目的 為貫徹落實衛生部《醫院感染管理辦法》、《抗菌藥物合理應用指導原則》，了解成都三六三醫院醫院感染的現狀，對醫院感染控制工作進行評價，提高醫務人員的感染控制意識。 方法 制定統一調查方案與措施，逐一查看2011年9月21日全院住院患者在架病歷，對全院住院患者通過床旁詢問和體檢的方式進行調查。 結果 全院共有住院患者621例，實查621例，實查率100%。發生醫院感染19例，現患率為3.06%。抗生素使用率46.38%。病原學送檢率21.88%。 結論 加強醫務人員醫院感染知識的培訓是提高其醫院感染防控意識的重要手段；提高感染患者病原學送檢率，減少經驗性用藥，依據藥敏結果合理使用抗生素，達到有效減少耐藥菌產生的目的。
Objective To investigate the relationship between the expression of hypoxia inducible factor 1α (HIF-1α) and the neuron apoptosis during a hypoxia ischemia brain damage and explore the role of HIF1α in regulating the neuron apoptosis and repairing the brain damaged by hypoxia and ischemia. Methods Forty SD rats aged 10 days were randomly divided into the experiment group and the control group, with 20 rats in each group. In the experimental group, the rats were anesthetized with ethylether. The right common carotid artery was exposed and ligated. Then, they were exposed to hypoxia ina normobaric chamber filled with 8% oxygen and 92% nitrogen for 2.5 hours. In the control group, the right common carotid artery was exposed but was not ligated or exposed to hypoxia. The brain tissues were harvested from the rats in the both groups at 4, 8, 24, 48 and 72 hours after the hypoxia and ischemia, and fromthe rats in the control group at the same time points. The HIF-1α protein expression and the cleaved caspase 3 (CC3) protein expression were detected with the immunohistochemistry method. The apoptosis cells were detected with the TUNEL staining method. Results In the experimental group, the HIF-1α expression was significantly increased at 4 hours after operation, at the peak level at 8 hours, and began to decrease at 24 hours. The CC3 protein was expressed at 4 hours after operation, and was slightly expressed at 8 hours, but was significantly increased at 24 hours; the higher levels were maintained at 48 and 72 hours. However, in the control group, both the expression levels of HIF-1α and the CC3 protein were extremely low. So, the expression levels of HIF-1α andthe CC3 protein were significantly higher in the experimental group than in the control group (P＜0.01). The TUNEL staining showed that in the experimentalgroup the positive cells were significantly increased after the hypoxia and ischemia, with a peak level at 72 hours after the hypoxia and ischemia; however, in the control group there were few positive cells.TUNEL positive cells in the experimental group were significantly more than that in the control group(P＜0.01).ConclusionThe expression tendency of HIF-1α is completely different from that of CC3.HIF-1α may have a protective role in regulating the neuron apoptosis in the neonatal hypoxia-ischemia brain damage and may promote the repairing and rebuilding process in the brain that was damaged by hypoxia and ischemia.
Objective To investigate the expression of hypoxia inducible factor 1α (HIF-1α) protein and the activation of phosphoinositid 3-kinase/Akt (PI3K/Akt) signal ing pathway in neurons under hypoxia ischemia condition,and to elucidate the role of PI3K/Akt on HIF-1α regulation in the developing neurons after hypoxia ischemia brain damage(HIBD). Methods Fifty-six SD rats aged 10 days were randomly divided into normal control group (n=12), sham operationgroup (n=12), experimental group (n=24), wortmannin treated group (n=4) and DMSO/PBS treated group (n=4). In theexperimental group, the rats were anesthetized with ethylether. The right common carotid artery was exposed and l igated. Then, they were exposed to hypoxia in a normobaric chamber filled with 8% oxygen and 92% nitrogen for 2.5 hours. In the sham control group, the right common carotid artery was exposed but was not l igated or exposed hypoxia. In the normal control group, the rats recevied no further processing. For wortmannin treated group and DMSO/PBS treated group, the rats received intraventricular injection of wortmannin or DMSO/PBS 30 minutes before hypoxia ischemia. The brain tissues were harvested from the rats in the normal control, sham operation and experimental groups at 4, 8 and 24 hours after hypoxia ischemia, but in the wortmannin and DMSO/PBS treated groups only at 4 hours. The HIF-1α protein expression and Akt protein expression were detected with immunohistochemistry method. HIF-1α, Akt and p-Akt protein expression were measured by Western blot analysis. Results In the experimental group, the HIF-1α expression was significantly increased at 4 hours after operation, reached the peak level at 8 hours, and began to decrease at 24 hours. The p-Akt protein was significantly increased at 4 hours, and began to decrease at 8 hours. However, the expression levels of HIF-1α and p-Akt protein in the normal control group were extremely low at each time point. So, the expression levels of HIF-1α in the experimental group was significantly higher than that in the normal control groups (P lt; 0.01), the expression of p-Akt protein in the experimental group at 4 and 8 hours was significant higher than that in the normal control group (P lt; 0.05). The change of Akt protein in the experimental group was not time-dependent, and no significant difference was evident when compared with that of the normal control group (P gt; 0.05). Using wortmannin, the PI3K/Akt specific inhibitor, HIF-1α protein expression was significantly decreased when compared with the DMSO/PBS treated group and experimental group (P lt; 0.01). Conclusion These results suggested that the HIBD of neonatal rats may activate PI3K/Akt signal ing pathway and further induce the expression of HIF-1α, indicating PI3K/Akt signal ing pathway and HIF-1α could be a potential target for treatment of neonatal HIBD.
目的 觀察右美托咪啶復合丙泊酚靶控靜脈麻醉在纖維支氣管鏡檢查術中的麻醉效果。 方法 2010年12月－2012年4月，將60例行纖維支氣管鏡檢查術的患者隨機分為丙泊酚麻醉組（對照組）和右美托咪啶復合丙泊酚麻醉組（觀察組），每組各30例。觀察記錄不同時點平均動脈壓（MAP）、心率、呼吸次數（RR）、脈搏血氧飽和度（SpO2），鎮靜評分、手術時間、蘇醒時間、丙泊酚總用量、不良反應發生率及患者滿意度。 結果 所有患者均能順利完成操作，誘導入睡后觀察組MAP、心率下降（P＜0.05），丙泊酚總用量、不良反應發生率均少于對照組（P＜0.05），鎮靜評分優于對照組（P＜0.05）；兩組RR、SpO2、蘇醒時間、手術時間及患者滿意度差異無統計學意義（P＞0.05）。 結論 右美托咪定復合丙泊酚靶控輸注適用于纖維支氣管鏡檢查術麻醉，是一種更加安全有效的麻醉方法。