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作 者:黄新冲[1] 曾因明[1] 张育才[1] 王公明[1]
机构地区:[1]徐州医学院江苏省麻醉学重点实验室,江苏徐州221002
出 处:《徐州医学院学报》2001年第3期175-178,共4页Acta Academiae Medicinae Xuzhou
基 金:江苏省卫生厅资助课题! (H9711)
摘 要:目的 观察梯度复氧对离体大鼠全心缺血再灌注损伤的影响。方法 SD大鼠 32只 ,采用Langendorff模型 ,全心缺血 2 0min后再灌注 ,根据再灌注开始时K -H液中氧分压 6 10mmHg(1mmHg =0 .133kPa)、10 0mmHg、15 0mmHg、2 40mmHg随机分成对照组 (Con)、梯度复氧组 (T1、T2、T3组 ) ,从功能、代谢等指标观察梯度复氧对心肌缺血再灌注损伤的影响。结果 左室发展压 (LVDP)及左室收缩压力变化最大速率 (±dp/dtmax)的恢复率T1组均显著低于Con组相应时点 (P <0 .0 1) ,T2组于再灌注 10、2 0min时也显著低于Con组 (P <0 .0 5 )。再灌注末心肌中ATP的含量、Na+ -K+ 依赖式ATP酶活性T1组较Con组减少 (P <0 .0 1) ,T2组较Con组减少 (P <0 .0 5 ) ;Ca2 + 依赖式ATP酶的活性T1组较Con组减少 (P <0 .0 5 ) ;SOD活性T1、T2组都比Con组增高 (P <0 .0 5 ) ;MDA含量T1、T2组都显著低于Con组 (P <0 .0 1)。结论 在Langendorff离体大鼠全心灌注模型上 ,以 10 0mmHg氧分压的K -H液开始复灌尽管减少了氧自由基的生成 ,但因ATP含量减少、ATP酶活性下降 ,对大鼠急性缺血再灌注心脏无保护作用 ,反而加重再灌注损伤 ;心肌缺血再灌注损伤除了氧自由基参与外 ,还有其他机制参与。Objective To study the effects of gradual reoxygenation on ischemia/reperfusion injury in Langendorff model of isolated rat hearts. Methods 32 rat hearts were randomly divided into four groups according to the PO 2 of K-H perfusate administered after sustained ischemia:control (Con) group (PO 2 in K-H 610 mmHg) and T1, T2 and T3 groups (gradual reoxygenation with K-H of PO 2 beginning from 100, 150 and 240 mmHg respectively) (n=8 in each group). The LVDP, LVEDP and ±dp/dtmax were recorded at 20 min of equilibration perfusion and 5, 10, 20 and 30 min after reperfusion with MacLab/4s. The content of ATP, MDA and the activities of Ca 2+-ATPase, Na+-K+-ATPase and SOD in myocardium were assessed. Results In T1 group the recovery of LVDP and ±dp/dt max of myocardium during reperfusion was significantly less than that in Con group (P<0.01). The ATP content and the activities of Na+-K+-ATPase and Ca 2+-ATPase of myocardium in T1 group were lower than in Con group (P<0.01,P<0.01 and P<0.05 respectively). The ATP content and Na+-K+-ATPase activity of myocardium in T2 group were also lower than in Con group (P<0.05). The activity of myocardial SOD was higher in T1 and T2 groups than in Con group (P<0.01 and P<0.05), while the MDA content was significantly lower compared with that in Con group (P<0.01). Conclusions Although the production of MDA in myocardium was reduced and the activity of SOD was maintained at a higher level in T1 group, the reperfusion injury was still aggravated, which apparently should be associated with the reduction of ATP content and the decrease of Na+-K+-ATPase and Ca 2+-ATPase activities in myocardium.
关 键 词:全心缺血 再灌注损伤 离体大鼠 梯度复氧 氧自由基 心肌
分 类 号:R542.2[医药卫生—心血管疾病]
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