低压低氧预处理对加速度暴露大鼠心肌损伤的保护作用

目的从心肌抗氧化系统及一氧化氮（NO）代谢通路研究低压低氧预处理对加速度环境下心肌细胞病理生理变化的影响，解释航空加速度环境下心肌组织的损伤机制，探讨低压低氧预处理的保护机制。方法24只雄性SD大鼠随机分为3组（n=8），C组为空白对照组,HHP＋10Gz组为5000m高空低压低氧预处理4h／d连续4d后暴露10Gz加速度组，10Gz组为直接暴露10Gz加速度组，各组按上述处理后，取大鼠心肌组织，委托北京华英生物技术研究室检测超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH—PX）、谷胱甘肽（GSH）、丙二醛（MDA）、热休克蛋白-70（HSP-70）以及一氧化氮（NO）、亚硝酸盐（NO2-）、硝酸盐（NO3-）、内皮型一氧化氮合酶（eNOS）、诱导型一氧化氮合酶（iNOS）、神经型一氧化氮合酶（nNOS）的变化。结果SOD水平：C组[（8．242±1．562）U／mg]和HHP＋10Gz组[（7．660±1．208）U／mg]高于10Gz组[（4．773±0．665）U／mg]，差异均有统计学意义（均P〈0．05）；CAT水平：C组[（2．348±0．382）U／mg]高于HHP＋10Gz组[（1．955±0．204）U／mg]和10Gz组[（1．749±0．165）U／mg]，HHP＋10Gz组高于10Gz组，差异均有统计学意义（均P〈0．05）；GSH—PX水平：C组[（91．864±38．788）U／mg]高于10Gz组[（47．821±8．208）U／mg]，差异有统计学意义（P〈0．05）；GSH水平：C组[（0．748±0．182）μmol／g]和HHP＋10Gz组[（0．593±0．205）μmol／g]高于10Gz组[（0．232±0．034）μmol／g]，差异均有统计学意义（均P〈0．05）；MDA水平：各组间差异无统计学意义（P〉0．054）；HSP-70水平：C组[（1．415±0．500）ng／mg]低于HHP＋10Gz组[（2．189±0．659）ng／mg]和10Gz组[（2．452±0．926）ng／mg]，差异均有统计学意义（均P〈0．05）；NO水平：C组[（1．932±0．496）μmol/g]低于HHP＋10Gz组[（2．751±0．784）μmol／g]和10Gz组[（3．185±0．769）μmol／g]，差异均有统计学意义（均P〈0．05）；NO2-水平：C组[（1．277±0．279）μmol/g]低于HHP＋10Gz组[（1．800±0．568）μmol／g]和10Gz组[（1．970±0．362）μmol／g]，差异均有统计学意义（均P〈0．05）；NO3-水平：C组[（2．191±0．426）μmol／g]低于HHP＋10Gz组[（2．898±0．500）μmol／g]和10Gz组[（2．995±0．445）μmol／g]，差异均有统计学意义（均P〈0．05）；eNOS水平：C组[（3．726±0．498）U／mg]低于HHP＋10Gz组[（5．081±0．994）U／mg]和10Gz组[（5．937±1．423）U／mg]，差异均有统计学意义（均P〈0．05）；iNOS水平：C组[（3．66±0．379）U／mg]低于HHP＋10Gz组[（4．382±0．567）U／mg]U/mg]和Gz组[（4．986±1．318）U／mg]，差异均有统计学意义（均P〈0．05）；nNOS水平：C组[（0．830±．117）U／mg]低于HHP＋10Gz组[（1．044±0．190）U／mg]和10Gz组[（1．226±0．300）U／mg]，差异均有统计学意义（均P〈0．05）。结论低压低氧预处理可以降低加速度对心肌造成的氧化损伤，对心肌具有保护作用，其机制与低压低氧预处理增强了大鼠体内抗氧化酶活性．减轻氧化应激对NOS的激活从而抑制NO的大量释放有关。

Protection of hypobaric hypoxia preconditioning on myocardial injuries of rats after acceleration exposured

Objective To evaluate the effect of hypobaric hypoxia preconditioning （HHP） on myocardial ceils pathological physiology changes under acceleration environment from myocardial antioxidant system and NO metabolic pathways. To explain the mechanism of myocardial tissue damage by acceleration environment, explore the protection mechanism of HHP. Methods 24 male SD rats were randomly divided into 3 groups （n=8）, C group was the blank control group, HHP＋10 Gz group was 5000 m altitude hypoxic preconditioning 4 h/d for 4 days then exposure to 10 Gz acceleration, 10 Gz group was directly exposed to 10 Gz acceleration. After the treatment above, SOD, CAT, GSH-PX,GSH, MDA, HSP-70 and NO, NO2-, NO3- , eNOS, iNOS, nNOS content of the cardiac muscle tissue of rats weredetermined by Beijing Huaying Biotechnology Research Company. Results SOD level： group C [（8.242±1.562） U/mg] was higher than group 10 Gz [（4.773±0.665） U/mg], group HHP＋10 Gz [（7.660±1.208） U/mg] was higher than group 10 Gz, the differences were statistically significant （P 〈 0.05）. CAT level： group C [（2.348±0.382） U/mg] was higher than group HHP＋10Gz [（1.955±0.204） U/mg] and group 10 Gz [（1.749±0.165） U/mg], group HHP＋10 Gz was higher than group 10Gz, the differences were statistically significant （P 〈 0.05）. GSH-PX level： group C [（91.864±38.788） U/rag] was higher than group 10 Gz [（47.821±8.208） U/mg] , the differencs was statistically significant （P 〈 0.05）. GSH level： group C [（0.748±0.182）μmol/g] and group HHP＋10 Gz [（0.593±0.205） μmol/g] were higher than group 10 Gz [（0.232± 0.034）μmol/g], the differences were statistically significant （P 〈 0.05）. MDA level： there was no statistically significant differences （P 〉 0.05）. HSP-70 levis： group C [（1.415±0.500） ng/mg] was lower than group HHP＋10 Gz [（2.189±0.659） ng/mg] and group 10 Gz [（2.452±0.926） ng/mg], the differences were statistically significant （P 〈 0.05）. NO level： group C [（1.932±0.496） μmol/g] was lower than group HHP＋10 Gz [（2.751±0.784） μmol/g] and group 10 Gz [（3.185±0.769） μmol/g], the differences were statistically significant （P 〈 0.05）. NO2-level： group C [（1.277±0.279） μmol/g] was lower than group HHP＋10 Gz [（1.800-±0.568） μmol/g] and group 10 Gz [（1.970±0.362）μmol/g], the differences were statistically significant （P 〈 0.05）. NO3-level： group C [（2.191±0.426） μmol/g] was lower than group HHP＋10 Gz [（2.898±0.500）μmol/g] and group 10 Gz [（2.995±0.445） μmol/g], the differences were statistically significant （P 〈 0.05）. eNOS level： group C [（3.726±0.498） U/mg] was lower than group HHP＋10 Gz [（5.081±0.994） U/nag] and group 10 Gz [（5.937±1.423） U/mg], the differences were statistically significant （P 〈 0.05）. iNOS level： group C [（3.668±0.379） U/ mg] was lower than group HHP＋10 Gz [（4.382±0.567） U/nag] and group 10 Gz [（4.986±1.318） U/mg], the differences were statistically significant （P 〈 0.05）. nNOS level： group C [（0.830±0.117） U/mg] was lower than group HHP＋10 Gz [（1.044±0.190） U/mg] and group 10 Gz [（1.226±0.300） U/mg], the differences were statistically significant （P 〈 0.05）. Conclusion HHP can reduce oxidative damage of myocardial tissue caused by acceleration and has myocardial protective effect, the mechanism is related to enhancing the activity of antioxidant enzymes and reducing oxidative stress on the activation of NOS and then inhibiting the release of NO in rats.