Platelets and acute cerebral infarction

Abstract

Stroke is worldwide a leading cause of death and disability. Its etiology is regarded as heterogeneous. Platelets are implicated in its pathophysiology, but our understanding of their specific role is incomplete. Only sparse and conflicting information exists about platelet reactivity and activity in acute stroke. Some scientists take the view that platelets activate in conjunction with acute cerebral infarctions. Others put forward evidence corroborating the contrary notion. Increased soluble P-selectin as a sign of platelet and/or endothelial activity seems to be a feature of the disease. The latter point of view is opposed by other researchers. Due to these conflicting opinions, this study is devoted to platelet characteristics in acute cerebral infarctions. We studied subjects (n ¼ 72; age 74 AE 10(SD) years; 31 females) having acute stroke. As controls served atrial fibrillation (AF) patients (n ¼ 58; age 69 AE 7(SD) years; 12 females) subject to electrical cardioversion, a flow cytometer was put to use for measuring platelet reactivity and activity. After agonist provocation, both platelet bound P-selectin and fibrinogen were employed as estimates of platelet reactivity. Dilutions of a thrombin-receptor-activating peptide (TRAP-6) (74 and 57 mmol/l) (P-selectin and fibrinogen) and ADP (8.5 and 1.7 mmol/l) (fibrinogen only) were put to use as platelet agonists. Membrane-bound P-selectin without agonist stimulation served as a measure of in vivo platelet activation. Soluble P-selectin, as determined from a commercial ELISA, was used to assess platelet and/or endothelial activity. In acute stroke neither platelet-bound P-selectin nor fibrinogen after stimulation, i.e. reactivity, differed from AF controls. In contrast, lower platelet activity as judged from surface attached and circulating P-selectin without agonist stimulation proved to be a feature of cerebral infarctions. The p-values were p < 0.001 and p < 0.01, respectively. It is concluded that acute stroke is not associated with platelet reactivity platelets circulate less activated during the disease. It is evident that the mechanisms reflecting platelet reactivity and activity being investigated in this study play minor roles in stroke pathophysiology. New powerful platelet inhibitory drugs are currently introduced. To avoid major bleeding studies on platelet, behavior in acute stroke are necessary before including these medications in stroke treatment protocols.

Platelet count and mean volume in acute stroke: a systematic review and meta-analysis

“…Three studies showed that patients with AS had higher PC than controls [24,35,36]. Eleven studies demonstrated lower PC in the patient group [12][13][14]23,[25][26][27]30,32,35,43], and 11 studies found no difference in PC between patients and controls (Table I, Supplementary Table VI) [11,15,28,29,33,37,41,42,44,46,47]. One study did not provide PC results.…”

Neurobiology of microglial action in CNS injuries: Receptor-mediated signaling mechanisms and functional roles

“…Our understanding of the roles of selectins in various neurological disorders lies in its infancy. In stroke, E-and P-selectin have been shown to affect platelet and endothelial activities (Beer et al, 2011;Jaremo et al, 2012), which in turn modulate inflammatory responses and degeneration (Ma et al, 2012). Interestingly, polymorphisms in L-selectin appear to increase the risk of stroke (Wei et al, 2011).…”

Very high-density platelets determine reactivity and activity of circulating platelets

“…Citrate anticoagulated whole blood was used for analysing reactivity and activity of all platelets and, to minimise deviations, due to sample aging the determinations were commenced approximately 2 hours after sampling. The number (%) of cells expressing P-selectin/ fibrinogen was visualised using a Beckman Coulter EPICS XL-MCL flow cytometer (Beckman Coulter, Inc., Brea, Cal, USA) [23], [24]. Platelets were identified with an antibody towards glycoprotein Ib.…”