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Enhanced contractility of intraparenchymal arterioles after global cerebral ischemia in rat - new insights into the development of delayed cerebral hypoperfusion

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AIM: Delayed cerebral hypoperfusion is a secondary complication found in the days after transient global cerebral ischemia that worsens the ischemic damage inflicted by the initial transient episode of global cerebral ischemia. A recent study demonstrated increased cerebral vasoconstriction in the large arteries on the brain surface (pial arteries) after global cerebral ischemia. However, smaller arterioles inside the brain (parenchymal arterioles) are equally important in the regulation of cerebral blood flow and yet their pathophysiology after global cerebral ischemia is largely unknown. Therefore, we investigated if increased contractility occurs in the intraparenchymal arterioles.

METHODS: Global cerebral ischemia was induced in male Wistar rats by bilateral common carotid occlusion for 15 minutes combined with hypovolemia. Regional cerebral blood flow was determined by quantitative autoradiography. Intraparenchymal arterioles were isolated, pressurized and concentration-response curves to endothelin-1 with and without the endothelin B receptor selective antagonist BQ788 was generated. Endothelin B receptor expression was investigated by quantitative flow cytometry and immunohistochemistry.

RESULTS: We observed increased endothelin-1 mediated contractility of parenchymal arterioles correlating with reduced cerebral blood flow of the cortex, hippocampus and caudate nucleus 48 hours after global cerebral ischemia. The increased endothelin-1 mediated contractility was abolished by BQ788 and the vascular smooth muscle cell-specific expression of endothelin B receptors was significantly increased after global cerebral ischemia.

CONCLUSION: Increased endothelin-1 mediated contractility and expression of endothelin B receptors in the intraparenchymal vasculature contributes to the development of delayed cerebral hypoperfusion after global cerebral ischemia in combination with vascular changes of the pial vasculature. This article is protected by copyright. All rights reserved.

OriginalsprogEngelsk
TidsskriftActa physiologica (Oxford, England)
Vol/bind220
Udgave nummer4
Sider (fra-til)417-431
ISSN1748-1708
DOI
StatusUdgivet - 2017

ID: 49473011