Acute development of collateral circulation and therapeutic prospects in ischemic stroke - PubMed (original) (raw)

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Acute development of collateral circulation and therapeutic prospects in ischemic stroke

Eri Iwasawa et al. Neural Regen Res. 2016 Mar.

Abstract

In acute ischemic stroke, collateral circulation plays an important role in maintaining blood flow to the tissue that is at risk of progressing into ischemia, and in increasing the successful recanalization rate without hemorrhagic transformation. We have reported that well-developed collateral circulation is associated with smaller infarct volume and better long-term neurological outcome, and it disappears promptly once the effective recanalization is achieved. Contrary to the belief that collateral vessels develop over time in chronic stenotic condition, there exists a phenomenon that collateral circulation develops immediately in acute stenosis or occlusion of the arteries and it seems to be triggered by fluid shear stress, which occurs between the territories of stenotic/occluded arteries and those fed by surrounding intact arteries. We believe that this acute development of collateral circulation is a target of novel therapeutics in ischemic stroke and refer our recent attempt in enhancing collateral circulation by modulating sphingosine-1-phosphate receptor 1, which is a known shear-stress mechanosensing protein.

Keywords: PCA laterality; S1PR1; collateral; hyperintensive vessels; ischemic stroke; leptomeningeal arteries; shear stress.

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Figures

Figure 1

Figure 1

A patient with occlusion of the right proximal middle cerebral artery. On magnetic resonance angiography, the right posterior cerebral artery (PCA) is 2 segments longer than the left PCA (arrow head); this presentation is defined as ‘PCA laterality’ (A). Hyperintensive vessels (HVs) are present along the cortex of the right middle cerebral artery perfusion territory, and are seen in 8 of 10 slices on fluid-attenuated inversion recovery magnetic resonance imaging (arrows) (B). After intravenous recombinant tissue plasminogen activator treatment, both PCA laterality (C) and HVs (D) disappeared.

Figure 2

Figure 2

Vessel occlusion increases fluid shear stress, consequently upregulating and activating sphingosine-1-phosphate receptor 1 (S1PR1) and leading to the growth of collateral vessels presumably through the phosphorylation of extracellular signal-regulated kinases (ERK), protein kinase B (Akt), and endothelial nitric oxide synthase (eNOS) activation.

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