BACKGROUND: Studies indicated that lipid peroxidation due to increase of free radical is the key factor of ischemia/reperfusion injury.Shinyleaf pricklyash root extracts, rutaceae plant, is bitter in taste, no stimulation, which has the effects of promoting qi, relieving pain, promoting blood circulation by removing blood stasis, dispelling wind and dredging collaterals and antioxidation.OBJECTIVE: To observe the influence of nitidine chloride on myocardial ischemia/reperfusion injury in rats and analyze its mechanism.DESIGN: Randomized controlled study.SETTING: Departmentof Pharmacology and Department of Chemistry,Guangxi Medical University.MATERIALS: A total of 60 healthy Wistar rats were selected, half male and half female, with the body mass of 250-300 g. Nitidine chloride was provided by Department of Chemistry, Guangxi Medical University, batch number 20050609. MS4000U biological signal quantitative record analysis system, 722N evident spectrophotometer, hydrochloric acid verapamil (batch number 020701, 2 mL in each), malondialdehyde (MDA) and superoxide dismutase (SOD) kit were purchased from Guangzhou Longfeida Technology Co., Ltd., Shanghai Precision Scientific Instruments Corporation, Shanghai Harvest Pharmaceutical Co, Ltd. and Nanjing Jiancheng Bioengineering Institute, respectively. Hitachi 7170A full automatic biochemistry analyzer was also applied.METHODS: The experiment was performed at the Department of Pharmacology and Department of Chemistry, Guangxi Medical University between June 2004 and May 2006. ①Totally 60 healthy Wistar rats with normal ECG (half male and half female) were randomly divided into 6 groups:sham operation group, model group, 2, 1, 0.5 mg/kg nitidine chloride groups, positive control group with 10 rats in each group. The rats in the sham operation group received threading without deligation, and 90 minutes later the experiment was accomplished. Other 50 rats received left anterior descending branch of coronary artery deligation, ischemia for 30 minutes reperfusion for 60 minutes. 2 mg/kg verapamil, 2,1,0.5 mg/kg, 5 mL/kgnitidine chloride, saline of the same volume were injected into femoral vein in rats of the positive control group, different doses nitidine chloride groups and model group, respectively 10 minutes before deligating left anterior descending branch of coronary artery. ②Monitoring was conducted successively with standard limb Ⅱ lead ECG when performing reperfusion. Type,incidence rate and duration of cardiac arrhythmia were recorded within 60minutes. Change of ST segment was also recorded after reperfusion for 15minutes and 60 minutes. ③At the end of experiment, serum myocardial enzymology indexes were measured wi th full automatic biochemistry analyzer.MDA content and SOD activity in myocardial tissues were examined with thiobarbituric acid(TBA) method and xanthine oxidase (XOD) method, respectively. ④Measurement data and enumeration data between two groups were compared with t test and x2 test. MAIN OUTCOME MEASURES: Occurrence of cardiac arrhythmia, ECG ST segment elevation, change of serum myocardial enzymology indexes, MDA content and SOD activity of myocardial tissues in rats of each group.RESULTS: A total of 60 rats were involved in the result analysis. ①Degree of cardiac arrhythmia and ECG ST segment elevation of rats: The emergency time of cardiac arrhythmia in 1 and 2 mg/kg nitidine chloride groups was significantly later than that in the model group (P ＜ 0.05,0.01). The duration of cardiac arrhythmia in the 1 and 2 mg/kg nitidine chloride groups and positive control group was obviously shorter than that in the model group (P ＜ 0.05-0.01). The incidence rates of various kinds of cardiac arrhythmia were markedly less than those in the model group (P ＜ 0.01). The degree of ST segment elevation at reperfusion for 15 and 60 minutes was remarkably lower than that in the model group (P ＜ 0.05-0.01). ②Serum myocardial enzyme level: It was significantly higher in the model than the sham operation group after 60-minute myocardial ischemia and reperfusion (P?.01). Activity of myocardial enzyme in the 1 and 2 mg/kg nitidine chloride groups was remarkably lower than that in the model group (P ＜ 0.01,P ＜ 0.05). The level of myocardial enzyme decreased with the increase of nitidine chloride. It was lower significantly in the positive control group than the model group (P ＜ 0.05-0.01 ). ③SOD activity of myocardial tissues: It was markedly lower in the model group than the sham operation group after 60-minute myocardialischemia and reperfusion (P ＜ 0.01); It was dramatically higher than in the 1 and 2 mg/kg nitidine chloride groups than the model group (P ＜ 0.01). The activity also increased with the increase of nitidine chloride. ④MDA content of myocardial tissues: It was distinctly higher in the model group than the sham operation group after myocardial ischemia reperftsion for 60 minutes (P ＜ 0.01). It was remarkably lower in the 1 and 2 mg/kg nitidine chloride groups than the model group (P ＜ 0.01). The content decreased with the increase of nitidine chloride. It was obviously lower in the positive control group than the model group (P ＜ 0.05 ).CONCLUSION: ①1 and 2 mg/kg nitidine chloride can reduce the incidence rate of cardiac arrhythmia in rats with myocardial ischemia and reperfusion, postpone the emergence time of cardiac arrhythmia and shorten its duration, decrease the degree of ST segment elevation after reperfusion for 15 minutes and 60 minutes, which have similar effect with verapamil.② 1 and 2 mg/kg nitidine chloride can reduce the release of myocardial enzyme, relieve the severity of oxygen-derived free radicals injury, and has the effect of protecting myocardial injury during ischemia-reperfusion, in which represents a dose-dependent effect.

Objective To explore the protective effect of thyroxin on severe traumatic brain injury of brain tissue by observing the effect of thyroxin on neuronal apoptosis,serum neuronal specific enolase(NSE),interleukin-6 (IL-6) and serum FT3 and FT4.Methods A total of 90 SD rats was randomly divided into control group,model group,low dosage of levothyroxine sodium tablets group,moderate dosage of levothyroxine sodium tablets group and high dosage of levothyroxine sodium tablets group,18 rats in each group.The animal model was reproduced by referring to Feeney's free fall impact modeling.Intragastric administration was performed at 6 h after injury.The levels of neuronal apoptosis and serum NSE,IL-6,FT3 and FT4 were detected by TUNEL method,ELISA method and radioimmunoassay at 24,72,168 h after intragastric administration.Results (1) After severe traumatic brain injury,the levels of serum FT3 and FT4 were under the normal and the level of FT4 was decreased to the lowest at 168 h.Thyroxine could increase the levels of FT3 and FT4.(2) Significant neuronal apoptosis was observed in rats with severe craniocerebral injury,and the apoptosis continued until 168 h.Moderate and high dose of thyroxine could improve neuronal apoptosis within 24 h,while low dose of thyroxine changed within 168 h.(3) The levels of serum NSE and IL-6 were increased significantly in rats after severe traumatic brain injury until 168 h,and they could be decreased by moderate and high dose of thyroxine within 72 h.Conclusion Exogenous thyroxine can protect brain tissue in rats with severe traumatic brain injury.

Objective:To explore the inconsistent and consistent classifications for lesions ≤2 cm by contrast-enhanced ultrasound(CEUS) Liver Imaging Reporting and Data System(LI-RADS) v2017 and contrast-enhanced computed tomography/contrast-enhanced magnetic resonance imaging(CECT/MRI) LI-RADS v2018.Methods:The focal liver lesions ≤2 cm underwent CEUS and CECT/MRI within 1 month were enrolled in this retrospective study.Each nodule was categorized according to the CEUS LI-RADS v2017 and CECT/MRI LI-RADS v2018. Intermodality agreement between the CEUS LI-RADS and CECT/MRI LI-RADS for each lesion was assessed with Cohen′s Kappa. Lesions with inconsistent classification for CEUS LI-RADS and CECT/MRI were analyzed.Results:A total of 145 lesions with a size of (1.65±0.33)cm in 145 patients were included. The numbers of lesions in LR-3, 4, 5 and M were 16, 23, 90 and 16 on CEUS LI-RADS, 25, 31, 87 and 2 on CECT/MRI, respectively. And 73.1% lesions were classified as LR-5 or M on CEUS, while 61.4% lesions were classified as LR-5 or M on CECT/MRI ( P=0.033). The incidences of HCC in LR-3, 4 and 5 were 37.5%, 52.2% and 97.8% on CEUS LI-RADS, 56.0%, 64.5% and 96.6% on CECT/MRI LI-RADS respectively. Among the 145 lesions, 56 lesions had inconsistent classifications of CEUS and CECT/MRI LI-RADS. Twenty-eight lesions in CECT/MRI LR-3 and 4 were escalated to LR-4 and 5 by CEUS and 82.1% of them were found to be HCC. Fourteen lesions on CEUS LR-3 and 4 were escalated to LR-4 and 5 by CECT/MRI and 85.7% of them were found to be HCC. Conclusions:The LR-5 of the CEUS and CECT/EOB-MRI LI-RADS has a comparable incidence of HCC. However, the inter-modality agreement of the LI-RADS category between CEUS and CECT/EOB-MRI is poor. The proportion of lesions in CEUS LR-5 and M is much higher than that in CECT/MRI LR-5 and M, while the proportion of lesions in CECT/MRI LR-3 and 4 is high than that in CEUS LR-3 and 4.