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Abstract: We examined in a rabbit model of transient spinal cord ischemia (SCI) whether isoflurane (Iso) preconditioning induces ischemic tolerance to SCI in a dose–response manner, and whether this effect is dependent on mitochondrial adenosine triphosphate-dependent potassium (KATP) channel. Eighty-six rabbits were randomly assigned to 10 groups: Control group (n =8) received no pretreatment. Ischemic preconditioning (IPC) group (n =8) received 5min of IPC 30min before SCI. The Iso 1, Iso 2 and Iso 3 groups (n =10, 9, 8) underwent 30min of 1.05, 2.1 and 3.15% Iso inhalation commencing 45min before SCI. The Iso 1HD, Iso 2HD and Iso 3HD groups (n =9, 9, 8) each received a specific mitochondrial KATP channel blocker, 5-hydroxydecanoic acid (5HD, 20mg/kg), 5min before each respective Iso inhalation. The 5HD group (n =8) received 5HD without Iso inhalation. The sham group (n =9) had no SCI. SCI was produced by infra-renal aortic occlusion via the inflated balloon of a Swan–Ganz catheter for 20min. The Iso 1, Iso 2 and Iso 3 groups showed a better neurologic outcome and more viable motor nerve cells (VMNCs) in the anterior spinal cord 72h after reperfusion than the control group (p <0.05). Iso 3 group showed a better neurologic outcome and more VMNCs than Iso 1 group (p <0.05). And, the Iso 1, Iso 2 and Iso 3 groups showed a better neurologic outcome and higher VMNC numbers than the corresponding Iso 1HD, Iso 2HD and Iso 3HD groups (p <0.05). This study demonstrates that Iso preconditioning protects the spinal cord against neuronal damage due to SCI in a dose–response manner via the activation of mitochondrial KATP channels. [Copyright &y& Elsevier]

Postoperative respiratory failure is a serious complication that could benefit from early accurate identification of high-risk patients. We developed and validated a machine learning model to predict postoperative respiratory failure, defined as prolonged (>48 h) mechanical ventilation or reintubation after surgery. Easily extractable electronic health record (EHR) variables that do not require subjective assessment by clinicians were used. From EHR data of 307,333 noncardiac surgical cases, the model, trained with a gradient boosting algorithm, utilised a derivation cohort of 99,025 cases from Seoul National University Hospital (2013–9). External validation was performed using three separate cohorts A–C from different hospitals comprising 208,308 cases. Model performance was assessed by area under the receiver operating characteristic (AUROC) curve and area under the precision-recall curve (AUPRC), a measure of sensitivity and precision at different thresholds. The model included eight variables: serum albumin, age, duration of anaesthesia, serum glucose, prothrombin time, serum creatinine, white blood cell count, and body mass index. Internally, the model achieved an AUROC of 0.912 (95% confidence interval [CI], 0.908–0.915) and AUPRC of 0.113. In external validation cohorts A, B, and C, the model achieved AUROCs of 0.879 (95% CI, 0.876–0.882), 0.872 (95% CI, 0.870–0.874), and 0.931 (95% CI, 0.925–0.936), and AUPRCs of 0.029, 0.083, and 0.124, respectively. Utilising just eight easily extractable variables, this machine learning model demonstrated excellent discrimination in both internal and external validation for predicting postoperative respiratory failure. The model enables personalised risk stratification and facilitates data-driven clinical decision-making. [ABSTRACT FROM AUTHOR]

Background Dexmedetomidine (DEX) is used as an adjunct to total intravenous anesthesia. However, its effect on intraoperative neurophysiologic monitoring (IOM) during brain tumor surgery remains controversial. The aim of this study was to explore the effect of DEX on IOM during brain tumor surgery. Methods Seventy-eight consecutive patients (DEX group, n = 40; control group, n = 38), who underwent brain tumor surgery with IOM, were retrospectively reviewed. The outcomes included the predictability, laterality of alterations, and stimulation parameters of transcranial motor evoked potentials (tcMEPs) and somatosensory evoked potentials (SSEPs). Results The predictability of tcMEPs for postoperative motor outcomes showed a higher false-positive rate in the DEX group than in the control group (27.5% vs. 5.3%, P = 0.047). Bilateral alterations were observed only in the DEX group (31.3%; P = 0.053). Compared with the control group, the DEX group required significantly higher intensity (377.5 ± 48.0 vs. 347.1 ± 30.0 mV; P = 0.001) and repetition rate (6.0 ± 0.2 vs. 5.7 ± 0.5 pulse/train; P = 0.001) of transcranial electric stimulation to evoke adequate tcMEPs. The SSEP results were comparable between both groups. In the DEX group, false-positive tcMEPs changes occurred 222.2 ± 70.5 minutes (range, 95–342 minutes) after the induction of anesthesia. In addition, the patients who were administered DEX under bispectral index monitoring (n = 12) showed a significantly higher false-positive rate than shown by the control group (50.5% vs. 5.3%; P = 0.003). CONCLUSIONS: This study showed that DEX had significant effects on tcMEPs during IOM in brain tumor surgery. Because the high false-positive rate could decrease the accuracy of IOM, outcomes after using DEX should be cautiously interpreted. [ABSTRACT FROM AUTHOR]

This study investigated the neuroprotective effect of pravastatin administration after forebrain ischemia in rats. Forebrain ischemia was induced by bilateral common carotid artery occlusion and systemic hypotension for 8 min. Pravastatin at 1 mg/kg (pravastatin group, n = 10), or an identical volume of normal saline (control group, n = 10), was injected 10 min, and 1–4 days after reperfusion. Arterial blood gas was analyzed 10 min before ischemia onset and 10 min after ischemia completion. Viable and apoptotic neuronal cells were evaluated 7 days after ischemia by hematoxylin and eosin (H&E) staining and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuracil triphosphate biotin in situ nick-end labeling (TUNEL) staining of the hippocampal Cornu Ammonis area (CA1). Expression of Bcl-2 and Bax proteins was quantified by Western blot analysis. The proportion of viable neuronal cells after ischemia was greater in the pravastatin vs . control group ( p < 0.01), with greater expression of apoptotic cells in the control vs . pravastatin group ( p < 0.05). Bax protein expression was significantly decreased in the pravastatin group ( p < 0.05), whereas, Bcl-2 expression was increased, but not significantly ( p > 0.05). Our findings suggest that pravastatin administration after forebrain ischemia confers neuroprotection in rats by inhibiting Bax protein expression. [ABSTRACT FROM AUTHOR]

Various experimental studies have reported neuroprotective effects of sevoflurane postconditioning against cerebral ischemia-reperfusion injury. We therefore investigated its neuroprotective effects on hyperperfusion-related transient neurologic deterioration, called symptomatic cerebral hyperperfusion (SCH), and also identified predictive factors for SCH in patients with moyamoya disease after revascularization surgery. A total of 152 adult patients with moyamoya disease undergoing anastomosis of the superficial temporal artery to middle cerebral artery were randomly allocated into 2 groups. The postconditioning group (group S, n = 76) inhaled sevoflurane of 1 minimum alveolar concentration for 15 minutes immediately after reperfusion and then washed it out slowly for 15 minutes. The control group (group C, n = 76) received no intervention. The incidence of SCH was compared between the 2 groups. The incidence of SCH was not significantly different between groups S and C (53.3% vs. 43.4%, respectively; P = 0.291). The incidence of postoperative complications and the Glasgow Outcome Scale score at hospital discharge also did not differ significantly. Predictive factors for SCH included a decreased vascular reserve in preoperative single-photon emission computed tomography scan (odds ratio [OR], 7.18; 95% confidence interval [CI], 1.78–29.02; P = 0.006), an operation performed on the dominant hemisphere (OR, 3.32; 95% CI, 1.57–6.98; P = 0.002), temporal occlusion time (OR, 1.06; 95% CI, 1.01–1.11; P = 0.017), and intraoperative minimum partial pressure of carbon dioxide (P a CO 2) (OR, 0.86; 95% CI, 0.78–0.94; P = 0.001). Sevoflurane postconditioning did not reduce the incidence of SCH after revascularization surgery in patients with moyamoya disease. Rather, a decreased vascular reserve, operation on the dominant hemisphere, increased temporal occlusion time, and decreased intraoperative minimum P a CO 2 were associated with SCH in these patients. [ABSTRACT FROM AUTHOR]

Objective Delayed hyponatremia can occur after transsphenoidal pituitary tumor surgery, resulting in unexpected readmission. Predictive factors for delayed hyponatremia after this type of surgery are not well established. In this retrospective study, predictive factors for delayed hyponatremia were investigated in patients undergoing transsphenoidal pituitary tumor surgery. Methods Preoperative data (demographics, comorbidities, and hormonal assessment), preoperative, intraoperative, and immediate postoperative sodium concentrations, the nadir sodium concentration on postoperative day (POD) 1–2, characteristics of pituitary tumor (size, cell type, optic chiasm compression, and cavernous sinus invasion), and intraoperative data (operation time and fluid balance) were retrospectively collected from 234 patients undergoing endoscopic transsphenoidal surgery for removal of nonfunctioning pituitary tumors. Delayed hyponatremia was defined as serum sodium concentration <135 mEq/L on POD 3 or later, and after discharge, postoperative sodium concentration was measured on POD 7–10. Results Delayed hyponatremia was observed in 53 patients (22.6%). Of these patients, 5 (9.4%) were readmitted because of delayed hyponatremia. In binary logistic regression analysis, age >60 years (odds ratio [OR], 2.22; 95% confidence interval [CI], 1.16–4.26; P = 0.017), the nadir sodium concentration on POD 1–2 (OR, 0.88; 95% CI, 0.77–0.99; P = 0.034), and operation time (OR, 1.01; 95% CI, 1.00–1.02; P = 0.018) were independent risk factors for delayed hyponatremia after endoscopic transsphenoidal pituitary surgery. Conclusions The incidence of delayed hyponatremia in patients with nonfunctioning pituitary tumor who underwent endoscopic transsphenoidal surgery was 22.6%. Old age, low sodium concentration on POD 1–2, and long operation time were associated with the development of delayed hyponatremia in such patients. [ABSTRACT FROM AUTHOR]

Dexmedetomidine (DXM) has anti-inflammatory effects, which is considered an important mechanism of DXM-induced neuroprotection from cerebral ischemia/reperfusion injury. We determined whether the anti-inflammatory effects of DXM are associated with inhibition of the toll-like receptor (TLR)-4/nuclear factor kappa B (NF-κB) pathway in a rat model of transient global cerebral ischemia/reperfusion injury. Fifty rats were randomly assigned to one of five groups (10 rats/group): Group S received no treatment; Group C underwent transient global ischemia (10 min); Group D received DXM 30 min before ischemia; Group R received resatorvid, a selective TLR-4 antagonist, 30 min before ischemia; and Group RD received resatorvid and DXM 30 min before ischemia. The numbers of necrotic and apoptotic cells and the levels of TLR-4, NF-κB, and caspase-3 were assessed 1 day after ischemia, and pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin 6 (IL-6) were measured before ischemia and 2, 6, and 24 h thereafter. The necrotic and apoptotic cell counts and levels of TLR-4, NF-κB, and caspase-3 were higher in Group C than in other groups. TNF-α were higher in Group C than in other groups 2 h after ischemia, whereas IL-6 were higher in Group C 6 h after ischemia. IL-1β was higher in Group C than in Group D 6 and 24 h after ischemia. Our findings suggest that the anti-inflammatory action of DXM via inactivation of the TLR-4/NF-κB pathway, in part, may explain DXM-induced neuroprotection after cerebral ischemia. [ABSTRACT FROM AUTHOR]

Introduction: The present study investigated the effects of induced hypertension on hippocampal cell death after forebrain ischaemia in rats.Materials and Methods: In this study, forebrain ischaemia was induced in 20 Sprague-Dawley rats by clamping the bilateral common carotid arteries to induce systemic hypotension for 8min. All rats then underwent reperfusion during which the induced hypertension group (n=10) received intermittent intravenous injections of phenylephrine (5μg) to maintain their mean arterial blood pressure at 20mmHg above baseline for 10min and the control group (n=10) did not receive any treatment. In both groups, the numbers of viable and apoptotic neuronal cells in the cornu ammonis 1 (CA1) area of the hippocampus were evaluated 7 days after the induction of ischaemia.Results: The mean percentage of viable neuronal cells was higher in the induced hypertension group than in the control group (35% vs. 26%, respectively; p=0.004), but there was no significant difference in the proportion of apoptotic neuronal cells between the groups (57% vs. 43%, respectively; p=0.165).Conclusions: Induced hypertension significantly attenuated necrotic cell death in the hippocampal CA1 area, but apoptotic cell death was not affected. [ABSTRACT FROM AUTHOR]

Background Red blood cell (RBC) transfusion, especially with “old” blood, is associated with adverse clinical outcomes. We compared the effects of fresh blood versus old blood transfusion on poor neurologic outcomes and symptomatic vasospasm in patients with ruptured cerebral aneurysms. Methods In this retrospective study, 211 patients with aneurysmal rupture were divided into 3 groups: nontransfusion ( n = 136), fresh blood (RBC storage ≤14 days) transfusion ( n = 39), and old blood (RBC storage >14 days) transfusion ( n = 36). Unfavorable neurologic outcomes (modified Rankin Scale score ≥3) and symptomatic cerebral vasospasm were assessed. Results The incidence of unfavorable neurologic outcomes was significantly higher in the fresh blood and old blood transfusion groups compared with the nontransfused group (71.8% and 58.3% vs. 21.3%; P < 0.01); the incidence of symptomatic vasospasm was significantly higher in the old blood group compared with the fresh blood and nontransfusion groups (57.1% vs. 26.7% and 22.2%; P < 0.05). On binary logistic regression, old age, Hunt and Hess grade 3–4, high postoperative C-reactive protein level, RBC transfusion, delayed infarction, and hydrocephalus were independent predictors of unfavorable neurologic outcomes. Young age, Fisher grade 3–4, old RBC transfusion, and surgical clipping were independent predictors of postoperative symptomatic vasospasm. Conclusions RBC transfusion itself, regardless of the duration of RBC storage, was associated with unfavorable neurologic outcomes in patients with ruptured cerebral aneurysms. Also, old blood transfusion, but not fresh blood transfusion, was associated with increased symptomatic cerebral vasospasm. [ABSTRACT FROM AUTHOR]