Author:
Göb Vanessa,Voll Maximilian G.,Zimmermann Lena,Hemmen Katherina,Stoll Guido,Nieswandt Bernhard,Schuhmann Michael K.,Heinze Katrin G.,Stegner David
Abstract
AbstractIschemic stroke is among the leading causes of disability and death worldwide. In acute ischemic stroke, successful recanalization of occluded vessels is the primary therapeutic aim, but even if it is achieved, not all patients benefit. Although blockade of platelet aggregation did not prevent infarct progression, cerebral thrombosis as cause of secondary infarct growth has remained a matter of debate. As cerebral thrombi are frequently observed after experimental stroke, a thrombus-induced impairment of the brain microcirculation is considered to contribute to tissue damage. Here, we combine the model of transient middle cerebral artery occlusion (tMCAO) with light sheet fluorescence microscopy and immunohistochemistry of brain slices to investigate the kinetics of thrombus formation and infarct progression. Our data reveal that tissue damage already peaks after 8 h of reperfusion following 60 min MCAO, while cerebral thrombi are only observed at later time points. Thus, cerebral thrombosis is not causative for secondary infarct growth during ischemic stroke.
Funder
Deutsche Forschungsgemeinschaft
Publisher
Springer Science and Business Media LLC
Cited by
7 articles.
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