Blood glucose and stroke.

Helgason, Cathy M.

doi:10.1161/01.str.19.8.1049

Cited by 81 publications

(11 citation statements)

References 51 publications

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“…Both acute and chronic hyperglycaemia are associated with increased oedema and infarct size20 and with reduced cerebral blood flow and cerebrovascular reserve 21. Ischaemia leads to a slowing of the oxidative glucose metabolism and an increase in anaerobic glycolysis.…”

Section: Discussionmentioning

confidence: 99%

Is hyperglycaemia an independent predictor of poor outcome after acute stroke? Results of a long term follow up study

Weir

Murray

Dyker

et al. 1997

BMJ

476

306

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Section: Discussionmentioning

confidence: 99%

Is hyperglycaemia an independent predictor of poor outcome after acute stroke? Results of a long term follow up study

Weir

Murray

Dyker

et al. 1997

BMJ

476

306

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“…In case of a time- limited total stop of cerebral blood flow, as seen in cardiac arrest, no differences in neuronal damage could be observed between normoglycemic and hyperglycemic animals [24, 28, 29, 30]. However, in humans as well as in animal studies of focal cerebral ischemia, the clinical outcome was worse in the hyperglycemic group [15, 28, 29, 30, 31, 32]. In contrast to global cerebral ischemia, focal cerebral ischemia is characterized by an almost complete loss of cerebral blood flow in the ischemic core, whereas the penumbra reveals a small residual blood flow [32, 33, 34, 35].…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia in Patients with Focal Cerebral Ischemia after Intravenous Thrombolysis: Influence on Clinical Outcome and Infarct Size

Klisch²,

Orszagh³

et al. 2002

Cerebrovasc Dis

123

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The aim of the present prospective study was to investigate whether hyperglycemia influences the clinical outcome or the infarct size after intravenous thrombolysis of focal cerebral ischemia. A consecutive series of hyperglycemic (n = 14) and normoglycemic patients (n = 17) with acute focal cerebral ischemia (<3 h) in the middle cerebral artery (MCA) territory received rtPA (0.9 mg/kg body weight) intravenously. Clinical outcome was measured using the NIH Stroke Score on admission and was followed up until day 28. Infarct volume was measured by diffusion-weighted MR imaging on admission, on days 3 and 7. There was a significantly better neurological outcome on day 28 in the normoglycemic patients than in the hyperglycemic group (NIH SS 4.0 versus 7.4; p < 0.05). The infarction volume increased significantly in the hyperglycemic patients Δ = 39.9 ± 17.4% compared to normoglycemic patients Δ = 27.1 ± 14.1% (p < 0.05). The present study suggests that hyperglycemia in patients with a focal MCA ischemia can cause a worse clinical outcome despite recanalization of the occluded vessel by thrombolysis therapy. This correlates with a markedly larger increase of the infarction volume in the hyperglycemic group. These results may be explained by an accentuated lactate accumulation and pH decrease by elevated energy levels which cannot be compensated by restoration of blood flow alone.

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“…Stroke damage caused by brain infarction is a devastating complication of diabetes mellitus, killing or permanently disabling more than 60% of diabetic patients who survive into their seventh decade (1)(2)(3)(4)(5)(6). Diabetic patients are more likely to develop a stroke than nondiabetic patients, and moreover, strokes in diabetic patients are larger and more disabling than those in nondiabetic patients.…”

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confidence: 99%

Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine.

Zimmerman

Meistrell

Bloom

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

100

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Cerebral infarction (stroke) is a potentially disastrous complication of diabetes mellitus, principally because the extent of cortical loss is greater in diabetic patients than in nondiabetic patients. The etiology of this enhanced neurotoxicity is poorly understood. We hypothesized that advanced glycation endproducts (AGEs), which have previously been implicated in the development of other diabetic complications, might contribute to neurotoxicity and brain damage during ischemic stroke. Using a rat model of focal cerebral ischemia, we show that systemically administered AGE-modified bovine serum albumin (AGE-BSA) significantly increased cerebral infarct size. The neurotoxic effects of AGE-BSA administration were dose-and time-related and associated with a paradoxical increase in cerebral blood flow. Aminoguanidine, an inhibitor of AGE cross-linking, attenuated infarct volume in AGE-treated animals. We conclude that AGEs may contribute to the increased severity of stroke associated with diabetes and other conditions characterized by AGE accumulation.Stroke damage caused by brain infarction is a devastating complication of diabetes mellitus, killing or permanently disabling more than 60% of diabetic patients who survive into their seventh decade (1-6). Diabetic patients are more likely to develop a stroke than nondiabetic patients, and moreover, strokes in diabetic patients are larger and more disabling than those in nondiabetic patients. Although a number of factors have been implicated in enhancing diabetic stroke-related neurotoxicity, a complete understanding of the biochemical basis for increased stroke size associated with diabetes remains elusive. Recent investigation into the pathogenesis of stroke indicates that a number of factors may directly influence the volume of brain infarction after occlusion of a cerebral artery (7-10). These studies suggest that such neurotoxic factors can transform ischemic but potentially viable brain tissue into an irretrievably infarcted lesion, resulting in larger strokes in terms of both parenchymal necrosis and corresponding functional impairment.Advanced glycation endproducts (AGEs) have been implicated in the development of diabetic complications such as accelerated atherosclerosis, renal dysfunction, and neuropathy (11,12). AGE modifications accumulate by nonenzymatic reactions as permanent adducts and cross-linking structures on long-lived body proteins (for instance, collagen) as a function of age and glucose concentration. AGE-modified proteins in tissues may subsequently undergo receptor-mediated or proteolytic cleavage into smaller, reactive AGE-peptides which are released into the circulation, where they may ultimately either reattach covalently to tissue proteins or be eliminated from the circulation by the kidneys (13, 14). Previous observations suggest that high levels of AGE-proteins and AGE-The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance wi...

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Blood glucose and stroke.

Cited by 81 publications

References 51 publications

Is hyperglycaemia an independent predictor of poor outcome after acute stroke? Results of a long term follow up study

Is hyperglycaemia an independent predictor of poor outcome after acute stroke? Results of a long term follow up study

Hyperglycemia in Patients with Focal Cerebral Ischemia after Intravenous Thrombolysis: Influence on Clinical Outcome and Infarct Size

Neurotoxicity of advanced glycation endproducts during focal stroke and neuroprotective effects of aminoguanidine.

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