The investigation of platelets in the thrombotic diatheses

O'Brien, J.R.; 博男, 山崎

doi:10.2491/jjsth1970.11.1

Cited by 5 publications

(4 citation statements)

References 5 publications

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“…This early absence of platelet hyperaggregability has not been observed in several other studies 4 ' 6 although O'Brien noted it and postulated that it could be due to an increased number of "empty exhausted platelets" which undergo release during thrombogenesis but continue to circulate for a normal time. 20 In confirmation of a previous report, 9 the plasma level of VIII:vWF was increased as well as the enhancement of RIPA, which requires VIII:vWF, in the patients with thrombotic CVD.…”

Section: Discussionsupporting

confidence: 85%

Platelet function tests in thrombotic cerebrovascular disorders.

Uchiyama¹,

Takeuchi²,

Ōsawa³

et al. 1983

Stroke

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A variety of platelet function tests were performed in patients with four forms of obstructive cerebrovascular disease (CVD); transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND), cerebral infarct, and cerebral embolism of cardiac source in rheumatic valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by ADP and ristocetin, spontaneous platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in acute stroke patients. The effect of aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic embolism and those with other forms of CVD. In patients with TIA, RIND, and cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to ADP and percent megathrombocytes developed slowly over a week following stroke. Induced and spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic embolism.

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Section: Discussionsupporting

confidence: 85%

Platelet function tests in thrombotic cerebrovascular disorders.

Uchiyama¹,

Takeuchi²,

Ōsawa³

et al. 1983

Stroke

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“…56 The lack of platelet hyperaggregability during the acute period has been ascribed to the consumption of active platelets during thrombogenesis. 5 Increased platelet activity has also been shown during the chronic period of stroke by measuring platelet aggregation 6 " 8 and platelet adhesiveness. 9 ' 10 In contrast, a trend toward a lower percentage sponFrom the Department of Neurology, Iwate Medical University, Morioka, Japan.…”

Section: Platelet Volume Aggregation and Adenosine Triphosphate Relmentioning

confidence: 99%

“…The decrease in whole blood platelet aggregation is not explained by the decrease in platelet count of approximately SxlOVmm 3 on average. 19 Nor is it ascribable to an increase in the number of "empty exhausted platelets" which have undergone release reaction during thrombogenesis 5 because the ATP release rate was significantly increased. Furthermore, we found that infarct size correlates positively with platelet aggregability during the acute period.…”

mentioning

confidence: 99%

Platelet volume, aggregation, and adenosine triphosphate release in cerebral thrombosis.

Tohgi

Suzuki

Tamura

et al. 1991

Stroke

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“…14 Previous studies have shown above-average levels of MPV among patients with acute stroke, myocardial infarction, and vascular risk factors such as diabetes mellitus (DM), hypercholesterolemia, and smoking 2,7,15-17 than in control subjects, whereas some studies observed no such effect. 18,19 Elevated MPV was found to be associated with a poor outcome, 1,11,20 whereas in some studies no significant relation between MPV and stroke outcome exist. 10,21 The significance of hematologic and biochemical parameters associated with spontaneous intracerebral hemorrhage (ICH) has not been studied extensively.…”

mentioning

confidence: 99%