Hyperglycemia Induces Progressive Changes in the Cerebral Microvasculature and Blood-brain Barrier Transport During Focal Cerebral Ischemia

Kawai, Nobuyuki; Keep, Richard F.; Betz, A. Lorris; Nagao, Seigo

doi:10.1007/978-3-7091-6475-4_63

Cited by 42 publications

(41 citation statements)

References 9 publications

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“…Similarly, oxidative damage in rat brain is increased by experimentally induced hyperglycemia (Aragno et al, 1997). It has been suggested that the modified oxidative state induced by chronic hyperglycemia may contribute to nervous tissue damage; free radical species impair the central nervous system, attacking neurons and schwann cells, and the peripheral nerves (Kawai et al, 1998;Kumar & Menon, 1998;Aragno, 2000). Because of high polyunsaturated lipid content, schwann cells and axons are particularly sensitive to oxygen free radical damage; lipid peroxidation may increase cell membrane rigidity and impair cell function.…”

Section: Resultsmentioning

confidence: 99%

Anthocephalus cadamba (Roxb.) Miq., Rubiaceae, extract shows hypoglycemic effect and eases oxidative stress in alloxan-induced diabetic rats

Alam¹,

Subhan²,

Chowdhury³

et al. 2011

Rev. bras. farmacogn.

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Abstract:The hydroethanolic extract of the flowering tops of Anthocephalus cadamba (Roxb.) Miq., Rubiaceae, a Bangladeshi medicinal plant, was studied for its potential hypoglycemic effect and antioxidant property in alloxan-induced diabetic rats. The extract induced significant reduction in serum glucose, and transaminases, e.g. aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatases (ALP), activities. Significant changes in the thiobarbituric acid reactive substances (TBARS), peroxidase and catalase levels during the experimental period were also observed. The results established that the hydroethanolic extract of the flowering tops of A. cadamba possesses hypoglycemic property and is able to protect liver and brain from oxidative damages caused by diabetes.

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Section: Resultsmentioning

confidence: 99%

Anthocephalus cadamba (Roxb.) Miq., Rubiaceae, extract shows hypoglycemic effect and eases oxidative stress in alloxan-induced diabetic rats

Alam¹,

Subhan²,

Chowdhury³

et al. 2011

Rev. bras. farmacogn.

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“…[20][21][22] In experimental studies, the detrimental role of hyperglycemia has typically been linked to accelerated infarct progression primarily in the penumbra area. [23][24][25] It is plausible that hyperglycemia may more greatly exacerbate infarct growth in patients with incomplete recanalization compared with patients with complete recanalization after MT.…”

Section: Strokementioning

confidence: 99%

Impact of Glucose on Outcomes in Patients Treated With Mechanical Thrombectomy

Kim

Jahan

Saver³

2016

Stroke

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6-8 perhaps because, among patients treated with intravenous thrombolysis, reperfusion occurs in only 40% to 50% and documentation of reperfusion timing and extent imprecise.Accordingly, the advent of mechanical thrombectomy (MT), which more frequently achieves reperfusion and permits more exact characterization of reperfusion timing and extent, offers an opportunity to more clearly evaluate the potential Background and Purpose-Sparse data are available regarding the association between hyperglycemia and outcomes in acute ischemic stroke patients receiving mechanical thrombectomy (MT). We investigated whether hyperglycemia affected the outcomes of subjects treated with MT in the Solitaire Flow Restoration With the Intention for Thrombectomy (SWIFT) multicenter randomized trial, overall and according to reperfusion status after MT. Methods-We analyzed the relationships between the presenting glucose level as a continuous variable and presenting hyperglycemia (>140 mg/dL glucose) as a binary variable and several outcomes of interest. Subjects were stratified according to the completeness of reperfusion (Thrombolysis In Myocardial Ischemia scale 3 versus 0-2) after MT. Excellent outcome at 3 months was defined as a modified Rankin scale score of 0-1. Results-Among all patients undergoing MT, patients with hyperglycemia less frequently exhibited an excellent outcome at 3 months than patients without hyperglycemia, 13% versus 34%; P=0.01. Presenting glucose levels did not differ among patients achieving complete reperfusion and incomplete reperfusion. Among patients with incomplete reperfusion, after adjustment for covariates, higher glucose levels were independently associated with worse outcome at 3 months (per 10 mg/dL increase in glucose: odds ratio for modified Rankin scale score 0-1 at 3 months 0.58, 95% confidence interval 0.34-0.99; P=0.047). In contrast, among patients with complete reperfusion, differences in presenting glucose levels by final outcome did not reach statistical significance. Conclusions-In patients treated with MT, hyperglycemia was independently associated with worse outcome at 3 months, and the negative effects of hyperglycemia may have been exacerbated in patients with incomplete reperfusion after MT. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01054560.

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“…The effects of hyperglycemia on CNS injury, 16,20,30,45 vascular injury, 8,16,17,24 and clinical morbidity in the surgical critical care setting 33,36,44 have been well studied. Acute hyperglycemia following ischemic and traumatic brain injury has been shown to be associated with larger infarct volume and worse neurological outcome.…”

Section: Discussionmentioning

confidence: 99%

Effect of hyperglycemia on progressive paraparesis in a rat metastatic spinal tumor model

McGirt¹,

Gok²,

Shepherd³

et al. 2009

SPI

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Object Hyperglycemia has been shown to potentiate ischemic injury of the spinal cord by quenching vasodilators and potentiating tissue acidosis and free radical production. Steroid-induced hyperglycemia is a common event in the surgical management of metastatic epidural spinal cord compression (MESCC). The goal in this study was to determine whether experimentally induced hyperglycemia accelerates neurological decline in an established animal model of MESCC. Methods Sixteen Fischer 344 rats underwent a transabdominal approach for implantation of a CRL-1666 breast adenocarcinoma cell line within the vertebral body of L-6. After 72 hours of recovery from tumor implantation, the animals received intraperitoneal injections every 12 hours of either 2 g/kg dextrose in 5 ml 0.09% saline (hyperglycemia, 8 rats) or 5 ml 0.09% saline alone (normoglycemia, 8 rats). Weights were taken daily, and the hindlimb function was tested daily after tumor implantation by using the Basso-Beattie-Bresnahan (BBB) scale (score range 1–21). Animals were killed at time of paralysis (BBB Score < 7), and the volume of epidural tumor growth within the spinal canal was measured. To determine the degree of hyperglycemia induced by this dextrose regimen, a surrogate group of 10 Fischer 344 rats underwent intraperitoneal injections of 2 g/kg dextrose (5 rats) or 0.09% saline (5 rats) every 12 hours, and serum glucose levels were assessed 1, 3, 6, 8, 10, and 12 hours after injections for 24 hours. Results Dextrose versus saline injections resulted in elevated mean serum glucose at 3 (259 vs 103 μg/dl), 6 (219 vs 102 μg/dl), 8 (169 vs 102 μg/dl), and 10 hours (118 vs 99 μg/dl) after injection, returning to normal levels by 12 hours (96 vs 103 μg/dl) just prior to subsequent injection. All rats had normal hindlimb function for the first 8 days after tumor implantation. Hyperglycemic versus normoglycemic rats demonstrated a worsened median BBB score by postimplantation Day 9 (Score 20 vs 21, p = 0.023) through Day 16 (Score 8 vs 12, p = 0.047). Epidural tumor volume demonstrated a near-linear growth rate across both groups; however, hyperglycemic rats developed paralysis earlier (median 15.5 vs 17.5 days, p = 0.0035), with significantly less epidural tumor volume (2.75 ± 0.38 cm3 vs 4 ± 0.41 cm3, p < 0.001) at time of paralysis. Conclusions In a rat model of metastatic epidural spinal cord compression, rats maintained in a hyperglycemic state experienced accelerated time to paralysis. Also, less epidural tumor volume was required to cause paralysis in hyperglycemic rats. These results suggest that hyperglycemic states may contribute to decreased spinal cord tolerance to compression resulting from MESCC. Clinical studies evaluating the effect of aggressive glucose control in patients with MESCC may be warranted.

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Hyperglycemia Induces Progressive Changes in the Cerebral Microvasculature and Blood-brain Barrier Transport During Focal Cerebral Ischemia

Cited by 42 publications

References 9 publications

Anthocephalus cadamba (Roxb.) Miq., Rubiaceae, extract shows hypoglycemic effect and eases oxidative stress in alloxan-induced diabetic rats

Anthocephalus cadamba (Roxb.) Miq., Rubiaceae, extract shows hypoglycemic effect and eases oxidative stress in alloxan-induced diabetic rats

Impact of Glucose on Outcomes in Patients Treated With Mechanical Thrombectomy

Effect of hyperglycemia on progressive paraparesis in a rat metastatic spinal tumor model

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