Increased damage after ischemic stroke in patients with hyperglycemia with or without established diabetes mellitus

Pulsinelli, William A.; Levy, David E.; Sigsbee, Bruce; Scherer, Priscilla; Plum, Fred

doi:10.1016/0002-9343(83)91007-0

Cited by 602 publications

(246 citation statements)

References 24 publications

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“…11,12 Once a stroke has begun, the coexistence of hyperglycemia at presentation, regardless of etiology, is associated with worse outcome. [3][4][5][6] But initiation of tight glucose control for improving an evolving stroke has largely been futile, and possibly counterproductive, in terms of neurologic outcome, although the single large prospective clinical study to date had limitations. 13 We hypothesized that hyperglycemia may trigger a downstream exacerbating agent for stroke which, once activated, would act independently of the prevailing glycemic status.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Coincidence of hyperglycemia at presentation for cerebral ischemia is associated with larger infarct size and worsened clinical outcome. [3][4][5][6] Persistent hyperglycemia in the postischemic period is an independent predictor of worse neurologic outcome and 90-day mortality. 7,8 Preexisting hyperglycemia also increases the ischemic brain infarct in numerous animal models, as recently reviewed.…”

Section: Introductionmentioning

confidence: 99%

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Role of Soluble Epoxide Hydrolase in Exacerbation of Stroke by Streptozotocin-Induced Type 1 Diabetes Mellitus

Jouihan

Zuloaga

Zhang

et al. 2013

J Cereb Blood Flow Metab

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Hyperglycemia worsens stroke, yet rigorous glycemic control does not improve neurologic outcome. An alternative is to target downstream molecular mediator(s) triggered by hyperglycemia but independent of prevailing glycemia. Soluble epoxide hydrolase (sEH) is a potential mediator of injury via its metabolism of neuroprotective epoxyeicosatrienoic acids (EETs). We tested whether hyperglycemia exacerbates cerebral injury by upregulating sEH and decreasing brain EET levels. Type 1 diabetes mellitus was modeled by streptozotocin (STZ; 50 mg/kg per day intraperitoneally, 5 days) in male mice. At 4 weeks, STZ-treated and control mice underwent 45-minute middle cerebral artery occlusion (MCAO) with or without sEH blockade by trans-4-[4-(3-adamantan-1-ylureido)-cyclohexyloxy]-benzoic acid (t-AUCB; 1 mg/kg intraperitoneally daily for 6 days before MCAO). The STZ-treated mice had increased sEH mRNA expression in cerebral vessels and decreased EET concentrations in brain. There was no difference in cortical perfusion between groups. The STZ-treated mice sustained larger brain infarct than controls. Pretreatment with t-AUCB eliminated the difference in infarct size and EETs concentration between STZ-treated mice and controls, without altering glycemia. We conclude that type 1 diabetes mellitus upregulates sEH mRNA and decreases concentrations of neuroprotective EETs within the brain, leading to worse stroke outcome. The data indicate that sEH antagonism may be beneficial in the setting of hyperglycemic stroke.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of Soluble Epoxide Hydrolase in Exacerbation of Stroke by Streptozotocin-Induced Type 1 Diabetes Mellitus

Jouihan

Zuloaga

Zhang

et al. 2013

J Cereb Blood Flow Metab

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“…Certainly, adult patients with established diabetes mellitus has been shown to have poorer neurological recovery after a stroke compared to non-diabetic patients. 73 In addition, neurological outcome was worse with higher serum glucose concentrations. Bush and Steward 7a reported severe and permanent neurological damage following an uneventful anaesthetic in a eight year old girl in whom the only significant intraoperative finding was hyperglycaemia.…”

Section: Glucose Managementmentioning

confidence: 99%

Cerebral physiology in paediatric cardiopulmonary bypass

Pua

Bissonnette

1998

Can J Anaesth

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FKCPCPurpose: To analyze studies of neurological injury after open-heart surgery in infants and children and to discuss the effects of cardiopulmonary bypass, hypothermia and deep hypothermic circulatory arrest on cerebral blood flow, cerebral metabolism and brain temperature. Source: Articles were obtained from the databases, Current Science and Medline, from 1966 to present. Search terms include cardiopulmonary bypass(CPB), hypothermia, cerebral blood flow(CBF), cerebral metabolism and brain temperature. Information and abstracts obtained from meetings on the topic of brain and cardiac surgery helped complete the collection of information. Principal findings: In adults the incidence of neurological morbidity is between 7 to 87% with stroke in about 2-5%, whereas the incidence of neurological morbidity increases to 30% in infants and children undergoing cardiopulmonary bypass. Besides the medical condition of the patient, postoperative cerebral dysfunction and neuronal ischaemia associated with cardiac surgery in infants and small children are a combination of intraoperative factors. Deep hypothermic circulatory arrest impairs CBF and cerebral metabolism even after termination of CPB. Inadequate and/or non-homogenous cooling of the brain before circulatory arrest, as well as excessive rewarming of the brain during reperfusion are also major contributory factors. Conclusion: Newer strategies, including the use of low-flow CPB, pulsatile CPB, pH-stat acid-base management and a cold reperfusion, are being explored to ensure better cerebral protection, Advances in monitoring technology and better understanding of the relationship of cerebral blood flow and metabolism during the different modalities of cardiopulmonary bypass management will help in the medical and anaesthetic development of strategies to improve neurological and developmental outcomes.Objectif: Examiner les Etudes portant sur les atteintes neurologiques survenues apr& une chirurgie b. coeur ouvert chez les bEbEs et les enfants et discuter des effets de la circulation extracorporelle, de l'hypothermie et de l'arr~t circulatoire sous hypothermie profonde sur le debit sanguin c&~bral, sur le m&abolisme c&Ebral et sur la temperature du cerveau. Sources documentaires : Des articles ont &E choisis ~ partir de bases de donnEes, Current Science et Medline, de 1966 ~ aujourd'hui. Les mots-cl& utilis& Etaient : circulation extracorporelle (CEC), hypothermie, debit sanguin cErEbral (DSC), mEtabolisme cErEbral et temperature du cerveau. Les informations et les rEsumEs obtenus & la suite de sEminaires sur le cerveau et la chirurgie cardiaque ont permis de completer la cueillette de donn&s. I)onn&s principales : Chez les adultes, l'incidence de morbiditE neurologique avec accident vasculaire est de 7 87 % clans 2 ~. S % des cas tandis que l'incidence de morbiditE neurologique augmente & 30 % chez les bEb~s et les enfants subissant une circulation extracorporelle. La condition mEdicale du patient raise & part, le d&~glement cErEbral postop&atoire et l'ischEmie neu...

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“…The immediate postoperative period was associated with hyperglycemia in our patients in the CSL/dextrose group. Hyperglycemia is known to reduce gastric emptying and increase sensation of gastric fullness 5 and is associated with adverse neurological, 6 cardiovascular, 7 gastrointestinal 5 and immunological 8 effects. The previously demonstrated small benefit in subjective postoperative recovery symptoms may be insufficient to justify administration of solutions that cause hyperglycemia.…”

mentioning

confidence: 99%

Intravenous fluid loading with or without supplementary dextrose does not prevent nausea, vomiting and pain after laparoscopy

McCaul

Moran

O’Cronin

et al. 2003

Can J Anesth/J Can Anesth

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Increased damage after ischemic stroke in patients with hyperglycemia with or without established diabetes mellitus

Cited by 602 publications

References 24 publications

Role of Soluble Epoxide Hydrolase in Exacerbation of Stroke by Streptozotocin-Induced Type 1 Diabetes Mellitus

Role of Soluble Epoxide Hydrolase in Exacerbation of Stroke by Streptozotocin-Induced Type 1 Diabetes Mellitus

Cerebral physiology in paediatric cardiopulmonary bypass

Intravenous fluid loading with or without supplementary dextrose does not prevent nausea, vomiting and pain after laparoscopy

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