant by control of the ambient pCO2 was designed and found effective in keeping both pH and quantitative ristocetin aggregation constant over a prolonged period of time. It can be adapted for use in platelet aggregation studies employing other reagents. The pH dependence of ristocetin-induced platelet aggregation is consistent with other data supporting an elctrostatic interaction between the platelet, von Willebrand factor, and ristocetin. We favor a model wherein ristocetin neutralizes some of the platelet's negative change and permits the von Willebrand factor to bridge sites on separate platelets to induce agglutination.

Blood Coagulation Tests↗
PubMed1979

Spontaneous platelet aggregation in cerebrovascular disease II. Further characterisation of the platelet defect.

A group of 186 patients with Transient Ischaemic Attacks (TIA) or cerebral infarction (CI) was found to demonstrate in vitro Spontaneous Platelet Aggregation (SPA) in 39% of those studied. Of the 176 normal subjects studied the incidence on in vitro SPA was found to be 5%. Further investigation of the phenomenon of SPA revealed that: 1. it is associated with ADP-hyperaggregability, i. e. the threshold concentration to induce second wave aggregation is decreased; 2. it is dependant on the increase in pH which occurs in platelet-rich plasma stirring in an aggregometer while concurrent ADP-hyperaggregability is independant of this change in pH; 3. it is associated with malondialdehyde production and the release of endogenous 5-hydroxytryptamine; and that 4. in addition Km and Vmax values for [14c]-5HT incorporation are normal; and that 5. no gross abnormalities of the platelet membrane glycoproteins were apparent although occasionally glycoprotein III was found to be increased. This study demonstrates abnormal platelet behaviour in patients with TIA and CI where the enzyme system involved in thromboxane production is sufficiently stimulated, by stirring alone, to induce aggregation of platelets and the release reaction. Acetylsalicylic acid abolishes SPA and prolongs the bleeding time with similar characteristics as has been described for normal individuals. Plasma beta-thromboglobulin levels are significantly increased in the patients studied. However, no correlation was established with the incidence of in vitro SPA.

Adenosine Diphosphate↗
PubMed1976

Ultrastructure of platelet aggregation in refractory anemia and myelomonocytic leukemia. II. Individual platelet abnormalities: thrombasthenia-like platelets, surface defects, and dissociation phenomena.

Studies of in vitro platelet aggregation were done in five patients with refractory anemia and two with acute myelomonocytic leukemia. The macroscopic results as well as the general ultrastructural findings were reviewed in a companion paper. Electron microscopic analysis of changes in the individual platelets within aggregates revealed a striking heterogeneity, both in the degree of response of each platelet are in the ultrastructural characteristics of the platelet population. Many of the unaggregated platelets had reacted individually, resembling the platelets of patients with Glanzmann's thrombasthenia. There were other abnormalities suggesting the presence of surface defects, such as the presence of areas of obliteration of the interplatelet space (so-called tight connections). One of the most striking findings was a peculiar dissociation between the different components of the aggregation sequence.

Anemia, Aplastic↗
PubMed1979

Inhibition of platelet aggregation during hypovolemic hypotension by acetylsalicylic acid and artificial respiration.

In vivo measurement of platelet aggregation was performed by a previously described photoelectric method. It is shown that platelet aggregation induced by arterial hypotension can be inhibited by i.v. administration of ASA and by artificial respiration. The inhibition of platelet aggregation following artificial ventilation is significantly more pronounced than by ASA given 24 h prior to the beginning of the experiments. Different sources of platelet aggregation in venous and arterial blood are informative about the canine lung not only as a filter for aggregates but also as a source of aggregating substances.

Adenosine Diphosphate↗
PubMed1975

Platelets fixed with paraformaldehyde: a new reagent for assay of von Willebrand factor and platelet aggregating factor.

Present methods for assay of platelet aggregating agents use freshly prepared platelets. Much time is spent in daily preparation of platelets and standardization presents problems. The preparation of fixed washed platelets (FWP) and their use in two bioassays are described in this report. Washed human platelets were fixed for 48 hours with 4 per cent paraformaldehyde, washed twice in phosphate buffer, pH 6.4, and stored at 4 degrees C. Aggregation of FWP was studied with a macroscopic test and a light absorbance measurement. FWP did not aggregate with adenosine diphosphate, collagen, adrenalin, and thrombin. FWP aggregated with bovine or porcine plasma, poly-L-lysine, and ristocetin with normal human plasma but not with von Willebrand's disease plasma. These observations confirm the direct aggregating effect of these agents. Macroscopic aggregation times were dependent on the amount of aggregating agent (bovine plasma, normal human plasma). A quantitative assay for bovine platelet aggregating factor (PAF) and von Willebrand factor (vWF) with FWP was developed. The ability of FWP to aggregate remained unchanged after 1 month of storage at 4 degrees C. Ristocetin alone caused a decrease in light transmission of FWP suspensions, depending upon the concentration of ristocetin, but did not cause aggregation. FWP constitute a stable reagent suitable for quantitative measurement of PAF and vWF.

Animals↗
PubMed1978

Some observations on the in vivo effect of propranolol on platelet aggregation and release.

Platelet function was investigated in four normal volunteers, one patient with a mild form of von Willebrand disease, and one with a thrombocytopathy, all taking propranolol. No effect on platelet function attributable to this drug could be demonstrated in any of these subjects. It is suggested that propranolol administered in conventional doses does not impair platelet hemostatic function.

Adult↗
PubMed1976

C1 and human platelets. III. Role of C1 subcomponents in platelet aggregation induced by aggregated IgG.

Studies have been performed with platelets using C1 haemolytic assays and platelet aggregation induced by anti-C1q, anti-C1s and aggregated IgG in the presence of C1 subcomponents C1q, C1r and C1s. C1q was removed by EDTA or modified by collagenase from human platelets while after the same treatment C1s remained bound to the platelets. EDTA treated platelets were no longer aggregated by aggregated IgG. The addition of C1q restored the reactivity of the platelets to aggregated IgG while the addition of C1r or C1s was without effect. Furthermore, the addition of C1r or C1s to C1q inhibited the action of C1q in platelet aggregation induced by IgG.The possible association between the different C1 subcomponents and human platelets is discussed.

Complement C1↗
PubMed1978

Effect of acid and pepsin on blood coagulation and platelet aggregation. A possible contributor prolonged gastroduodenal mucosal hemorrhage.

In a series of in vitro studies, both the soluble (plasmatic) coagulation system and the cellular (platelet-mediated) aspect of coagulation were shown to be extremely sensitive to relatively minor increases in hydrogen ion concentration. All studies became abnormal at pH 6.8. At pH 6.4, assays of the intrinsic and extrinsic coaglution systems, the polymerization of fibrinogen, and assay of the availability of platelet phospholipid (platelet factor 3) were twice prolonged over control values. Platelet aggregation was reduced by more than 50%. At pH 5.4 in vitro, platelet aggregation and plasma coagulation were both virtually abolished. Furthermore, previously formed platelet aggregates disaggregated at a slightly acid pH. Pepsin further enhanced platelet disaggregation. Because gastric acidity is normally two to four orders of magnitude greater than that which abolishes platelet aggregation and plasma clotting in vitro, and pepsin is present in abundance, we call attention to the probable antihemostatic effect of hydrocloric acid and pepsin in the upper gastrointestinal tract. This in vitro study may provide a rationale for meticulous regulation of intragastric pH in an effort to control upper gastrointestinal hemorrhage.

Blood Coagulation↗
PubMed1978

Venom coagglutinin: an activator of platelet aggregation dependent on von Willebrand factor.

A platelet-aggregating activity was found in many snake venoms, predominantly those of the genus Bothrops, that is apparent only in the presence of the platelet-aggregating von Willebrand factor of plasma. It is designated "venom coagglutinin." The coagglutinin can be largely separated from the thrombin-like enzyme of the venoms by ion-exchange chromatography. The venom factor acts on formaldehyde-fixed platelets and is effective with decalcified, heparinized, and afibrinogenemic plasmas but not with severe von Willebrand disease plasmas or with normal plasmas in which the von Willebrand factor has been neutralized by specific antibodies. Use of this coagglutinin permits the assay of von Willebrand factor without the many disadvantages of the ristocetin test. The coagglutinin is active with human, dog, pig, and bovine plasmas and with platelets of any one of these species. This broad-spectrum activity without regard to species contrasts with the ristocetin-resistance of many combinations of plasma and platelets from various species. The assay provides a procedure for studying human, porcine, and canine von Willebrand disease. The lack of species specificity of the coagglutinin suggests that it may be a universal activator of the von Willebrand factor-platelet reaction.

Animals↗
PubMed1977

Human platelet aggregation induced by prostaglandin endodisulfide.

The effect on human platelet functions of 9,11-dithio analogues of prostaglandin endoperoxide was investigated. Methyl (5Z, 9alpha, 11alpha, 13E, 15S)-9,11-epidithio-15-hydroxyprosta-5,13-dienoate induced platelet aggregation, while the 9beta,11beta-epimer was inactive. The platelet aggregation caused by the 9alpha,11alpha-dithio analogue was associated with serotonin release from platelets, and was inhibited by methyl ester of prostaglandin I2 (prostacyclin) but not by indomethacin.

Blood Platelets↗
PubMed1978

Burro aortic collagen: platelet aggregating activity and ultrastructural changes induced by plasma.

A fibrillar collagen molecule was extracted from the upper thoracic aorta of an old burro (Equus asinus). Presence of the collagen in the extract was determined by amino acid analysis, scanning and transmission electron microscopy, incubation with collagenase, and assays of its platelet-aggregating capacity by "aggregometry". Based on the amino acid rations of proline/hydroxyproline and lysine/hydroxylysine, the collagenous protein most nearly resembles type I of 4 main published types of collagen. Quantitative assays of the collagen as a mediator of platelet aggregation showed human platelets more sensitive and sheep platelets slightly less sensitive than burro platelets. Incubation with collagenase abolished platelet aggregation capacity and converted the fibrillar collagen to a gel-like mass. Incubation with galactose oxidase neither lessened nor intensified the collagen-mediated platelet aggregation. Incubation with burro plasma decreased platelet aggregating activity and changed the collagen ultrastructure (demonstrated with scanning electron microscopic imaging). The significance of a naturally occurring plasma (protein) factor(s) which may have a regulatory role in reducing the chemical activity of the fibrillar collagen molecule with platelets is also discussed.

Animals↗