NADPH-oxidase activity is elevated in penumbral and non-ischemic cerebral arteries following stroke

Miller, A. A. , Dusting, G. J., Roulston, C. L. and Sobey, C. G. (2006) NADPH-oxidase activity is elevated in penumbral and non-ischemic cerebral arteries following stroke. Brain Research, 1111(1), pp. 111-116. (doi: 10.1016/j.brainres.2006.06.082) (PMID:16879806)

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Abstract

Reactive oxygen species play a role in neuronal damage following cerebral ischemia–reperfusion. We tested whether activity of the superoxide-generating enzyme, NADPH-oxidase, is enhanced in cerebral arteries within, adjacent and distant from the ischemic core. The right middle cerebral artery (MCA) of conscious rats was temporarily occluded by perivascular injection of endothelin-1 to induce stroke (ET-1; n = 19). Control rats were injected with saline (n = 9). At 24 h or 72 h post-administration of ET-1, the MCA and its branches within the ipsilateral penumbra and infarcted core, corresponding arteries in the contralateral hemisphere, and basilar artery were excised. Anatomically similar arteries were excised from saline-injected rats. At 24 h after stroke, NADPH-stimulated superoxide production by arteries from the infarcted core did not differ from levels generated by arteries from control rats, whereas levels were significantly lower 72 h after stroke. However, at both time points after stroke, superoxide production by arteries from the ischemic penumbra was 8-fold greater than levels generated by arteries from control rats. Surprisingly, even in the non-ischemic arteries from the contralateral hemisphere and in the basilar artery, superoxide production was increased ∼ 4- to 6-fold at 24 h, but had returned to normal 72 h after stroke. The NADPH-oxidase inhibitor, diphenyleneiodonium, virtually abolished superoxide production by all arteries. Thus, the activity of NADPH-oxidase is enhanced in cerebral arteries from the ischemic penumbra at 24 h and 72 h following cerebral ischemia. Additionally, NADPH-oxidase activity is temporarily enhanced after cerebral ischemia within arteries from non-ischemic parts of the brain.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Miller, Dr Alyson
Authors: Miller, A. A., Dusting, G. J., Roulston, C. L., and Sobey, C. G.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:Brain Research
Publisher:Elsevier
ISSN:0006-8993
ISSN (Online):1872-6240
Published Online:01 July 2006

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