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Objective:To explore the application of computer simulation teaching based on GasMan @ software in anesthesiology standardized nursing training. Methods:Thirty-six anesthesia nurses undergoing standardized training were selected as research objects. They were randomly divided into the traditional teaching group (group C) and the computer simulation teaching based on GasMan @ software group (group G), with 18 nurses in each group. All the nurses received the theory test before and after the training, and the practical operation assessment and the teaching satisfaction survey were conducted after the training. SPSS 17.0 was used for independent-samples t test and chi-square test. Results:There was no significant difference in the theoretical test scores of the anesthesia nurses before class between the two groups ( P > 0.05); the theoretical test, practical performance and satisfaction survey of group G were significantly better than those of group C, with statistical significance ( P < 0.05). Conclusion:Computer simulation teaching based on GasMan @ software is in favor of the anesthesia nurse to learn and master the relevant theory of inhalation general anesthesia, especially to improve practical skills.
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Objective To investigate the effect of dexmedetomidine on minimum alveolar concentration (MAC) of isoflurane required to inhibit the body movement during skin incision. Methods Forty-eight ASA Ⅰ or Ⅱ patients aged 40-60 yr with body mass index of 22-27 kg/m2 undergoing elective upper abdominal surgery under general anesthesia were randomly divided into 3 groups: control group (group C, n = 15);low dose dexmedetomidine group (group D1, n = 17) and high dose dexmedetomidine group (group D2, n = 16). The patients were unpremedicated. Dexmedetomidine 0.4 and 0.8 μg/kg in normal saline (NS) 15 ml was infused over 15 min before induction of anesthesia in D1 and D2 groups respectively. Anesthesia was induced with fentanyl-propofol-succinylcholine. The patients were mechanically ventilated after tracheal intubation. Anesthesia was maintained with isoflurane. MAC of isoflurane was determined by up-and-down technique. The initial end-tidal isofiurane concentration was set at 1.0%, 0.8% and 0.6% in C, D1 and D2 groups respectively. Each time the end-tidal isoflurane concentration was increased/decreased by 0.2%. Skin incision was made after 15 min of equilibration, when the twitch height returned to more than 90% of its control value. Movement of body and limbs including swallowing and coughing were carefully looked for when skin incision was made. MAC of isoflurane was the mean of end-tidal concentration of isoflurane of each crossover pair, and 95 % CI was calculated. Results MAC of isoflurane was significantly decreased in D1 and D2 groups as compared with group C and in group D2 as compared with group D1( P ＜ 0.05 or 0.01 ). Conclusion Dexmedetomidine can significantly decrease MAC of isoflurane required to inhibit the body movement during skin incision in a dose-dependent manner.
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Objective To investigate the effect of nicorandil pretreatment on myocardial mitochondria in a rabbit model of myocardial ischemia-reperfusion (I/R). Methods Tirty-two healthy male New Zealand white rabbits weighing 2.0-2.5 kg aged 4 months were randomly allocated into 4 groups ( n = 8 each): Ⅰ group sham operation (group S); Ⅱ group I/R; Ⅲ group nicorandil pretreatment (group N) and Ⅳ group nicorandil + 5 hydroxydecanoic acid (group N + 5-HD). Myocardial I/R was induced by 30 min occlusion of left circumflex coronary artery followed by 120 min reperfusion. In group N and N + 5-HD a bolus of nicorandil 100 μg/kg was given iv at 10 min before myocardial ischemia followed by continuous infusion at 10 μg· kg-1 · min-1 until the beginning of myocardial ischemia. In group Ⅳ a bolus of 5-HD 5 mg/kg was injected iv at 20 min before myocardial ischemia.The animals were sacrificed at the end of 120 min reperfusion. The mitochondrial membrane potential was measured by flow cytometry using JC-1 fluorescence probe as indicator. Bcl-2, Bax and cytochrome c protein expression was determined by immuno-histochemistry. Myocardial ultrastructure was examined with transmission electron microscope. Results Red fluovescence intensity indicating normal live cells was significantly higher, the green fluorescence intensity indicating apoptotic cells was lower and red/green fluorescence intensity ratio was higher; the Bcl-2/Bax ratio was significantly higher and cytochrome c protein expression lower in group N than in group I/R.5-HD administration negated the protective effect of nicorandil pretreatment against myocardial I/R injury. Conclusion Nicorandil stabilizes mitochondrial membrane potential, decreases cytochrome c protein releasing, and suppresses mitochondrial apoptotic signal transduction by opening the mito-KATP channels.
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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.