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Objective To explore the direction value of endovascular pressure differences in endovascular management of subclavian steal syndrome (SSS).Methods Eleven SSS patients accepted endovascular management,admitted to our hospital from January 2016 to December 2017,were collected in this study.Before and after operation,pressure-sensing wire was used to measure endovascular pressure differences (mean distal stenosis pressure minus mean proximal pressure),digital substraction angiography (DSA) was used to assess the stenotic rate,transcranial doppler (TCD) was used to assess the steal degrees,and electronic sphygmomanometer was used to measure the systolic pressure differences between bilateral brachial arteries.The pressure differences before and after endovascular management were compared.Before operation,the relations of pressure differences with stenotic rate,steal degrees and systolic pressure differences between bilateral brachial arteries were analyzed.After operation,the relations of pressure differences with stealing and clinical symptom improvements were analyzed.The predictive values of pressure differences and residual stenosis in clinic success were compared.Results (1) After operation,the blood stealing disappeared and the clinical symptoms improved in 10 patients;although residual stenotic rate of one patient decreased obviously,blood stealing and clinical symptoms still existed after operation;the clinic success rate was 90.9％(10/11).(2) Pressure differences before surgery ([11.2±5.7] mmHg) were significantly higher as compared with those after the surgery ([2.5±5.3] mmHg,P＜0.05).(3) Before operation,pressure differences were significantly correlated with stenotic rate (r=0.757,P=0.007) and bilateral systolic pressure differences (r=0.701,P=0.016).Six patients had pressure differences of 6-9 mmHg,enjoying degree I and Ⅱ of stealing,and 5 patients had pressure differences ≥ 10 mmHg,enjoying degree Ⅲ of stealing.(4) After operation,pressure difference was 18 mmHg in one patient without clinic success,but pressure differences were ≤ 3 mmHg in 10 patients with clinic success.(5) Significant difference was noted between the two clinic success indexes (residual stenotic rate ≤ 30％ by DSA and pressure differences ≤ 3 mmHg,P＜0.05).Conclusion Endovascular pressure differences can reflect the hemodynamic changes before and after endovascular management;as compared with residual stenosis,it is better to predict the clinic success after operation;it is useful to guide the endovascular management in the SSS patients.
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Histones can be released into the extracellular space,and lead to lethal sepsis, ischemia reperfusion injury, trauma, pancreatitis, coagulation and thrombosis.In addition, the increase of serum histone is related to the pathological and pathophysiological process of autoimmune diseases, nervous system diseases and tumors.Therefore, extracellular histone can be used as biomarkers and therapeutic targets for a variety of human diseases.
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Objective To investigate the correlation between the-1562 C/T polymorphism of matrix metalloproteinase-9 (MMP-9) and the risk of ischemic stroke.Methods All the relevant literatures published were searched from PubMed,Embase,MEDLINE,Web of Science as well as CBMdisc and CNKI before May 2013.After extracting data,a meta-analysis of the studies meeting the requirements was conducted by using Review Manager Version 5.0 and Stata 11.0 software.The effect size was pooled and odds ratio (OR) and 95％ confidence interval (CI) were calculated.Results Six studies were enrolled,including 1115 patients and 979 controls.The ORs after pooled analysis (95％ CIs) were C/T vs.C/C:1.10 (0.71-1.71) and T/T vs.C/C:1.78 (0.89-3.57) of the codominant genetic model,respectively; C/T + T/T vs.C/C:1.13 (0.76-1.67) of the dominant genetic model; T/T vs.C/T + C/C:1.79 (0.90-3.57) of the recessive genetic model,which suggested that there was no significant correlation between the-1562 C/T polymorphism of MMP-9 gene and the risk of ischemic stroke.The analysis of 5 studies in Chinese populations showed that the ORs (95％ CIs) of the above 4 genetic models were 1.24 (0.76-2.04),1.43 (0.52-3.92),1.25 (0.80-1.97),and 1.33 (0.49-3.62),respectively.There were also no significant differences.Conclusions According to the analysis of the available literatures,there was no significant correlation between the-1562 C/T polymorphism of MMP-9 gene and the risk of ischemic stroke.
ABSTRACT
BACKGROUND: In recent years, there are many studies designed to explain the protective effect of lidocaine on brain, but few about the therapeutic effect on traumatic cerebral edema. The content of aquaporin-4(AQP-4) in brain tissue is the highest and it has been proved that AQP-4participants in the formation of cerebral edema induced by cerebral trauma, cerebral infarction, eerebrai tumor and other reasons.OBJECTIVE: To observe the effect of lidocaine on the expression of AQP-4 of experimental rats following brain injury and analyze the therapeutic effect of lidocaine on brain edema.DESIGN: A randomized and control animal experiment.SETTING: Department of Anesthesiology, Affiliated Hospital of Medical College of Qingdao University.MATERIALS: The experiment was carried out in the Institute of Brain Disease, the Medical School Hospital of Qingdao University between January and July 2004. Totally 65 three-month-old healthy male Wistar rats,were enrolled in the experiment and randomly divided into 3 groups: normal control group (n=5), model group (n=30) and treatment group (n=30). Thirty rats in the model group and treatment group were respectively assigned into 6 subgroups according to 6 different time points: 1,4,6,12,24 and 48 hours following brain injury, with 5 rats at each time point.METHODS: Animal models of brain injury at right parietal lobe were created according to the method from Feeney et al. As for the rats of normal control group, they only underwent operation to be injured at the corresponding part. Rats recovered the access to food and water 2 to 8 hours after operation. For the rats in the treatment group, they were intraperitoneally injected of lidocaine at the 1st, 4th,6th, 12th, 24th, and 48th hours following injury, 5 rats at each time point. The initial dosage was 30 mg/kg, then 15 mg/kg was maintained . Administration was conducted every 6 hours in 3 days; For the rats in the model group, they were intraperitoneally injected of 30 mg/kg normal saline and rats in the normal control group were given no special treatments. Water content of brain was calculated 5 days following brain injury with dry and wet weight method:water content of brain=[brain mass (wet)-brain mass (dry)]/brain mass(wet)×100%. Expression of AQP-4 of brain tissue of rats was detected with immunohistochemical method and cytomorphological change of brain tissue was observed under optical microscope.MAIN OUTCOME MEASURES: ① Water content of brain of rats in each group. ② Expression of AQP-4 of brain tissue of rats in each group.③ Pathological results of brain tissue of rats in each group.RESULTS: No rats died accidentally or for other factors in the process of experiment, finally, all the 65 rats entered the stage of result analysis. ①Compared with model group, administration of lidocaine within 6 hours following brain injury could significantly decrease the water content of brain tissue [1 hour after brain injury: (81.09±0.29)%, (83.04±0.25)% ,P ＜ 0.05];[4 hours after brain injury: (81.34±0.35)%, (83.31±0.48)%,P ＜ 0.05] ;[6 hours after brain injury: (82.01±0.21)%, (83.25±0.37)% ,P ＜ 0.05]. Compared with model group, administration of lidocaine could significantly decrease the expression of AQP-4 [1 hour after brain injury:(0.19±0.02), (0.24±0.03),P ＜ 0.05]; [4 hours after brain injury: (0.21±0.05 ), (0.25±0.05) ,P ＜ 0.05]; [6 hours after brain injury: (0.21±0.03 ),(0.24±0.02) ,P ＜ 0.05]. There were no significant differences of AQP-4expression and water content of brain tissue when administration was conducted at the 12th, 24th and 48th hours following brain injury (P ＞ 0.05). ②Under the microscope, AQP-4 positive cells presented vacuolus, they mainly lay in the edema area of peripheral part of trauma, cortex of traumatic side and around the blood vessel as well as astrocyte of white substance, choroid plexus and ependymal layer. ③ Necrosis was found in most cells in the central area of trauma and apoptosis in most cells in the peripheral area. Compared with model group, necrotic and apoptotic cells were significantly less within 6 hours following trauma, but not at the 12th,24th and 48th hours following trauma in the treatment group.CONCLUSION: High dosage of lidocaine can decrease the expression of AQP-4 and lighten cerebral edema following brain injury, but administration should be given as early as possible.