Platelet Size in Stroke Patients

O’Malley, Tom; Langhorne, Peter; Elton, R. A.; Stewart, Carolyn

doi:10.1161/01.str.26.6.995

Cited by 216 publications

(175 citation statements)

References 33 publications

Supporting

Mentioning

140

Contrasting

Unclassified

Order By: Relevance

“…It has been shown that epinephrine can increase platelet volume, 11 and platelets isolated from individuals with a history of stroke are indeed larger than those platelets found in patients with no history of stroke. 12 In addition, the interrelationship of intraplatelet chloride and calcium remains to be determined. We found that epinephrine-dependent increases in [Cl -] i relied on the presence of calcium in the extracellular buffers.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Epinephrine-Induced Platelet Aggregation

et al. 1998

View full text Add to dashboard Cite

Abstract-We report that a genetic polymorphism of the ␣ 2 -adrenergic receptor (A2AR) encoded by chromosome 10 is associated with hypertension and an increase in epinephrine-mediated platelet aggregation in humans. The mechanism responsible for this heritable contrast in sensitivity to epinephrine is unknown. We tested our hypothesis that epinephrine-induced platelet aggregation is mediated by activation of chloride transport. We measured epinephrinemediated increases in optical density of gel-filtered platelets suspended in a bicarbonate-buffered physiological salt solution.Compared with platelets incubated in the control buffer (130 mmol/L NaCl), platelets incubated with either bumetanide, a Na/K/2Cl cotransport inhibitor; anthracene-9-carboxylic acid, a chloride channel blocker; or acetazolamide, an agent that blocks ATP-dependent chloride transport had significantly decreased aggregation responses to epinephrine. When measured fluorometrically, epinephrine significantly increased intraplatelet chloride concentrations. Chloride-dependent modifications of epinephrine-induced platelet aggregation were not attributable to changes in A2AR ligand binding characteristics or to the concentration of platelet cAMP. Finally, subthreshold concentrations of epinephrine also potentiated thrombin-induced platelet aggregation, and blockade of chloride transport diminished this synergistic action of epinephrine on thrombin-stimulated platelet aggregation. Heritable differences in epinephrine-mediated platelet aggregation may be attributable to genetic differences in chloride transport in platelets. Furthermore, because we observed a necessary role for chloride transport in epinephrine-mediated platelet aggregation, pharmacological agents that block chloride transport, such as diuretics, may provide salutary protection against vascular thrombosis in patients with hypertension independent of the effect of these drugs on blood pressure. (Hypertension. 1998;31:603-607.)Key Words: adrenergic receptor Ⅲ diuretics Ⅲ thrombosis Ⅲ chloride Ⅲ humans Ⅲ polymorphism Ⅲ blacks Ⅲ genetics T he mechanism by which epinephrine induces platelet aggregation is unknown. In some tissues, such as the respiratory epithelium, activation of the A2AR increases transcellular sodium and chloride cotransport. 1 We reasoned that epinephrine-induced platelet aggregation could also be mediated by A2AR-dependent sodium and chloride cotransport. Accordingly, we tested our hypothesis by measuring epinephrine-mediated platelet aggregation under experimental conditions that would inhibit A2AR-mediated sodium chloride transport, and we measured epinephrine-mediated changes in intracellular chloride concentrations fluorometrically in platelets. Because platelet aggregation may also be dependent on A2AR-mediated changes in the accumulation of intracellular cAMP, we determined the effect of chloride transport inhibition on postreceptor signal transduction by cAMP. Methods Subject RecruitmentWe recruited healthy, fasting, male and female college-age subjects who were...

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanism of Epinephrine-Induced Platelet Aggregation

et al. 1998

View full text Add to dashboard Cite

show abstract

“…[17][18][19] It's a new emerging risk factor for atherosclerosis. 20 Patient with larger platelets can be easily identified during routine hematological analysis and could possibly benefit from the treatment for predicting the possibility of impending acute events.…”

Section: Introductionmentioning

confidence: 99%

A study to find correlation of platelet indices with HbA1c in diabetic patients with absence/presence of vascular complications

2017

View full text Add to dashboard Cite

Background: Diabetes Mellitus is a global pandemic disease. The increased platelet activity is emphasized to play a role in the development of vascular complications of the metabolic disorder. Mean platelet volume (MPV) is an indicator of average size and activity of platelets. This study was conducted to find correlation of platelet indices with HbA1c in diabetic patients with absence/presence of vascular complications.Methods: Total of 100 subjects was enrolled in the study. Sample for glucose estimation and platelet indices were collected and estimation were carried out by the auto-analyzers. The statistical evaluation is done using SPSS version 22. Student t- test was used for doing comparison between two variables namely HbA1c <7 and HbA1c ≥7 and diabetics with vascular complications v/s without vascular complications.Results: MPV, is significantly higher in patients with type -2 diabetes mellitus with HbA1C ≥7 and those with vascular complications in comparison to patients having HbA1c <7 and those without vascular complications ( p- value <0.001 which is highly significant).Conclusions: MPV might be used as a simple and cost-effective laboratory test in the follow up of diabetes mellitus along with HbA1c and thereby help to reduce the morbidity and mortality.

show abstract

“…Moreover, several groups showed that, compared with age-matched healthy controls, platelets of stroke patients show morphologic and metabolic alterations (Joseph et al, 1988(Joseph et al, , 1989O'Malley et al, 1995) likely linked to energy exhaustion.…”

Section: Introductionmentioning

confidence: 99%

Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Aliprandi

Longoni

Stanzani

et al. 2005

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Experimental studies have shown the role of excitotoxicity in the pathogenesis of ischemic brain lesions, and glutamate levels have been found to be elevated in CSF and plasma from patients, early after stroke. In this study, we investigated whether platelets could be involved in the mechanism of altered plasma glutamate levels after stroke. Forty four patients, from 6 hours to 9 months after ischemic stroke, 15 age-related healthy controls and 15 controls with stroke risk factors or previous transient ischemic attack were enrolled. Glutamate plasma levels, platelet glutamate release after aggregation and platelet glutamate uptake were assessed. Plasma glutamate levels were increased up to 15 days after the ischemic event in stroke patients, and the levels at day 3 were inversely correlated with the neurologic improvement between day 3 and 15. Ex vivo platelet glutamate release was decreased by 70% in stroke patients, suggesting previous in vivo platelet activation. Moreover, platelet glutamate uptake in these patients was decreased by 75% up to 15 days and was still reduced 90 days after stroke. Our data show a prolonged increase of glutamate in plasma after stroke, which might presumably be linked to altered platelet functions, such as excessive release of the amino acid or impaired uptake.

show abstract

Platelet Size in Stroke Patients

Cited by 216 publications

References 33 publications

Mechanism of Epinephrine-Induced Platelet Aggregation

Mechanism of Epinephrine-Induced Platelet Aggregation

A study to find correlation of platelet indices with HbA1c in diabetic patients with absence/presence of vascular complications

Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Contact Info

Product

Resources

About