Author(s)

D. Tarr, D. Graham, L. A. Roy, W. M. Holmes, C. McCabe, I. M. Macrae, K. W. Muir, D. Dewar

ISBN

0271-678X

Publication year

2013

Periodical

Journal of Cerebral Blood Flow and Metabolism

Periodical Number

10

Volume

33

Pages

1556-1563

Author Address

Dewar, D Univ Glasgow, Inst Neurosci & Psychol, Coll Med Vet & Life Sci, Garscube Estate, Glasgow G61 1QH, Lanark, Scotland Univ Glasgow, Inst Neurosci & Psychol, Coll Med Vet & Life Sci, Glasgow G61 1QH, Lanark, Scotland Univ Glasgow, BHF Glasgow Cardiovasc Res Ctr, Inst Cardiovasc & Med Sci, Glasgow G61 1QH, Lanark, Scotland

Full version

Poststroke hyperglycemia is associated with a poor outcome yet clinical management is inadequately informed. We sought to determine whether clinically relevant levels of hyperglycemia exert detrimental effects on the early evolution of focal ischemic brain damage, as determined by magnetic resonance imaging, in normal rats and in those modeling the ‘metabolic syndrome’. Wistar Kyoto (WKY) or fructose-fed spontaneously hypertensive stroke-prone (ffSHRSP) rats were randomly allocated to groups for glucose or vehicle administration before permanent middle cerebral artery occlusion. Diffusion-weighted imaging was carried out over the first 4 hours after middle cerebral artery occlusion and lesion volume calculated from apparent diffusion coefficient maps. Infarct volume and immunostaining for markers of oxidative stress were measured in the fixed brain sections at 24 hours. Hyperglycemia rapidly exacerbated early ischemic damage in both WKY and ffSHRSP rats but increased infarct volume only in WKY rats. There was only limited evidence of oxidative stress in hyperglycemic animals. Acute hyperglycemia, at clinically relevant levels, exacerbates early ischemic damage in both normal and metabolic syndrome rats. Management of hyperglycemia may have greatest benefit when performed in the acute phase after stroke in the absence or presence of comorbidities.