Changes of cortical perfusion in the early phase of subarachnoid bleeding in a rat model and the role of intracranial hypertension

Title:

Changes of cortical perfusion in the early phase of subarachnoid bleeding in a rat model and the role of intracranial hypertension

Creator:

Kolar, M., Nohejlova, K., Duska, F., Mares, J., and Pachl, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:41e3cf0a-cd33-4a3b-8f13-39134a2f097a
uuid:41e3cf0a-cd33-4a3b-8f13-39134a2f097a

Subject:

subarachnoid hemorrhage, decompressive craniectomy, early brain injury, laser speckle-contrast analysis, and rat

Type:

article, model:article, and TEXT

Description:

Brain perfusion is reduced early after subarachnoid hemorrhage (SAH) due to intracranial hypertension and early vasospasm. The contribution of these two mechanisms is unknown. By performing a prophylactic decompressive craniectomy (DC) in a rat model of SAH we aimed to study brain perfusion after the component of intracranial hypertension has been eliminated. We used 2x2 factorial design, where rats received either decompressive craniectomy or sham operation followed by injection of 250 μl of blood or normal saline into prechiasmatic cistern. The cortical perfusion has been continually measured by laser speckle-contrast analysis for 30 min. Injection of blood caused a sudden increase of intracranial pressure (ICP) and drop of cerebral perfusion, which returned to baseline within 6 min. DC effectively prevented the rise of ICP, but brain perfusion after SAH was significantly lower and took longer to normalize compared to non-DC animals due to increased cerebral vascular resistance, which lasted throughout 30 min experimental period. Our findings suggest that intracranial hypertension plays dominant role in the very early hypoperfusion after SAH whilst the role of early vasospasm is only minor. Prophylactic DC effectively maintained cerebral perfusion pressure, but worsened cerebral perfusion by increased vascular resistance.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:Suppl 4

Harvested from:

CDK

Metadata only:

false