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Results for “Platelet Function Tests”

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At least 1,261 records · Page 70Linked to original sources
PubMed1984

Thrombocytopathic purpura associated with eosinophilia.

An acquired bleeding syndrome associated with eosinophilia occurs in South-east Asia, mainly in children. Bleeding is known to result from impaired platelet function. This paper reports seven previously healthy young adults from Singapore who exhibited this syndrome. Bleeding was confined mainly to the skin and mucosal surfaces; no unusual clinical findings were noted. The bleeding tendency was transient. Intestinal helminths were found in four cases; five were mildly thrombocytopenic at onset. Platelet aggregation abnormalities were transient and the pattern suggested storage pool disease; this is discussed in relation to recent studies of the syndrome. The possible pathogenic role of eosinophilia and parasitism is also discussed.

Adult↗
PubMed1982

Kinetic analysis of alpha-granule secretion by platelets. A methodological report.

A method is described for the kinetic measurement of alpha-granule secretion by platelets. The method uses formaldehyde as a secretion-blocking reagent. This treatment alters the antigenecity of beta-thromboglobulin but not of Platelet Factor 4, both measured with commercially available reagents. Evidence is shown that this formaldehyde effect does not alter the secretion kinetics when the data are expressed as a percentage of a similarly treated reference sample. The method shows that following stimulation with thrombin or A 23187 alpha-granule secretion is much slower than dense granule secretion.

Blood Platelets↗
PubMed1982

Dosage frequency for suppression of platelet function by low dose aspirin therapy.

A study of platelet aggregation and MDA production after an oral dose of 300 mg aspirin indicated that partial recovery of platelet function occurred when approximately one third of the circulating platelets had been replaced by new (uninhibited) platelets. In vitro studies on mixtures of normal and aspirin inhibited platelets indicated partial restoration of platelet aggregation and thromboxane B2 production with as little as 10% of normal platelets in some subjects. Restoration of full function required a higher proportion of normal platelets. There was considerable variation between subjects. These data suggest that complete suppression of platelet functions in all normal subjects requires daily administration of the drug.

Adenosine Diphosphate↗
PubMed1983

Verapamil does not alter platelet function in patients with recent myocardial infarction.

Reports concerning the influence of the calcium antagonist verapamil on platelet function are conflicting. In a randomized double blind trial including 52 patients with acute myocardial infarction the effect of verapamil 120 mg given perorally three times a day for three months was investigated. There were no alterations in cutaneous bleeding time, platelet aggregate ratio or platelet aggregation induced by ADP or collagen. Verapamil administered in therapeutic doses does not seem to affect platelet function in patients with ischaemic heart disease.

Aged↗
PubMed1983

Warfarin-induced factor VII deficiency and the bleeding time.

The effect of warfarin-induced factor VII deficiency on the skin bleeding time was investigated in 10 consecutive patients with mean prothrombin times of 33 sec and factor VII levels of 7%. Bleeding times in all but one subject were entirely within the normal range. We conclude that warfarin administration, even to the point of prolonging the prothrombin time beyond the therapeutic range, is not associated with an abnormal bleeding time. Furthermore, from the above evidence and a review of the literature, it is considered doubtful that factor VII plays a major role in primary hemostasis.

Bleeding Time↗
PubMed1984

A pharmacokinetic and platelet function study of the combined administration of metoprolol and sulfinpyrazone to healthy volunteers.

In a double-blind study on healthy subjects who underwent three 3-week periods of treatment with metoprolol (M) + sulfinpyrazone (S), M + placebo, and S + placebo, pharmacokinetics and plasma levels of M were not affected by concurrent administration of S. Analysis of variance change-over demonstrated a significant difference between treatments only for serum uric acid levels. Analysis of post-treatment and baseline data within each treatment showed: decreased platelet count by M, lowered serum 6-keto PGF1 alpha by all three treatments, decreased serum TXB2 generation and arachidonic acid-induced platelet aggregation by S + M. No negative interaction between S + M was found.

Adult↗
PubMed1984

Purified -SH-activated toxins (streptolysin O, alveolysin): new tools for determination of platelet enzyme activities.

The purpose of this study was to examine the lytic effect on human platelet preparations (washed, gel-filtered and dextran-isolated) of two sulfhydryl-activated bacterial protein toxins, streptolysin 0 and and alveolysin, and to compare their efficacy with that of other disruptive procedures (freezing and thawing, ultrasonic, mechanical, or nystatin-toluene treatment) as a method for the determination of various platelet enzyme activities. The enzymes assayed were alkaline and acid phosphatases, monoamine oxidase, phenolsulfotransferase, N-acetyltransferase, hydroxyindole-O-methyltransferase, glutathione peroxidase and lactate dehydrogenase. In all cases, the lowest activities were found after freezing and thawing and/or ultrasonic disruption. The highest activities were always observed in the platelet lysates obtained after toxin, and in some instances after nystatin-toluene treatment. Intermediate values were obtained for mechanical disruption. The -SH-activated cytolysins thus appear to be appropriate and gentle tools for the assay of platelet enzymes when compared to the physical or chemical procedures generally employed.

Bacterial Proteins↗
PubMed1986

Defective contact activation of platelets from dogs with basset hound hereditary thrombopathy.

Basset Hound Hereditary Thrombopathy (BHT) is an autosomally inherited disorder of platelet function characterized by a thrombasthenia-like defect in aggregation but normal clot retraction. Glycoprotein IIb-IIIa (GP IIb-IIIa) is detectable in BHT platelets but may be functionally defective. In order to further characterize this potential model for human Glanzmann's thrombasthenia, contact reactivity of BHT platelets was studied by whole mount electron microscopy. Gel filtered BHT platelets, after 30 minutes of contact activation, attached poorly to a formvar substrate. There was an 8 fold difference in the number of adherent BHT platelets and normal platelets. In addition, contact induced shape change was inhibited when compared to control dogs. Almost 95% of control platelets reached fully dendritic or spread forms after 30 minutes of contact; in contrast only 63.7% of BHT platelets reached this degree of activation. The addition of 8.2 uM ADP to BHT platelets induced nearly a 4 fold increase in the number of spread forms and a 5 fold increase in the number of adherent BHT platelets, but did not cause aggregate formation. Both the defect in adhesion and shape change and the ability of ADP to stimulate both adhesion and contact-induced shape change in BHT platelets are similar to recent observations in our laboratory in patient's with type II Glanzmann's thrombasthenia.

Adenosine Diphosphate↗
PubMed1987

Effects of low doses of aspirin, 10 mg and 30 mg daily, on bleeding time, thromboxane production and 6-keto-PGF1 alpha excretion in healthy subjects.

To compare the long term effects of two low doses of aspirin taken daily, we performed a placebo-controlled cross-over study in 19 normal subjects. Aspirin 10 mg daily for 3 weeks caused a significant inhibition by 61 +/- 12 percent of platelet thromboxane B2 generation but had no effect on the Simplate bleeding time. Aspirin 30 mg daily for 3 weeks reduced thromboxane B2 production by 94 +/- 5 percent and caused a significant prolongation of the bleeding time, 1.6 times the control value. No cumulative inhibitory effects were observed after the first week of treatment. Both doses did not effect the urinary excretion of 6-keto-PGF1 alpha.

6-Ketoprostaglandin F1 alpha↗