Effect of contrast media on renal function in patients with cerebrovascular disease complicated by diabetes mellitus after receiving interventional treatment / 介入放射学杂志

Objective To evaluate the effect of contrast medium on the renal function in patients with cerebrovascular disease accompanied by diabetes mellitus after receiving neuro - interventional therapy. Methods The clinical data of a total of 108 patients with cerebrovascular disease complicated by diabetes mellitus type 2, who were treated with neuro - interventional therapy during the period from March 2013 to March 2016, were retrospectively analyzed. The contrast dose used in interventional procedures was less than 250ml in each patient. The preoperative and 24 h -postoperative serum creatinine (sCr), serum cystatin C (Cys C) levels were determined, and based on the modification of dietary renal disease (MDRD) equation and Larsson equation the estimated glomerular filtration rates (eGFR) were separately calculated. Results Compared with preoperative values, the 24 h - postoperative mean sCr and Cys C levels were increased significantly (P=0. 001, P=0. 015 respectively), while the average eGFR rates were remarkably decreased (P＜ 0. 000 1 by using MDRD equation, and P=0. 021 by using Larsson equation). No kidney damage that needed to be treated occurred in all patients. Conclusion The contrast dose used in neuro - interventional procedures can cause decline of renal function in patients with type 2 diabetes mellitus. The combined determination of sCr and Cys C levels is helpful for the detection of contrast - induced changes in renal function as early as possible. The use of conventional dose of contrast agent in neuro - interventional procedures is safe for patients with type 2 diabetes mellitus. (J Intervent Radiol, 2018, 27:277-280)

Changes of cerebral white matter in patients with medication-overuse headache / 中国神经精神疾病杂志

Objective To investigate the microstructural abnormalities of cerebral white matter in patients with medication-overuse headache with diffusion tensor imaging.Methods Diffusion tensor magnetic resonance imaging (DT-MRI) was carried out in 80 migraine patients with medication-overuse headache (case group) and 80 age-and sex-matched healthy controls (control group).Fractional anisotropy (FA) and apparent diffusion coefficient (ADC) were measured and the correlation between clinical characteristics and the changes was examined.Results ① The FA values at the bilateral orbitofrontal cortex,cingulate cortex,splenium of the corpus callosum and the right anterior limb of the capsula interna were significantly lower than those in the controls(P＜0.05).② The ADC values at the right orbitofrontal cortex,left inferior frontal gyrus and anterior cingulate cortex were significantly higher than those in the controls (P＜0.05).③ There were negative correlations between FA values at the bilateral orbitofrontal cortex and right hind legs of the capsula interna and headache course as well as frequency.There was negative correlation between FA values at the left hind legs of capsula interna and headache frequency.④ There were positive correlations between ADC values at the left orbitofrontal cortex and headache course as well as frequency.There were positive correlations between ADC values at the right orbitofrontal cortex and prior cingulate cortex and headache frequency.There was positive correlation between ADC values at the posterior cingulate cortex and headache course.Conclutions There might be an integrity change of neurofibrotic microstructures in the bilateral orbitofrontal cortex and cingulate cortex in patients with medication-overuse headache,FA values are negatively associated with headache course and frequency whereas ADC values are positively associated with headache course and frequency.

Effect analysis of multi-interventional modes mainly with mechanical thrombectomy for large artery occlusive acute cerebral infarction / 中国脑血管病杂志

Objective To investigate the effectiveness and safety in patients with largeartery occlusive acute cerebral infarction who received multi-interventional modes mainly with mechanical thrombectomy and its related factors affecting prognosis. Methods The clinical data of 56 patients with large artery occlusive acute cerebral infarction were analyzed retrospectively. The clinical characteristics (gender,age,and underlying diseases),timing of treatment (time from ictus to puncture,time from puncture to recanalization), multi-interventional mode therapies (intra-arterial thrombolysis,thrombectomy,balloon dilation,and stenting, etc. ),and distribution of offending vessels were observed. The modified Thrombolysis in Cerebral Ischemia Scale (mTICI)grade was used to evaluate revascularization. The National Institute of Health Stroke Scale (NIHSS)score was used to observe the neurological function at 24 h before and after procedures. The modified Rankin scale (mRS)was used to evaluate the prognosis at 3 months after procedure. The safety of the treatment was evaluated with operative complications (mainly symptomatic intracranial hemorrhage)and mortality. The patients were divided into either a good prognosis group (n = 34;mRS≤2)or a poor prognosis group (n =22;mRS≥3)according to the prognosis at 3 months after procedure. They were analyzed with univariate analysis. The factors influencing the prognosis were further analyzed with multivariate logistic regression analysis. Results (1)The recanalization rate in 56 patients was 78. 6%(n = 44),in which basilar artery was the highest,reaching 93. 8% (15 / 16),middle cerebral artery was 87. 0% (20 / 23). The NIHSS score at 24 hours was 10 ± 7,it was lower than 16 ± 6 on admission. There was significant difference (t =6. 401,P <0. 01). At 3 months,34 patients (60. 7%)had good prognosis,4 (7. 1%)died,and 8 (14. 3%) had symptomatic intracranial hemorrhage. (2)Multiple factor analysis showed that the high level of recanalization was a protective factor for good prognosis (OR,0. 465,95% CI 0. 267 -0. 809,P =0. 007). Diabetes was an independent risk factor for poor prognosis (OR,5. 535,95% CI 1. 101 -27. 835, P = 0. 038). Conclusion Acute large artery occlusive cerebral infarction treated with the intra-arterial multi-interventional modes may quickly and effectively restore intracranial blood flow. It has the characteris-tics of high recanalization rate and good prognosis,and the higher the level of recanalization,the better the prognosis. Diabetes is an independent risk factor for poor prognosis.

Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-κB and Inflammation Response

Dexmedetomidine is an α2-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of 1 μg/kg load dose, followed by 0.05 μg/kg/min infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-1β, interleukin-6 and tumor nevrosis factor-α as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κBp65, inhibitor of κBα and phosphorylated of κBα in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-κB pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.

Neuroprotection of Dexmedetomidine against Cerebral Ischemia-Reperfusion Injury in Rats: Involved in Inhibition of NF-κB and Inflammation Response

Dexmedetomidine is an α2-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of 1 μg/kg load dose, followed by 0.05 μg/kg/min infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-1β, interleukin-6 and tumor nevrosis factor-α as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κBp65, inhibitor of κBα and phosphorylated of κBα in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-κB pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.

Effect of dexmedetomidine on expression of iNOS and COX-2 during focal cerebral ischemia-reperfusion in rats / 中华麻醉学杂志

Objective To evaluate the effect of dexmedetomidine on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty pathogen-free male Sprague-Dawley rats,aged 12-16 months,weighing 300-360 g,were randomly divided into 3 groups (n =10 each) using a random number table:sham operation group (group Sham),focal cerebral I/R group (group I/R),and dexmedetomidine group (group D).Focal cerebral I/R was induced by occlusion of the right middle cerebral artery.In group D,dexmedetomidine was given as a loading dose of 1 μg/kg (over 10 min) starting from 1 h of ischemia,followed by an infusion of 0.05 μg · kg-1 · h-1 until 2 h of reperfusion.Neurological deficit was assessed and scored at 24 h of reperfusion,and then the rats were sacrificed.Brains were removed for determination of cerebral infarct size and expression of iNOS and COX-2 in the hippocampus (by Western blot).The percentage of cerebral infarct size was calculated.Results Compared with group Sham,the neurological deficit score,percentage of head swing to the left,percentage of cerebral infarct size,and expression of iNOS and COX-2 in the hippocampus were significantly increased in I/R and D groups (P＜0.05).Compared with group I/R,the neurological deficit score,percentage of head swing to the left,percentage of cerebral infarct size,and expression of iNOS and COX-2 in the hippocampus were significantly decreased in group D (P＜0.05).Conclusion The mechanism by which dexmedetomidine mitigates focal cerebral I/R injury may be related to inhibition of iNOS and COX-2 expression in rats.

Role of oxLDL/LOX-1 system and NF-κB pathway in early diabetic vascular endothelial dysfunction / 中华内分泌代谢杂志

Diabetic rat model was established by peritoneal injection of streptozocin.At the end of 2 weeks,oxidized low-density lipoprotein (oxLDL) level in diabetic rats was raised [ ( 2.87 ± 0.40 vs 2.27 ± 0.36 ) μg/dl,P＜0.05 ] and endothelium-dependent relaxation was sluggish compared with normal rats.At the end of 6 weeks,oxLDL level continued to increase [ 4.32 ±0.66 ) μg/dl,P＜0.01] and endothelium-dependent maximum relaxation ( Rmax ) was decreased obviously ( P ＜0.01 ).Meanwhile,the protein and mRNA expressions of lectin-like oxidized lowdensity lipoprotein receptor-1 ( LOX-1 ),NF-kB,and ICAM-1 on vessel wall of diabetic rats were higher than those in normal rats,and LOX-1 mRNA was positively correlated with the levels of oxLDL,NF-kB,and ICAM-1 mRNA,while negatively correlated with Rmax,indicating that OxLDL/LOX-1 system may cause early endothelial dysfunction in diabetes via activating NF-kB and up-regulating ICAM-1 expression.