山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2015年
6期
1-3
,共3页
刘雪聪%刘福林%李志林%周晓东%申文增%周程
劉雪聰%劉福林%李誌林%週曉東%申文增%週程
류설총%류복림%리지림%주효동%신문증%주정
心肌缺血再灌注损伤%氢气饱和生理盐水%丙二醛%超氧化物歧化酶
心肌缺血再灌註損傷%氫氣飽和生理鹽水%丙二醛%超氧化物歧化酶
심기결혈재관주손상%경기포화생리염수%병이철%초양화물기화매
myocardial ischemia reperfusion injury%hydrogen-rich saline%malondialdehgde%superoxide dismutase
目的:探讨氢气对心肌缺血再灌注( I/R )损伤的保护作用。方法将48只大鼠随机分为实验组和对照组各24只。取两组大鼠心脏,按逆灌注10 min,常温旷置20 min、再灌注20 min的方法建立心肌缺血再灌注模型。对照组灌注液用K-R液,实验组灌注液用K-R液+氢气饱和生理盐水。监测两组大鼠心脏缺血前期、缺血期、再灌注期心肌组织丙二醛(MDA)、超氧化物歧化酶(SOD)水平及左室舒张末期压力(LVEDP)。结果对照组缺血期心肌MDA水平高于缺血前期(P<0.05),再灌注期心肌MDA水平低于缺血期(P<0.05),但仍高于缺血前期(P<0.05)。实验组各期心肌MDA水平无统计学差异;缺血期、再灌注期心肌MDA水平较对照组同期下降(P均<0.05)。两组缺血期与缺血前期心肌SOD水平无统计学差异,缺血再灌注期心肌SOD水平低于缺血前期和缺血期(P均<0.05)。实验组缺血期与再灌注期心肌SOD水平较对照组同期升高(P均<0.05)。对照组再灌注期LVEDP高于缺血前期(P<0.05);实验组再灌注期与缺血前期LVEDP无统计学差异,但与对照组同期比较下降明显(P<0.05)。结论氢气对大鼠离体心脏心肌I/R损伤有明显的保护作用。其机制可能为抑制心肌组织MDA表达,提高心肌组织SOD水平。
目的:探討氫氣對心肌缺血再灌註( I/R )損傷的保護作用。方法將48隻大鼠隨機分為實驗組和對照組各24隻。取兩組大鼠心髒,按逆灌註10 min,常溫曠置20 min、再灌註20 min的方法建立心肌缺血再灌註模型。對照組灌註液用K-R液,實驗組灌註液用K-R液+氫氣飽和生理鹽水。鑑測兩組大鼠心髒缺血前期、缺血期、再灌註期心肌組織丙二醛(MDA)、超氧化物歧化酶(SOD)水平及左室舒張末期壓力(LVEDP)。結果對照組缺血期心肌MDA水平高于缺血前期(P<0.05),再灌註期心肌MDA水平低于缺血期(P<0.05),但仍高于缺血前期(P<0.05)。實驗組各期心肌MDA水平無統計學差異;缺血期、再灌註期心肌MDA水平較對照組同期下降(P均<0.05)。兩組缺血期與缺血前期心肌SOD水平無統計學差異,缺血再灌註期心肌SOD水平低于缺血前期和缺血期(P均<0.05)。實驗組缺血期與再灌註期心肌SOD水平較對照組同期升高(P均<0.05)。對照組再灌註期LVEDP高于缺血前期(P<0.05);實驗組再灌註期與缺血前期LVEDP無統計學差異,但與對照組同期比較下降明顯(P<0.05)。結論氫氣對大鼠離體心髒心肌I/R損傷有明顯的保護作用。其機製可能為抑製心肌組織MDA錶達,提高心肌組織SOD水平。
목적:탐토경기대심기결혈재관주( I/R )손상적보호작용。방법장48지대서수궤분위실험조화대조조각24지。취량조대서심장,안역관주10 min,상온광치20 min、재관주20 min적방법건립심기결혈재관주모형。대조조관주액용K-R액,실험조관주액용K-R액+경기포화생리염수。감측량조대서심장결혈전기、결혈기、재관주기심기조직병이철(MDA)、초양화물기화매(SOD)수평급좌실서장말기압력(LVEDP)。결과대조조결혈기심기MDA수평고우결혈전기(P<0.05),재관주기심기MDA수평저우결혈기(P<0.05),단잉고우결혈전기(P<0.05)。실험조각기심기MDA수평무통계학차이;결혈기、재관주기심기MDA수평교대조조동기하강(P균<0.05)。량조결혈기여결혈전기심기SOD수평무통계학차이,결혈재관주기심기SOD수평저우결혈전기화결혈기(P균<0.05)。실험조결혈기여재관주기심기SOD수평교대조조동기승고(P균<0.05)。대조조재관주기LVEDP고우결혈전기(P<0.05);실험조재관주기여결혈전기LVEDP무통계학차이,단여대조조동기비교하강명현(P<0.05)。결론경기대대서리체심장심기I/R손상유명현적보호작용。기궤제가능위억제심기조직MDA표체,제고심기조직SOD수평。
Objective To explore the protective effects of hydrogen saturated saline in induced myocardial ischemia reperfusion injury in rats .Methods Forty-eight rats were divided randomly into the experimental group (24) and the con-trol group (24).The rats of experimental group were treated with K-R solution combined with hydrogen saturated saline , the controls were given K-R solution only .After the treatment , the hearts were excised rats and Langendorff model .And the heart of the in vitro by inverse perfusion for 10 minutes, normal temperature place for 20 minutes, 20 minutes of reper-fusion.The solution of the cardiac muscle tissue of the rats were treated with saline and then the accounts of malondialde -hyde (MDA)and the activity of superoxide dismutase (SOD) , and the changes of left ventricular end-diastolic pressure ( LVEDP) were determined to compare the different protective effects .Results The accounts of MDA in the control group were the highest , there was a significant difference between the experimental group and the controls concerning with the re -sults of ischemia period and reperfusion period (P<0.01, P<0.05).There were differences among the ischemia period and reperfusion period and preischemia period in the control group (P<0.05).In the experimental group, there was not significant difference among the ischemia period and reperfusion period and the preischemia period .There was a significant difference between the experimental group and the controls considering the activity of SOD (P<0.01).The accounts of LVEDP of the control group was obviously high (P<0.05).The level of LVEDP in experimental group was obviously lower than in the control group (P<0.05),but had no significant difference to ischemia period .Conclusion Hydrogen rich sa-line is quite effective in alleviating myocardial ischemia reperfusion injury .