2017
DOI: 10.1093/neuros/nyx016
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Hyperglycemia Aggravates Cerebral Vasospasm after Subarachnoid Hemorrhage in a Rat Model

Abstract: Hyperglycemia exacerbated cerebral vasospasm and was associated with poorer neurological outcomes following SAH. Our findings also suggested the nitric oxide pathway as a potential underlying mechanism via the dysregulation of eNOS and iNOS.

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Cited by 30 publications
(19 citation statements)
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“…[ 15 ] In our experimental study, hyperglycemia-preconditioned rats had worse neurological functions following SAH than those with either hyperglycemia or SAH alone, which reinforced clinical findings. [ 16 ] It is reasonable to hypothesize that factors affecting the prognosis of patients following SAH also may be responsible for an increased risk of tracheotomy, and the connection between diabetes mellitus and tracheostomy shown in this study seems not surprising. The acute phase of stroke is usually accompanied by a humoral surge in cortisol and catecholamines, [ 17 ] which results in elevated blood glucose levels regardless of a previous diabetes diagnosis.…”
Section: Discussionmentioning
confidence: 74%
“…[ 15 ] In our experimental study, hyperglycemia-preconditioned rats had worse neurological functions following SAH than those with either hyperglycemia or SAH alone, which reinforced clinical findings. [ 16 ] It is reasonable to hypothesize that factors affecting the prognosis of patients following SAH also may be responsible for an increased risk of tracheotomy, and the connection between diabetes mellitus and tracheostomy shown in this study seems not surprising. The acute phase of stroke is usually accompanied by a humoral surge in cortisol and catecholamines, [ 17 ] which results in elevated blood glucose levels regardless of a previous diabetes diagnosis.…”
Section: Discussionmentioning
confidence: 74%
“…70 Hyperglycemia increases the chance of cerebral vasospasm after SAH, mainly through the NO pathway as a potential underlying mechanism via the dysregulation of eNOS and iNOS. 71 A study found that aminoguanidine inhibits iNOS activity and reduces cerebral vasospasm after SAH in rabbits after abnormal endothelial cell repair. 72 …”
Section: Echanisms Of No In Smentioning
confidence: 99%
“…Moreover, hyperglycemia provides an abundant substrate for anaerobic glycolysis in ischemic brain tissue, which leads to excessive lactate accumulation, acidosis, and cell death [34]. In a rat SAH model, hyperglycemia exacerbated cerebral vasospasm by dysregulating endothelial nitric oxide synthase (eNOS) and inducing nitric oxide synthase (iNOS) [35]. Another experimental study indicated that hyperglycemia may activate the extrinsic caspase cascade through the extracellular regulated kinase (ERK) signal pathway to contribute to neuronal apoptosis after SAH [36].…”
Section: Discussionmentioning
confidence: 99%