Regional cerebral blood flow decreases during hyperglycemia

Duckrow, Robert B.; Beard, Daniel Carter; Brennan, Robert W.

doi:10.1002/ana.410170308

Cited by 108 publications

(49 citation statements)

References 36 publications

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“…Hyperglycemia leads to an increase in cerebrovascular resistance due to hyperviscosity and higher brain water content, resulting in a global reduction of cerebral blood flow leading to intracellular acidosis secondary to impaired metabolism (5). Hyperglycemia further leads to dysfunction of the gabaminergic projection neurons from striatum (6).…”

Section: Discussionmentioning

confidence: 99%

Concepts and controversies in nonketotic hyperglycemia‐induced hemichorea: Further evidence from susceptibility‐weighted MR imaging

Cherian

Thomas

Baheti

et al. 2009

Magnetic Resonance Imaging

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Hyperglycemia-induced hemichorea can show T1 hyperintensity of the contralateral striatum on MRI. This is thought to be due to petechial hemorrhages or gemistocytic astrocyte accumulation. This study explores the utility of susceptibility-weighted imaging (SWI) and diffusionweighted imaging (DWI) in identifying the nature of these lesions. Three patients underwent MR imaging of the brain with SE T1, F SE T2, DWI, and SWI. T1 images showed hyperintensity predominantly involving the contralateral striatum, where mild (two cases) to moderate (one case) restricted diffusion (low apparent diffusion coefficient [ADC]) was detected on DWI. SWI demonstrated bilateral symmetrical hypointensities in the first two cases, suggesting age associated mineralization. In addition, increased susceptibility change (hypointensity) was also noted in the right putamen in the first and the third cases, suggesting paramagnetic mineral deposition. T1 hyperintensity may be from the protein hydration layer inside the cytoplasm of swollen gemistocytes appearing after an acute cerebral injury. These astrocytes also express metallothionein with zinc, which is thought to be the cause of asymmetric hypointensity of the posterior putamen on SWI. ADC values were thought to be useful for prognostication; however, they should be interpreted cautiously in the presence of susceptibility changes.

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Section: Discussionmentioning

confidence: 99%

Concepts and controversies in nonketotic hyperglycemia‐induced hemichorea: Further evidence from susceptibility‐weighted MR imaging

Cherian

Thomas

Baheti

et al. 2009

Magnetic Resonance Imaging

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“…This finding agrees with the findings of and Duckrow and Bryan (1987), who re- ported a 13-14% decrease of lCBF and lCMR g iu in the rat brain following 3 weeks of streptozotozin diabetes. During acute hyperglycemia (induced by intraperitoneal injection of glucose), lCBF declined by 30% (Duckrow et at., 1985), whereas Orzi et al (1986) found levels not different from those in con trol animals. Possibly, this discrepancy can be ex plained by the absence of steady state in acutely induced hyperglycemia.…”

Section: Discussionmentioning

confidence: 99%

Autoradiographic Determination of Cerebral Glucose Content, Blood Flow, and Glucose Utilization in Focal Ischemia of the Rat Brain: Influence of the Plasma Glucose Concentration

Jakobsen

Diemer

1988

J Cereb Blood Flow Metab

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Summary: Focal cerebral ischemia was produced by oc clusion of the middle cerebral artery in rats, Cerebral blood flow measured with [14C]iodoantipyrine was se verely reduced in the lateral portion of neostriatum. This area of dense ischemia was sharply demarcated against the surroundings. The adjacent cortex was perfused at one-third of normal, whereas blood flow in the medial neostriatum was only slightly reduced. This pattern of perfusion was independent of the plasma glucose concen tration of the animal. In contrast, the glucose utilization calculated from the 2-pH]deoxyglucose accumulation de pended on the plasma glucose concentration. Enhanced glucose utilization was evident in the border areas sur rounding the ischemic focus in normoglycemic animals. Neither acutely nor chronically diabetic animals had such an increase of metabolism in the borderzone. Moderately hyperglycemic rats had a narrow rim of enhanced glucose Occlusion of the middle cerebral artery (MCA) causes nearly complete ischemia in the center of the vascular territory. The ischemic area is sur rounded by tissue with reduced flow and a pe riphery with almost normal perfusion. In rats, the cerebral blood flow is severely reduced in the lat eral part of the striate body, whereas the adjacent cortex reveals flow values about one-third of normal (Nedergaard et aI., 1986). Earlier, we have

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“…20 Additionally, hyperglycemia is seen to cause reduction in blood circulation to the marginal ischemic areas after occlusion of the middle cerebral artery. 21 This suggests that penumbra around the infarct area converts to infarct in hyperglycemia.…”

Section: Hyperglycemia-associated Reduction In Perfusionmentioning

confidence: 99%

Hyperglycemia, Insulin, and Acute Ischemic Stroke

Garg

Chaudhuri

Munschauer

et al. 2006

Stroke

206

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Background and Purpose-Hyperglycemia is associated with increased mortality and morbidity in acute ischemic stroke. Summary of Review-Hyperglycemia induces a pro-oxidative and proinflammatory state that can cause direct neuronal toxicity. Hyperglycemia-mediated increase in matrix metalloproteinase-9 can cause neuronal damage by an increase in cerebral edema. Moreover, hyperglycemia may be responsible for a procoagulant state that can further compromise blood supply to the penumbral areas in acute ischemic stroke. Insulin infusion has an effect that is opposite to that of hyperglycemia. It not only lowers blood glucose levels but also exerts an antioxidant and anti-inflammatory effect. Insulin also improves NO production and results in improved blood circulation to the ischemic areas. This article focuses on the potential mechanisms underlying the injurious effects of glucose and the beneficial effects of insulin. Conclusions-In the absence of other potential beneficial therapies, there is an urgency to institute trials with insulin infusion in acute ischemic stroke. (Stroke. 2006;37:267-273.)

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Regional cerebral blood flow decreases during hyperglycemia

Cited by 108 publications

References 36 publications

Concepts and controversies in nonketotic hyperglycemia‐induced hemichorea: Further evidence from susceptibility‐weighted MR imaging

Concepts and controversies in nonketotic hyperglycemia‐induced hemichorea: Further evidence from susceptibility‐weighted MR imaging

Autoradiographic Determination of Cerebral Glucose Content, Blood Flow, and Glucose Utilization in Focal Ischemia of the Rat Brain: Influence of the Plasma Glucose Concentration

Hyperglycemia, Insulin, and Acute Ischemic Stroke

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