Publications (2)0 Total impact
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ABSTRACT: Dexmedetomidine and midazolam have been widely used in clinical anesthesia and intensive care unit sedation. These two drugs differ in sedative mechanism. We hypothesized that the neurotoxicity of repeated exposure to dexmedetomidine or midazolam for neonatal mice might be different. Twenty four mice of postnatal day 8 were randomly divided into control (n=8), dexmedetomidine (n=8) and midazolam group (n=8) respectively. In the three groups, saline(10mL/kg), dexmedetomidine(10microg/kg) or midazolam(40mg/kg) was injected intraperitoneally once a day, in the next five days, respectively. Then the brains of the mice in the three qroups were removed and cryosectioned. Apoptotic neural cell in hippocampus region was detected with terminal deoxynucleotydyl transferase -mediated dUTP nick end labeling(TUNEL). Bcl2 and Bax protein expression level in the hippocampus were determined by immunofluorescent staining. In the present study, the number of TUNEL-positive cells from midazolam group ((20 +/-3) /mm2) was larger than that from dexmedetomidine group ((15+/-2) /mm2, P<0. 05) and control group((13+/-3) /mm2, P<0. 05); Bcl-2 protein quantity in hippocampus from control group((790+/-103)/mm2)was significantly lower than that in midazolam group((1187+/- 162)/mm2, P<0.05)and dexmedetomidine group((890+/-125)/mm2, P<0. 05). Bax protein level in control group((942+/-104)/mm2) was also significantly lower than that in midazolam group((1839+/-160)/mm2, P<0. 05)and dexmedetomidine group((1143+/-125)/mm2, P<0. 05); Bax/Bcl-2 ratio in midazolam group(0. 64+/-0. 13) was significantly lower than that in dexmedetomidine group(0. 78 +/-0. 14, P<0. 05) and control group(0. 84+/-0. 15, P<0. 05). Our results suggest that dexmedetomidine has lower neurotoxicity than midazolam for neonatal mice.Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi 06/2013; 30(3):607-10.
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ABSTRACT: The maintenance of the balance between oxygen supply and oxygen consumption is a key measure in preventing acute kidney hypoxic/reoxygenation injury. Morphine can inhibit metabolism and reduce the oxygen consumption. We tried to investigate the protective effects of morphine hypoxic preconditioning on acute kidney hypoxic/reoxygenation injury in rabbit and its influence on expression of caspase-3 protein. Kidney hypoxic and reoxygenation were induced by making the tested rabbits inhale 8% oxygen for three hours firstly, and then putting them in the air to breathe in normal oxygen for another three hours. Morphine hypoxic preconditioning was induced by administering morphine 3 mg/kg, and then hypoxic of 8% oxygen was induced. Caspase-3 protein expression in renal tissue was assessed by immunohistochemical method. In the present study, the expressions of caspase-3 protein were significantly higher in saline-control hypoxic group than in morphine hypoxic preconditioning group ((29.3+/-5.7)% vs. (12.16+1.23)%, P<0.05). These observations suggested that morphine hypoxic preconditioning can protect rabbit against acute kidney hypoxic/reoxygenation injury by decreasing expression of caspase-3 protein.Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi 06/2011; 28(3):531-3.