【摘要】 目的 :探讨异丙酚对肺缺血 -再灌注损伤 (PIRI)时蛋白激酶C基因表达的影响。方法 :采用在体兔单肺原位缺血 -再灌注模型。实验兔 2 7只 ,随机均分为假手术对照组 (sham)、肺缺血 -再灌注组 (I-R)和肺缺血 -再灌注加异丙酚治疗组 (PPF)。再灌注 6 0min时取肺组织 ,观察蛋白激酶C(PKC)mRNA定位表达、超氧化物歧化酶(SOD)活性、丙二醛 (MDA)浓度、一氧化氮 (NO)含量、肺组织湿干重比 (W/D)、肺损伤组织学定量评价指标 (IQA)及光镜、电镜下的组织形态学改变。结果 :肺再灌注 6 0min ,PPF组PKCmRNA在肺小动脉内膜、外膜及薄壁小血管 (主要是肺小静脉 )强阳性表达 ,其吸光度值与sham组及I-R组比较有显著差异 (P <0 0 5和P <0 0 1) ;SOD活性明显高于I-R组 (均P <0 0 1) ;MDA浓度、W/D和IQA值显著低于I-R组 (P <0 0 1和P <0 0 5 ) ;肺组织形态学异常改变不同程度减轻。结论 :异丙酚可上调肺组织PKC -α、δ、θmRNA的表达 ,而提高体内NO水平、降低氧自由基水平、减轻脂质过氧化反应 ,对PIRI发挥积极的防护作用。更多还原

【Abstract】 AIM: To investigate the effect of propofol on expression of protein kinase C (PKC) mRNA during pulmonary ischemia and reperfusion injury (PIRI) in rabbits. METHODS: Single lung ischemia and reperfusion animal model was used in vivo. The rabbits were randomly divided into three groups ( n =9 in each): sham operated group (sham), PIR group (I-R) and PIR+ propofol group (PPF). Changes of several parameters including malondialdehyde (MDA), superoxide dismutase (SOD), wet to dry ratio of lung tissue weight (W/D) and index of quantitative assessment of histologic lung injury (IQA) were measured at 60 minutes after reperfusion in lung tissue. Meanwhile the location and expression of PKC mRNA were observed. Lung tissue was also prepared for light microscopic and electron microscopic observation at 60 minutes after reperfusion. RESULTS: As compared with group I-R, PKC mRNA strongly expressed in intima and extima of small pulmonary artery as well as thin-wall vessels (mostly small pulmonary veins) in PPF group. The average optical density values of PKC-α、δ and θ mRNA in small pulmonary veins PPF in group showed significantly higher than that in I-R group (all P <0 01). SOD increased and MDA, W/D and IQA decreased at 60 minutes after reperfusion in lung tissue ( P <0 01 and P< 0 05). Abnormal changes of the lung tissue in morphology were lessen markedly in PPF group. CONCLUSIONS: Propofol produces notable protective effects on PIRI in rabbits by activating PKC-α, δ and θ mRNA expression in lung tissue, raising NO level, dropping OFR level and decreasing lipid peroxidation.更多还原