Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage

So you described a problem. WHOM  is going to followup and provide solutions to prevent that problem? Specific names only.

Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage

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Ari Dienel, Peeyush Kumar T, Spiros L Blackburn, ...

First Published June 10, 2021 Review Article 

https://doi.org/10.1177/0271678X211020865

Article information

Abstract

Aneurysmal subarachnoid hemorrhage (aSAH) patients develop delayed cerebral ischemia and delayed deficits (DCI) within 2 weeks of aneurysm rupture at a rate of approximately 30%. DCI is a major contributor to morbidity and mortality after SAH. The cause of DCI is multi-factorial with contributions from microthrombi, blood vessel constriction, inflammation, and cortical spreading depolarizations. Platelets play central roles in hemostasis, inflammation, and vascular function. Within this review, we examine the potential roles of platelets in microthrombi formation, large artery vasospasm, microvessel constriction, inflammation, and cortical spreading depolarization. Evidence from experimental and clinical studies is provided to support the role(s) of platelets in each pathophysiology which contributes to DCI. The review concludes with a suggestion for future therapeutic targets to prevent DCI after aSAH.

Keywords Subarachnoid hemorrhage, aneurysm, delayed deficits, delayed cerebral ischemia, platelets

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Different Stages of Platelet Adhesion to the Site of Vascular Injury

See what this changes about your blood thinning from your doctor.
http://scholar.google.com/scholar_url?hl=en&q=http://www.ijbc.ir/browse.php%3Fa_id%3D349%26slc_lang%3Den%26sid%3D1%26ftxt%3D1&sa=X&scisig=AAGBfm1NSIJ29JuI8RU45NjsvCaS-cMqvg&oi=scholaralrt
Abstract
Platelet activation and adhesion to the site of vascular injury is a dynamic process comprising reversible and irreversible
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of neutrophils. This phenomenon is highly regulated and influenced by the cross-talk between platelets and injured
endothelium. This cross-talk involves a variety of mediators including adhesion molecules and receptors, agonists,
chemokines, shed proteins and various proinflammatory lipids.
This review briefly discuses the main adhesion molecules and receptors involved in both reversible and irreversible
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http://www.ncbi.nlm.nih.gov/pubmed/22621230

Abstract

Activated platelets shed microparticles, which contain variety of growth factors central to angiogenesis and neurogenesis. The aim of this study was to explore whether platelet derived microparticles (PMP) can boost endogenous neural stem cells dependent repair mechanisms following stroke in a rat model. To examine the effects of PMP therapy in-vivo, we delivered PMP or vehicle via a biodegradable polymer to the brain surface after permanent middle cerebral artery occlusion (PMCAO) in rats. Rats were tested with the neurological severity score and infarct volumes were measured at 90 days post-ischemia. Immunohistochemistry was used to determine the fate of newborn cells and to count blood vessels in the ischemic brain. The results show that PMP led to a dose dependent increase in cell proliferation, neurogenesis and angiogenesis at the infarct boundary zone and significantly improved behavioral deficits.