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作 者:杨丽丽[1] 刘志[1] 戢新平[1] 刘刚[2] 关福兰[3]
机构地区:[1]中国医科大学第一临床学院急诊科,辽宁沈阳110001 [2]中国医科大学呼吸疾病研究所,辽宁沈阳110001 [3]中国医科大学药理学教研室,辽宁沈阳110001
出 处:《中国病理生理杂志》2004年第6期1057-1061,共5页Chinese Journal of Pathophysiology
基 金:辽宁省教育厅高等学校科学研究项目 (No .2 0 2 0 1315 2 )
摘 要:目的 :探讨高碳酸血症对急性肺损伤 (ALI)动物模型是否具有拮抗作用 ,并从氧化 /抗氧化失衡、细胞凋亡等方面探求其可能的机制。方法 :2 2只新西兰兔随机分为对照组 (C组 )、非高CO2 通气组 (N组 )、高CO2 (8% )通气组 (H组 )。采用油酸静脉注射复制肺损伤模型。观察 3组肺力学、血气指标的变化 ,检测肺组织丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活性 ,观察肺组织细胞凋亡情况。结果 :(1)肺力学指标的变化 :气道峰压H组显著低于N组 ,动态胸肺顺应性显著高于N组。 (2 )动脉血氧分压H组明显高于N组。 (3)肺组织中MDA含量H组明显低于N组 ,SOD活性H组明显高于N组。 (4 )细胞凋亡指数H组明显低于N组。 (5 )H组病理组织学改变明显轻于N组。 (6 )相关分析表明PaCO2 与pH的相关性最明显 ,与PaO2 、动态顺应性均呈正相关 ,与气道峰压、肺通透指数呈负相关。结论 :机械通气时吸入 8%的CO2 所致高碳酸血症对ALI动物肺有保护作用 ,其机制可能与增强了肺组织抗氧化能力 ,减轻脂质过氧化损伤 ,减少细胞凋亡有关。AIM: To investigate whether hypercapnia is protective against acute lung injury (ALI) in a rabbit model, and study it's potential mechanisms. METHODS: Twenty-two healthy New Zealand white rabbits were involved in this study, and randomly allocated to control group (group C), normocapnic group (group N) and hypercapnic group (group H). Oleic acid (0 1 mL/kg) was injected intravenously to establish ALI model. Lung mechanics, hemodynamics, blood-gas analysis, the content of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in lung tissue were measured. Apoptosis was analyzed after 3h mechanical ventilation. RESULTS: (1) Peak airway pressure in group H was significantly lower than that in group N (P<0 05) and the dynamic lung compliance was significantly higher than that in group N (P<0 05). (2) PaO 2 in group H was significantly higher than that in group N(P<0 05). (3) The content of MDA was significantly lower but the activity of SOD was significantly higher in group H than that in group N (P<0 05). (4) Apoptosis index in group H was significantly lower than that in group N (P<0 01). (5) Histologic damage was significantly severer in group N than group H. (6) PaCO 2 was correlated with pH, PaO 2, dynamic lung compliance, peak airway pressure and pulmonary permeability index (r=-0 928, P<0 01; r=0 511, 0 526, -0 506, -0 556, P<0 05, respectively). CONCLUSION: Hypercapnia protects lung from oleic acid-induced injury in rabbits. The mechanisms of protection might be associated with improvement of oxidation/anti-oxidation imbalance and inhibition of apoptosis.
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