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作 者:杨镒宇[1] 曾其毅[1] 洪婕[1] 陶建平[1] 张剑珲[1] 曾萍[1] 吴艳兰[1] 谢志伟[1]
出 处:《岭南急诊医学杂志》2007年第2期81-82,85,共3页Lingnan Journal of Emergency Medicine
基 金:广东省中医药局科研课题(1050064);广州市中医药中西医结合科研课题(2005A026);广东省卫生厅基金资助(A2001579);广东省自然科学基金资助(2000-261);广州市科技局科技攻关计划基金资助(2003Z2-E0181)
摘 要:目的:探讨儿科急性肺损伤(ALI)的病理生理和发病机制。方法:比较小儿ALI与呼吸功能正常儿的呼吸功能与炎症因子的变化。结果:(1)ALI患儿血气分析显示氧合或通气功能不同程度的恶化。氧合功能(PaO2/FiO2)下降有47例;指标PaCO2上升有27例。(2)机械通气所需气道峰压(PIP)和呼气末正压(PEEP)呈不同程度的上升,PIP上升26例,ALI患儿与呼吸功能正常儿为(28.62±6.38)cmH2O比(20.90±3.60)cmH2O,P<0.05;PEEP为(5.0±1.6)cmH2O比(2.0±0.6)cmH2O,P<0.01。(3)ALI患儿血清TNF-α较正常对照组升高,分别为(32.60±8.62)pg/mL和(8.54±3.04)pg/mL,P<0.001。结论:(1)ALI的肺病理生理变化特点除氧合功能下降或肺泡有效通气减少外,还有小气道阻力升高;(2)全身炎症反应可能参与小儿ALI。Objective: To investigate the pathophysiology and pathogeneses of pediatrics acute lung injury (ALI). Methods: To compare the differences of the pulmonary function and inflammatory factor between pediatric patients with ALI and cases with normal pulmonary function. Results: (1)The blood gases analysis in pediatric patients with ALI revealed deteriorative oxygenation and ventilation in different levels, There were 47 cases with decreased PaO/FiO2, while there were 27 with increased PaCO2. (2)There were 26 cases with increased peak inspiratory pressure during mechanical ventilation, which valve compared with control group was (28.62±6.38)cmH2O vs. (20.90±3.60)cmH2O, P 〈 0.05, while the positive expiratory ending pressure compared with control group was (5.0±1.6)cmH2O vs. (2.0±0.6) cmH2O,P 〈 0.01. (3)There was an increased serum concentration of TNF-α compared to normal children, which was (32.60±8.62)μg/mL vs, (8.54±3.04)μg/mL,P〈0,001, Conclusions: (1)The pulmonary pathophysiology of ALI indicates either increased resistance of small airway, or decreased oxygenation and effective alveolar ventilation, (2)The systemic inflammatory response may induce pediatrics ALI.
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