血管内皮细胞在氧自由基所致肺内动脉收缩反应中的作用

应用生物测定法观察黄嘌呤(X)-黄嘌呤氧化酶(XO)系统产生的氧自由基对正常、缺氧(5000m,10d)Wistar大鼠肺内动脉环张力的影响及内皮细胞在其中的作用。发现XO在一定浓度范围内产生的氧自由基可引起肺内动脉剂量依赖性收缩。正常鼠肺内动脉去内皮或加内皮舒张因子 (EDRF) 灭活剂后,此剂量依赖性收缩明显增强。慢性缺氧大鼠肺内动脉无论内皮完整与否,上述收缩反应均增强。提示缺氧使内皮细胞和(或)EDRF的功能受到损害。应用超氧化物歧化酶(铜锌SOD),在正常或缺氧鼠肺内动脉上可分别加强或恢复内皮细胞抑制氧自由基的缩血管作用。提示慢性缺氧时,内皮细胞和(或)EDRF受到超氧阴离子的严重破坏,这一机制可能在缺氧性肺动脉高压的形成中起重要作用。     

抗氧化剂丹酚酸A对缺氧鼠肺内动脉ACh舒张反应的影响

应用微量生物测定法观察了丹酚酸A(salvinolic acid A,Sal.A)对慢性缺氧(5000m,10d)大鼠(200～300g)肺内动脉ACh舒张反应的影响,并对其机制进行了初步探讨。实验发现,慢性缺氧可明显减弱大鼠肺内动脉ACh(10~(-8)～10~(-4)mol/L)舒张反应(P<0.01～0.001),在浴槽内先加入Sal.A(10~(-4)mol/L),缺氧鼠肺内动脉ACh舒张反应明显增强(P<0.01),而在浴槽内同时加入血管内皮舒张因子(EDRF)灭活剂phenidon(5×10~(-5)mol/L),则Sal.A上述增强缺氧鼠肺内动脉ACh舒张反应的作用消失。此外,本实验还发现,在以黄嘌呤(X,10~(-4)mol/ L)-黄嘌呤氧化酶(XO,0.01U/ml)系统产生氧自由基损伤正常大鼠肺内动脉ACh舒张反应的基础上,Sal.A(10~(-4)mol/L)同样可明显减弱氧自由基对大鼠肺内动脉ACh舒张反应的损伤作用。结果表明,Sal.A可消除氧自由基对肺血管内皮细胞释放的EDRF的破坏作用而具有保护慢性缺氧鼠肺内动脉ACh舒张反应的作用。     

急性缺氧所致大鼠肺动脉内皮依赖性收缩反应

本实验初步证实,急性缺氧可使大鼠肺动脉产生内皮衍生收缩因子,并对其性质作了初步探讨。急性缺氧可使离体大鼠肺内和肺外动脉产生收缩反应,当灌流液氧分压从约17.3kPa降低到4kPa时(pH7.40～7.48),肺内和肺外动脉的基础张力分别比原来静息张力增加了37.5±5.1mg(n=4)和33.2±1.9mg(n=6);当氧分压恢复到约17.3kPa时,肺动脉基础张力也降到缺氧前的静息张力水平,即肺内动脉约300mg,肺外动脉约400mg。去掉内皮细胞后,急性缺氧引起的肺动脉收缩反应消失。消炎痛、去甲二氢愈创木脂酸、阿托品和酚妥拉明均不能阻断急性缺氧所致大鼠肺动脉内皮依赖性收缩反应。急性缺氧可诱发大鼠肺动脉内皮细胞产生释放非花生四烯酸环氧酶和脂氧酶代谢产物的内皮衍生收缩因子。     

慢性缺氧对肺动脉内皮依赖性和非内皮依赖性舒张反应的影响

本实验用生物测定法观察了模拟海拔5000m高度连续缺氧20d对大鼠肺动脉内皮依赖性和非内皮依赖性舒张反应的影响。结果显示慢性缺氧明显抑制了肺内和肺外动脉对乙酰胆碱、ATP、硝普钠和异丙肾上腺素舒张反应的敏感性和反应性。在浓度为10~(-6)mol/L时,缺氧组大鼠肺内动脉对乙酰胆碱、硝普钠和异丙肾上腺素的舒张反应分别只有对照组大鼠的61.3％、75.9％和61.7％,对浓度为1.8×10~(-5)mol/L的ATP的舒张反应只有对照组大鼠的64.9％。研究表明,ATP和乙酰胆碱主要是通过内皮舒张因子使肺动脉产生内皮依赖性舒张反应,硝普钠和异丙肾上腺素分别通过直接激活血管平滑肌细胞鸟苷酸环化酶和β受体使血管产生非内皮依赖性舒张反应。缺氧同时抑制了肺动脉内皮依赖性和非内皮依赖性舒张反应,提示慢性缺氧可能抑制了正常肺内舒血管活性物质的生理作用。     

慢性缺氧对大鼠肺动脉内皮依赖性舒张反应及cGMP含量的影响

本实验观察了慢性缺氧对大鼠肺动脉内皮依赖性舒张反应和肺动脉内环磷酸鸟苷(cGMP)含量的影响。乙酰胆碱(ACh)和三磷酸腺苷(ATP)可使正常大鼠的离体肺动脉产生内皮依赖性舒张反应,其舒张作用不受消炎痛的影响,但被甲烯蓝完全抑制。慢性缺氧明显减低了 ACh 和 ATP 诱发的大鼠肺内和肺外动脉的内皮依赖性舒张反应。当 ACh 浓度为10~(-6)mol/L 时,缺氧组大鼠肺内和肺外动脉舒张百分数分别为对照组的61.3%和59.2%;当 ATP浓度为1.8×10~(-5)mol/L 时,缺氧组大鼠肺内和肺外动脉舒张反应分別为对照组的64.9%和55.3%。慢性缺氧也减低了硝普钠(SNP)诱发的大鼠肺动脉非内皮依赖性舒张反应。慢性缺氧显著减低了大鼠肺动脉内 cGMP 的含量。缺氧组和对照组大鼠肺动脉内 cGMP 的基础含量分别是51.9±5.7 pmol/g wet wt.(n=14)和84.9±9.7 pmol/g wet wt.(n=14),p<0.01;经 10~(-7)mol/L ACh 刺激后分别是91.4±7.3 pmol/g wet wt.(n=5)和240.8±30.6pmol/g wet wt.(n=5),p<0.01。慢性缺氧可能抑制了肺动脉平滑肌细胞胞浆中可溶性鸟苷酸环化酶,从而减低了肺动脉对内皮舒张因子和 SNP 的舒张反应性。     

缺氧复氧对家兔胸主动脉环张力的影响及其机制

生物测定法观察家兔胸主动脉环经缺氧－复氧后血管张力的变化及这种变化与内皮的关系,并初步探讨了缺氧复氧对血管张力影响的机制。结果表明急剧缺氧可使苯肾上腺素（ＰＥ）预收缩的主动脉环出现短暂的收缩,随即自发舒张,复氧后立即舒张,随后持续收缩;去除内皮或经一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ,ＮＯ）合成酶抑制剂Ｎ－硝基－精氨酸－甲基酯（Ｌ－ＮＡＭＥ）或鸟苷酸环化酶抑制剂美蓝（ＭＢ）孵育后的血管环,缺氧性收缩反应消除或明显抑制,复氧性舒张也受到明显抑制,而复氧性收缩显著增强;加入ＮＯ合成底物Ｌ－精氨酸（Ｌ－Ａｒｇ）孵育后,有内皮血管环缺氧复氧性张力变化与对照组相比无明显变化。表明缺氧性血管收缩是内皮依赖性的,与ＮＯ释放的迅即减少有关;复氧早期引起的舒张是由于内皮释放ＮＯ引起的,而随后的收缩可能因复氧后大量氧自由基灭活ＮＯ所致。     

川芎嗪对慢性缺氧大鼠肺动脉和主动脉的离体舒张作用

用生物测定法观察了川芎嗪对慢性缺氧大鼠肺动脉和主动脉环的舒张效应,并与乙酰胆碱的舒血管作用进行了比较。结果表明:川芎嗪对慢性缺氧大鼠肺动脉和主动脉的舒张作用均与平原组无明显差异。慢性缺氧明显减低了乙酰胆碱诱发的肺动脉内皮依赖性舒张反应,但不影响川芎嗪对肺血管的舒张作用。提示川芎嗪对肺血管的舒张作用不依赖于内皮。川芎嗪对肺动脉的舒张作用明显大于体动脉。这些特性有利于川芎嗪对肺动脉高压的治疗。     

慢性缺氧对自发性高血压大鼠血液动力学和血管反应性的影响

本研究观察了鼠龄10周的自发性高血压大鼠(SHR)在慢性缺氧条件下(模拟海拔5000m,15d)体动脉压(SBP)、平均肺动脉压(MPAP)、左、右心室收缩指数(LVIC、RVIC)和舒张指数(LVIR、RVIR)以及血管反应性的变化。结果表明,慢性缺氧明显阻抑SHR大鼠SBP升高(P<0.05),但使SHR大鼠MPAP升高(P<0.001)。慢性缺氧还可增大SHR大鼠LVIC和LVIR,增强SHR大鼠胸主动脉对乙酰胆碱(ACh)的舒张反应,减弱其对5-羟色胺(5-HT)的收缩反应。SHR大鼠肺动脉对ACh和5-HT的反应则与主动脉相反。实验结果提示,慢性缺氧阻抑SHR大鼠血压升高与血管反应性的改变有关。     

蛋白激酶C对大鼠离体肺动脉环张力及其反应性的调节作用

目的 :观察蛋白激酶C(PKC)对大鼠离体肺动脉环张力及反应性的调节作用。方法 :取Wistar大鼠肺动脉 ,观察在离体情况下PKC激活剂PMA及PKC抑制剂RO3 182 2 0对肺动脉环张力的直接作用 ;对氯化钾 (KCl)、5 羟色胺 (5 HT)和缺氧引起的收缩反应的影响 ;以及PMA对乙酰胆碱 (ACh)介导的内皮依赖性舒张 (EDR)和硝普钠(SNP)介导的内皮非依赖性舒张 (EIDR)反应的影响。结果 :①PMA(5 0 0nmol/L)使肺动脉环产生缓慢增强、持久的收缩 ,随PMA浓度增加而增强 ,RO3 182 2 0 (5 μmol/L)可完全阻断PMA的上述作用 ;②PMA可增强肺动脉对KCl、5 HT的收缩反应 ,该作用随PMA浓度增加而增强 ;③RO3 182 2 0 (5 μmol/L)几乎可以完全阻断离体肺动脉环对缺氧的第二相收缩反应 ;④PMA(10nmol/L)在 10min内完全逆转ACh(10 μmol/L)介导的EDR ,PMA(10nmol/L)还可使ACh的浓度一反应显著减弱 ,达到最大舒张反应的一半时对应的ACh浓度 (EC50 )显著增加 ,最大舒张反应明显减小 ;而PMA对SNP介导的EIDR无显著影响。结论 :PKC在与肺动脉张力及反应性的调节有关的细胞内生物信号传递过程中具有重要作用。     

缺血/缺氧对自发性高血压大鼠肠系膜动脉血管舒缩功能的影响及其可能机制

高血压引起的脑卒中、冠心病等严重并发症的发生,均与组织缺血/缺氧导致的动脉血管痉挛有关。为了研究高血压大鼠肠系膜血管缺血/缺氧后的功能学改变,本研究采用三气培养箱模拟缺血/缺氧条件处理自发性高血压大鼠(spontaneously hypertensive rats,SHR)肠系膜动脉血管环,运用敏感的肌张力描记技术测定血管环对不同血管活性物质的反应性。结果显示:与WKY组大鼠相比,SHR组大鼠肠系膜动脉血管对收缩剂KCl和苯肾上腺素(phenylephrine,PE)的反应性明显提高,对内皮依赖的血管舒张剂乙酰胆碱(acetylcholine,ACh)的反应性显著降低;而与SHR组和急性缺血/缺氧对照(WKY+H)组相比较,高血压合并急性缺血/缺氧(SHR+H)组对KCl和PE的收缩反应显著性增加,对ACh的舒张反应明显降低。N-硝基-L-精氨酸甲酯(L-NAME)存在时,SHR+H组和SHR组血管环对ACh的舒张反应没有明显变化,而WKY组血管对ACh的舒张反应显著降低。与SHR组相比,SHR+H组CaCl2诱导的钙依赖性收缩曲线明显左移。在无钙K-H液中,SHR+H组PE和咖啡因(caffeine)诱导的...     

血管内皮舒张因子在氧自由基所致慢性缺氧大鼠肺内动...

The role of endothelium-derived relaxing factor (EDRF) on the effect of oxygen-derived free radicals (generated by xanthine-xanthine oxidase system) on intrapulmonary arterial in chronic hypoxic rats was studied by a microbioassay method. Intrapulmonary artery rings with intact or denuded endothelium of hypoxic (5,000 m, 10 days) and normoxic rats were prepared for observation of oxygen-derived free radicals induced contraction. It was shown that oxygen-derived free radicals induced contractions of intrapulmonary arterial rings with intact endothelium were obviously augmented in hypoxic rats than in normoxic controls. The augmented responses could be further potentiated by the addition of EDRF inactivator reduced hemoglobin (RHb), but diminished or even abolished by applying superoxide dismutase (Cu-Zn SOD). However, no effect on denuded rings was observed when RHb or SOD was added. It is concluded that chronic hypoxia may attenuate the action of EDRF in the enhancement of the reactivity of intrapulmonary artery to oxygen-derived free radicals.     

L－NNA和还原型Hb对SHRsp肠系膜动脉内皮依赖性舒张的影响

我们以往的工作证实成年自发高血压大鼠（ＳＨＲ与ＳＨＲｓｐ）肠系膜动脉由乙酰胆碱引起的内皮依赖性舒张（ＥＤＲ）减弱。为进一步探讨ＥＤＲ减弱的机制，本文观察了一氧化氮（ＮＯ）合成酶抑制剂左旋硝基精氨酸（Ｌ－ＮＮＡ）及ＥＤＲＦ灭活剂还原型血红蛋白（ＲＨｂ）对卒中易感型自发高血压大鼠（ＳＨＲｓｐ）与常压对照（ＷＫＹ）大鼠肠系膜动脉ＡＣｈ内皮依赖性舒张（ＥＤＲ）的影响。发现Ｌ－ＮＮＡ（１０（－３）ｍｏｌ／Ｌ）可使ＳＨＲｓｐ弱于ＷＫＹ的ＡＣｈＥＤＲ（１０（－８）－１０（－５）ｍｏｌ／Ｌ）的差异消失，ＲＨｂ（１０（－５）ｍｏｌ／Ｌ）则仅在１０（－７）－１０（－８）ｍｏｌ／ＬＡＣｈ时使ＳＨＲ（ｓｐ）肠系膜动脉ＥＤＲ弱于ＷＫＹ的差异消失。将ＷＫＹ在加入Ｌ－ＮＮＡ后的与加入ＲＨｂ后的ＡＣｈ（１０（－８）－１０（－５）ｍｏｌ／Ｌ）ＥＤＲ进行比较，无显著差异。而将ＳＨＲｓｐ在Ｌ－ＮＮＡ后的与ＲＨｂ后的ＡＣｈ（１０（－８）－１０（－６）ｍｏｌ／Ｌ）ＥＤＲ进行比较，则有显著差异。并且，ＳＨＲｓｐ的有内皮肠系膜动脉条对ＲＨｂ的敏感性与ＷＫＹ接近，对Ｌ－ＮＮＡ的敏感性则低于ＷＫＹ。表明高血压时肠系膜动脉内皮依赖性舒张减弱中，ＥＤＲＦ机制与     

氧自由基在应激性胃溃疡中的发病学意义

本工作研究了氧自由基在大鼠冷冻束缚应激性胃溃疡中的发病学意义。实验结果如下:(1)以超氧自由基清除剂超氧化物歧化酶(SOD)或羟自由基清除剂二甲亚砜和甘露醇预先处理大鼠,均可显著地减轻胃粘膜损伤;(2)应激时,胃粘膜内的脂质过氧化分解产物丙二醛的含量显著升高;(3)组织化学的研究显示,胃粘膜层含有丰富的黄嘌呤氧化酶,其活性在应激时明显升高,预先用别嘌呤醇处理大鼠以抑制黄嘌呤氧化酶的活性,可使胃粘膜损伤显著减轻。上述结果提示,氧自由基是应激性胃溃疡的重要致病因子,而黄嘌呤氧化酶活性的升高似可能为应激时氧自由基生成增加的重要原因。     

内皮舒张因子与氧自由基在脑血管痉挛发病中的作用

实验性兔蛛网膜下腔出血后,基底动脉壁丙二醛（ＭＤＡ）含量及超氧化物峻化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）活性发生改变,基底动脉出现痉挛,应用ＳＯＤ后上述变化减轻。离体采用生物检定法发现,基底动脉受自由基损伤后,去甲肾上腺素（ＮＥ）诱导的血管收缩效应增强,而ＡＣｈ诱导的血管舒张效应减弱。用ＳＯＤ防止了ＡＣｈ诱导的血管舒张效应的减弱。结果表明,氧自由基参与了脑血管痉挛的发生,而脑血管受自由基损伤后,其内皮舒张因子释放减少是脑血管痉挛发病的重要因素。     

Apelin对大鼠离体肺动脉环的舒张作用及与一氧化氮的关系

目的：探讨新的小分子活性肽Apelin对大鼠离体肺动脉环的舒张作用及与一氧化氮（NO）途径的关系,并比较低氧大鼠的肺动脉环对Apelin的舒张反应与正常大鼠的差异。方法：36只大鼠随机分为正常组与低氧组;采用离体血管环灌流法,检测Apelin对去甲肾上腺素（NE）预收缩的大鼠离体肺主动脉环的舒张效应,观察去内皮或用一氧化氮合酶抑制剂（L-NAME）、可溶性鸟苷酸环化酶（sGC）抑制剂（ODQ）孵育后该舒张率的变化。结果：①在正常组大鼠肺动脉环,Apelin（0.01~100 nmol/L）具有浓度依赖性的舒张效应。去除内皮后,Apelin对NE预先收缩的肺血管舒张效应明显减弱（P〈0.01）。L-NAME或ODQ预孵育后,Apelin的舒张效应均明显减弱（P均〈0.01）。②低氧组大鼠的肺动脉环对Apelin的舒张反应明显低于正常组大鼠,在最大浓度100 nmol/L时,Apelin的效应低60.45%（P〈0.01）,而两组EC50相比差异无显著性（P〉0.05）。结论：Apelin具有内皮依赖性的舒张肺动脉环的作用,该效应与NO-sGC-cGMP信号途径有关;低氧大鼠的离体肺动脉环对Apelin的舒张反应减弱。     

Cytoprotective function of nitric oxide: inactivation of superoxide radicals produced by human leukocytes.

The oxygen-derived free radical superoxide anion (.O2-) plays an important role in the pathogenesis of various diseases. Recent demonstrations that .O2- inactivates the potent vasodilator endothelium-derived relaxing factor (EDRF) and that EDRF is probably nitric oxide (NO) suggest that EDRF(NO) may act as an endogenous free radical scavenger. This hypothesis was tested in an in vitro system by analyzing the effect of authentic NO (dilutions of a saturated aqueous solution) on .O2- production (detected spectrophotometrically as reduction of cytochrome c) by fMet-Leu-Phe-activated human leukocytes (PMN). NO depressed the rate of reduction of cytochrome c by .O2- released from PMN's or generated from the oxidation of hypoxanthine by xanthine oxidase. This effect was concentration-dependent and occurred at dilutions of the saturated NO solution (1:250 to 1:10) which inhibited platelet aggregation. NO had no direct effect on cytochrome c or on xanthine oxidase. These observations indicate that NO(EDRF) can be regarded as a scavenger of superoxide anion and they suggest that EDRF(NO) may provide a chemical barrier to cytotoxic free radicals (.O2-).     

Increased activity of H2O2 in aorta isolated from chronically streptozotocin-diabetic rats: effects of antioxidant enzymes and enzymes inhibitors.

The effects of hydrogen peroxide (H2O2, 1 nM-5 mM) on the tone of the rings of aorta precontracted with phenylephrine (PE) were studied in 4-5 months streptozotocin (STZ)-diabetic rats and their age-matched controls. H2O2 induced brief contraction before relaxation in endothelium-containing rings that was more pronounced in diabetic rats. Removal of the endothelium or pretreatment of rings with N(G)-nitro-L-arginine methyl ester (L-NAME, 100 microM) abolished H2O2-induced immediate and transient increase in tone, but preincubation with indomethacin (10 microM) had no effect on contractions induced by H2O2 in both group of animals. Pretreatment with L-NAME or indomethacin as well as absence of endothelium produced an inhibition of H2O2-induced relaxation that was more pronounced in diabetic rings. Chronically STZ-diabetes resulted in a significant increase in H2O2-induced maximum relaxation that was largely endothelium-dependent. Decreased sensitivity (pD2) of diabetic vessels to vasorelaxant action of H2O2 was normalized by superoxide dismutase (SOD, 80 U/ml). Pretreatment with SOD had no effect on H2O2-induced maximum relaxations in both group of animals but led to an increase in H2O2-induced contractions in control rats. When the rings pretreated with diethyldithiocarbamate (DETCA, 5 mM), H2O2 produced only contraction in control rats, and H2O2-induced relaxations were markedly depressed in diabetic rats. H2O2 did not affect the tone of intact or endothelium-denuded rings in the presence of catalase (2000 U/ml). Aminotriazole (AT, 10 mM) failed to affect H2O2-induced contractions or relaxations in all rings. Our observations suggest that increased production of oxygen-derived free radicals (OFRs) in diabetic state leads to a decrease in SOD activity resulting an increase in endogenous superoxide anions (O2*-), that is limited cytotoxic actions, and an increase in catalase activity resulting a decrease in both H2O2 concentrations and the production of harmful hydroxyl radical (*OH) in diabetic aorta in long-term. Present results indicate that increased vascular activity of H2O2 may be an important factor in the development of vascular disorders associated with chronically diabetes mellitus. Enhanced formation of *OH, that is a product of exogenous H2O2 and excess O2*, seems to be contribute to increased relaxations to exogenously added H2O2 in chronically diabetic vessels.     

Oxygen-derived free radicals and 'stunned myocardium'

A brief, transient period of coronary artery occlusion (less than 20 minutes in duration) followed by reperfusion does not result in irreversible myocyte injury or death, yet the regional contractile function and high energy phosphate content of the previously ischemic tissue remains depressed or 'stunned' for hours to days following reperfusion. It has been suggested that this prolonged postischemic dysfunction of viable, previously ischemic myocardium may be a consequence of oxygen-derived free radicals generated during occlusion or at the time of reperfusion. Recent evidence demonstrates that free radical scavenging agents such as superoxide dismutase (SOD) + catalase, N-2-mercaptopropionylglycine, and allopurinol, administered prior to coronary artery occlusion, significantly enhance recovery of regional contractile function of the stunned, previously ischemic tissue. This improved contractile function was not, however, accompanied by improvements in high energy phosphate metabolism: infusion of SOD + catalase did not preserve ATP stores in the previously ischemic tissue. These data support the hypothesis that oxygen-derived free radicals contribute, at least in part, to the phenomenon of the stunned myocardium. The source or mechanisms of free radical production in the setting of brief, transient ischemia, however, remains to be elucidated.     

Phosphodiesterase 5 inhibition restores impaired ACh relaxation in hypertensive conduit pulmonary arteries

Responses to acetylcholine (ACh) and sodium nitroprusside (SNP) were compared in large (LPA) and small pulmonary artery (SPA) rings from normoxic and chronically hypoxic (CH) rats. In addition, the effects of a selective phosphodiesterase (PDE) 5 inhibitor, E-4021, on ACh-induced relaxation were evaluated. Chronic hypoxia markedly decreased both ACh- and SNP-induced relaxations in LPA but not in SPA rings. Pretreatment with E-4021 caused a much greater leftward shift of the concentration-response curve for ACh in hypoxic than in normoxic LPA rings, eliminating the difference in response to ACh between these two vessels. These results suggest that cGMP-dependent relaxation is impaired in the proximal but not in the distal pulmonary artery of CH rats and that increased PDE5 activity could be a mechanism responsible for this impaired responsiveness.     

生长抑素对胃粘膜的保护作用可能与清除自由基有关

本文观察到生长抑素对大鼠冷冻－束缚应激性胃粘膜损伤具有明显的保护作用,同时显著地抑制应激引起的胃粘膜丙二醛含量的升高。应激时大鼠胃粘膜内黄嘌呤氧化酶的生增高,同时谷胱甙肽过氧化物酶的活性降低,但超氧化物歧化酶的活性未见明显变化,生长抑素预处理可使应激时ＧＳＨ－ＰＸ活性的降低恢复到正常水平,但对ＸＯ和ＳＯＤ未见明显影响。上述结果提示,生长抑素对应激性胃粘膜损伤的保护作用似与增强胃粘膜对自由基的清除有