The Stabilization of Central Sympathetic Nerve Activation by Renal Denervation Prevents Cerebral Vasospasm after Subarachnoid Hemorrhage in Rats

Takemoto, Yushin; Hasegawa, Yu; Hayashi, Kenyu; Cao, Cheng; Hamasaki, Tadashi; Kawano, Takayuki; Mukasa, Akitake; Kim‐Mitsuyama, Shokei

doi:10.1007/s12975-019-00740-9

Cited by 30 publications

(21 citation statements)

References 57 publications

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“…25 Several studies examining post-SAH EBI have shown that EBI is an important factor affecting the prognosis of patients with SAH. 26,27 Therefore, improved understanding of the mechanisms driving EBI may provide novel therapies for improving the prognosis of patients with SAH.…”

Section: Discussionmentioning

confidence: 99%

Acyl‐CoA synthetase long chain family member 4 plays detrimental role in early brain injury after subarachnoid hemorrhage in rats by inducing ferroptosis

Liang

et al. 2020

CNS Neurosci Ther

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Section: Discussionmentioning

confidence: 99%

Acyl‐CoA synthetase long chain family member 4 plays detrimental role in early brain injury after subarachnoid hemorrhage in rats by inducing ferroptosis

Liang

et al. 2020

CNS Neurosci Ther

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“…A cohort study showed that using a beta-blocker to inhibit sympathetic activity was associated with a lower incidence of cerebral vasospasm in patients with aSAH [31]. An experimental study also con rmed the correlation between sympathetic suppression and decreased cerebral vasospasm after SAH [32]. Therefore, elevated serum glucose after SAH may re ect the stress response and severity of the neurological insult.…”

Section: Discussionmentioning

confidence: 97%

Serum glucose as an important predictor of delayed cerebral ischemia in angiogram-negative subarachnoid hemorrhage

Zhang

Wang

et al. 2021

Preprint

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Background Despite benign overall course, angiogram-negative subarachnoid hemorrhage (AN-SAH) still companies with risk of delayed cerebral ischemia (DCI). Serum glucose was previously found to be related to DCI occurrence in aneurysmal subarachnoid hemorrhage (aSAH), but this has not been confirmed in AN-SAH. The aim of this study was to clarify the significance of serum glucose in DCI prediction in AN-SAH patients. Methods We included patients with AN-SAH admitted to our hospital between January 2013 and December 2018. According to different bleeding patterns, patients were divided into perimesencephalic AN-SAH (PAN-SAH) and non-perimesencephalic AN-SAH (NPAH-SAH) patients. DCI was defined as symptomatic vasospasm or/and delayed cerebral infarction. A statistical analysis of the clinical, radiological, and laboratory risk factors of DCI was conducted. Logistic regression analysis was performed to identify the independent predictors of DCI. Results A total of 244 AN-SAH patients (mean age 55.7 years, 55.7% men) were included with 164 (67.2%) PAN-SAH patients and 80 (32.8%) NPAN-SAH patients. There were significant correlations between high DCI incidence and high serum glucose levels in the first five days after admission in both PAN-SAH patients and NPAN-SAH patients (p < 0.05). High admission serum glucose was significantly related to higher World Federation of Neurosurgeons Scale (WFNS) (p < 0.05). Multivariate logistic regression analysis showed that admission serum glucose (p = 0.001, OR 1.705, 95% CI 1.232–2.360) and WFNS (p = 0.008, OR 2.889, 95% CI 1.322–6.311) were both significant and independent predictors for DCI occurrence in PAN-SAH patients. Admission serum glucose (p = 0.016, OR 2.307, 95% CI 1.167–4.562), standard deviation (SD) of the serum glucose in the first three days after admission (p = 0.049, OR 5.684, 95% CI 1.006–32.114) and modified Fisher scale (mFS) (p = 0.033, OR 1.859, 95% CI 1.051–3.288) were significant and independent predictors for DCI occurrence in NPAN-SAH patients. Conclusions Serum glucose is an early biomarker to predict DCI risk in both PAN-SAH and NPAN-SAH patients, which has an important value in guiding intensive care in AN-SAH patients.

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“…It was found that inhibition of sympathetic activity by beta-blockers could reduce cerebral vasospasm rates and improve functional outcomes after aSAH [31,32]. In an animal study, inhibition of central sympathetic nerve activation through renal denervation signi cantly prevented cerebral vasospasm after SAH [33]. In addition, hyperglycemia may aggravate early brain injury (EBI) after SAH.…”

Section: Discussionmentioning

confidence: 99%

Effect of stress-induced hyperglycemia after non-traumatic non-aneurysmal subarachnoid hemorrhage on clinical complications and functional outcomes

Zhang

Zhao

Liu

et al. 2021

Preprint

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Background Despite having an overall benign course, non-traumatic non-aneurysmal subarachnoid hemorrhage (naSAH) is still accompanied by a risk of clinical complications and poor outcomes. Risk factors and mechanisms of complications and poor outcomes after naSAH remain unknown. Our aim was to explore the effect of stress-induced hyperglycemia (SIH) on complication rates and functional outcomes in naSAH patients. Methods We retrospectively reviewed patients with naSAH admitted to our institution between 2013 and 2018. SIH was identified according to previous criterion. Symptomatic vasospasm, delayed cerebral infarction, and hydrocephalus were identified as main complications. Outcomes were reviewed using a modified Rankin Scale (mRS) at discharge, 3 months, and 12 months. A statistical analysis of clinical, radiological, and laboratory risk factors of complications and outcomes was conducted. Results 244 naSAH patients were incorporated in the cohort with 74 (30.3%) SIH. After adjusting for age, gender, hypertension, Hunt and Hess (HH) grade, modified Fisher Scale (mFS), intraventricular hemorrhage (IVH), and subarachnoid blood distribution, SIH was significantly associated with symptomatic vasospasm (P < 0.001, 12.176 [4.904–30.231]), delayed cerebral infarction (P < 0.001, 12.434 [3.850-40.161]), hydrocephalus (P = 0.008, 5.771 [1.570-21.222]), and poor outcome at 12 months (P = 0.006, 5.506 [1.632–18.581]), whereas the correlation between SIH and poor outcome at discharge (P = 0.064, 2.409 [0.951-6.100]) or 3 months (P = 0.110, 2.029 [0.852–4.833]) was not significant. Incorporation of SIH increased the area under curve (AUC) of ROC in the combined model for predicting symptomatic vasospasm (P = 0.002), delayed cerebral infarction (P = 0.024), hydrocephalus (P = 0.037), and 12-month poor outcome (P = 0.087). Conclusions SIH is a significant and independent risk factor for symptomatic vasospasm, delayed cerebral infarction, hydrocephalus, and long-term poor outcome in naSAH patients. Identifying SIH early after naSAH is important for decision-making and treatment planning.

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The Stabilization of Central Sympathetic Nerve Activation by Renal Denervation Prevents Cerebral Vasospasm after Subarachnoid Hemorrhage in Rats

Cited by 30 publications

References 57 publications

Acyl‐CoA synthetase long chain family member 4 plays detrimental role in early brain injury after subarachnoid hemorrhage in rats by inducing ferroptosis

Acyl‐CoA synthetase long chain family member 4 plays detrimental role in early brain injury after subarachnoid hemorrhage in rats by inducing ferroptosis

Serum glucose as an important predictor of delayed cerebral ischemia in angiogram-negative subarachnoid hemorrhage

Effect of stress-induced hyperglycemia after non-traumatic non-aneurysmal subarachnoid hemorrhage on clinical complications and functional outcomes

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