Cortical spreading depression aggravates early brain injury in a mouse model of subarachnoid hemorrhage

Cortical spreading depression (CSD) has been observed during the early phase of subarachnoid hemorrhage (SAH). However, the effect of CSD on the cerebral blood flow (CBF) and cerebral oxyhemoglobin (CHbO) during the early phase of SAH has not yet been assessed directly. We, therefore, used laser spe...

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Veröffentlicht in:Journal of biophotonics 2021-04, Vol.14 (4), p.e202000379-n/a
Hauptverfasser: Tang, Yue, She, Deyuan, Li, Pengcheng, Pan, Li, Lu, Jinling, Liu, Peng
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creator Tang, Yue
She, Deyuan
Li, Pengcheng
Pan, Li
Lu, Jinling
Liu, Peng
description Cortical spreading depression (CSD) has been observed during the early phase of subarachnoid hemorrhage (SAH). However, the effect of CSD on the cerebral blood flow (CBF) and cerebral oxyhemoglobin (CHbO) during the early phase of SAH has not yet been assessed directly. We, therefore, used laser speckle imaging and optical intrinsic sinal imaging to record CBF and CHbO during CSD and cerebral cortex perfusion (CCP) at 24 hours after CSD in a mouse model of SAH. SAH was induced by blood injection into the prechiasmatic cistern. When CSD occurred, the change trend of CBF and CHbO in Sham group and SAH group was the same, but ischemia and hypoxia in SAH group was more significant. At 24 hours after SAH, the CCP of CSD group was lower than that of no CSD group, and the neurological function score of CSD group was lower. We conclude that induction of CSD further aggravates cerebral ischemia and worsens neurological dysfunction in the early stage of experimental SAH. Our study underscores the consequence of CSD in the development of early brain injury after SAH. Using LSI and OISI technology, we found that the response trend of CBF and CHbO to CSD in mice under SAH and physiological conditions was consistent, but cerebral ischemia and hypoxia under SAH condition were more serious. At the same time, it was found that CSD induced in the early phase of SAH aggravated cerebral hypoperfusion and neurological dysfunction 24 hours after SAH.
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However, the effect of CSD on the cerebral blood flow (CBF) and cerebral oxyhemoglobin (CHbO) during the early phase of SAH has not yet been assessed directly. We, therefore, used laser speckle imaging and optical intrinsic sinal imaging to record CBF and CHbO during CSD and cerebral cortex perfusion (CCP) at 24 hours after CSD in a mouse model of SAH. SAH was induced by blood injection into the prechiasmatic cistern. When CSD occurred, the change trend of CBF and CHbO in Sham group and SAH group was the same, but ischemia and hypoxia in SAH group was more significant. At 24 hours after SAH, the CCP of CSD group was lower than that of no CSD group, and the neurological function score of CSD group was lower. We conclude that induction of CSD further aggravates cerebral ischemia and worsens neurological dysfunction in the early stage of experimental SAH. Our study underscores the consequence of CSD in the development of early brain injury after SAH. 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subjects Blood flow
Brain
Brain injury
Cerebral blood flow
Cerebral cortex
cerebral oxyhemoglobin
Cortical spreading depression
early brain injury
Head injuries
Hemorrhage
Hypoxia
Ischemia
Mental depression
Neuroimaging
Neurological complications
Oxyhemoglobin
Perfusion
Subarachnoid hemorrhage
Traumatic brain injury
title Cortical spreading depression aggravates early brain injury in a mouse model of subarachnoid hemorrhage
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