毛冬青素L7抗小鼠缺氧作用

目的:研究毛冬青素L7抗小鼠缺氧作用。方法:通过常压耐缺氧、亚硝酸钠中毒、氰化钾中毒、利多卡因中毒、夹闭气管小鼠心电消失时间、断头小鼠张口动作持续时间等实验观察其抗小鼠缺氧作用。结果:毛冬青素L7可明显延长小鼠在常压缺氧条件下的存活时间;延长亚硝酸钠、氰化钾、利多卡因中毒后的小鼠存活时间;延长夹闭气管小鼠心电消失时间及断头小鼠的喘气时间。结论:毛冬青素L7对缺氧有保护作用。     

小檗碱的抗整体小鼠缺氧作用

硫酸小檗碱(Ber)sc能延长常压密闭缺氧小鼠存活时间,但ig无效。Ber sc能对抗异丙肾上腺素或酚妥拉明缩短密闭缺氧小鼠存活时间,延长断头小鼠张口动作持续时间及氰化钾、亚硝酸钠或利多卡因中毒小鼠的存活时间。Ber ig也能延长张口动作持续时间和利多卡因中毒小鼠的存活时间,但作用均较sc弱。Ber的抗缺氧作用表现为减慢机体的耗氧速度及提高异常状态机体对低氧的利用能力。     

咖啡酸和阿魏酸的抗缺氧作用

咖啡酸和阿魏酸能延长断头小鼠张口动作持续时程和氰化钾（ＫＣＮ），中毒小鼠存活时间。两者对小鼠常压密闭缺氧耐受力无提高作用。阿魏酸不延长亚硝酸钠（ＮａＮＯ２）中毒小鼠存活时间，但咖啡酸能延长之。此外咖啡酸还能对抗脑垂体后叶素引起大鼠急性心肌缺血。     

麦利平的抗缺氧作用

目的为探讨麦利平对心肌缺血缺氧的作用 ,用小白鼠制备模型进行耐缺氧研究。方法采用小鼠常压缺氧模型、垂体后叶素 (PIT)致小鼠急性心肌缺血模型、氰化钾 (KCN)致小鼠组织缺氧模型、亚硝酸钠 (NaNO2 )致小鼠组织缺氧模型 ,考察了麦利平对心肌缺氧缺血的保护作用。结果麦利平能延长小鼠常压缺氧条件下的存活时间 ;能降低垂体后叶素致小鼠急性心肌缺血的死亡率 ;对腹腔注射氰化钾、亚硝酸钠引起小鼠组织中毒性缺氧均有明显的缓解作用。结论麦利平对心肌缺血缺氧具有保护作用。     

抗癫痫药物卡马西平的抗缺氧作用研究

目的研究卡马西平对缺氧小鼠的保护作用。方法采用常压缺氧、断头缺血和亚硝酸钠中毒缺氧方法,观察卡马西平对小鼠耐缺氧作用的影响。结果100mg.kg-1和50mg.kg-1卡马西平能显著延长常压耐缺氧小鼠的存活时间(P<0.01);100mg.kg-1和50mg.kg-1卡马西平能显著延长断头小鼠的存活时间(P<0.01);100mg.kg-1卡马西平能显著延长亚硝酸钠中毒小鼠的存活时间(P<0.01)。结论卡马西平对常压、急性脑缺血性缺氧和化学性缺氧小鼠有一定保护作用。     

黄芩苷的耐缺氧作用

为探讨黄芩苷对心肌缺血有无治疗作用 ,用小白鼠制备模型进行了耐缺氧研究。本文采用常压耐缺氧法 ;对抗异丙肾上腺素法 ;对抗亚硝酸钠法 ;断头法 ;失血性休克法研究了黄芩苷对小鼠耐缺氧作用的影响。结果表明 ,黄芩苷能非常显著延长常压耐缺氧条件下小白鼠的存活时间 (P<0 0 1) ;能非常显著延长腹腔注射异丙肾上腺素的小白鼠在常压缺氧条件下的生存时间 (P <0 0 1) ;能非常显著缩短失血性休克小鼠心跳时间 (P <0 0 1) ;对小白鼠的亚硝酸钠中毒无显著的缓解作用 (P >0 0 5 ) ;对断头小鼠的呼吸时间无显著影响 (P >0 0 5 )。这些结果提示因黄芩苷可拮抗儿茶酚胺类化合物 ,所以对心肌氧供不足及因心肌耗氧增加引起的心肌缺氧均有非常显著的改善作用 (P <0 0 1) ;对脑缺氧无显著的改善作用 (P >0 0 5 ) ;对亚硝酸钠引起的组织中毒性缺氧无显著的缓解作用 (P >0 0 5 )。     

蛙血清去蛋白提取物抗缺氧作用的初步研究

目的 研究蛙血清去蛋白提取物对小鼠的抗缺氧作用.方法 通过建立小鼠常压缺氧模型、急性脑缺血性缺氧模型及亚硝酸钠中毒缺氧模型,以生理盐水为空白对照,盐酸普萘洛尔为阳性对照,观察蛙血清去蛋白提取物3个剂量组(10,30,90 mg/kg)对小鼠的抗缺氧作用.结果 蛙血清去蛋白提取物能显著延长模型小鼠在常压缺氧、急性脑缺血性缺氧及亚硝酸钠中毒缺氧时的存活时间.结论 蛙血清去蛋白提取物具有抗缺氧作用.     

黄芪水提液对大鼠体外神经细胞缺氧损伤的保护作用

<正>黄芪是中医常用益气药之一,具有免疫调节、抗菌、利尿、降压、强心等作用。近年来的研究还发现黄芪可延长常压缺氧小鼠存活时间,延长氰化钾(KCN)中毒小鼠(细胞内缺氧)及亚硝酸钠(NaNO2)中毒小鼠(细胞外液缺氧)的存活时间,同时,还可延长断头小鼠张口动作(脑缺氧)的持续时间[1]。体外实验已证实黄芪对体外培养的心肌细胞、血管内皮细胞具有明显的保护作用。     

异紫堇定的抗整体小鼠缺氧作用

异紫堇定能延长断头小鼠张口动作持续时间,对正常小鼠的常压缺氧存活时间及氧利用能力都无明显影响,但能对抗异丙肾上腺素降低小鼠对氧的利用能力。对于酚妥拉明缩短小鼠存活时间和降低氧利用能力,异紫堇定只能对抗其缩短存活时间作用。异紫堇定还能延长KCN、NaNO_2或利多卡因中毒小鼠的存活时间,其抗缺氧作用可能与罂粟碱样结构有关。     

大豆苷元耐缺氧的实验研究

目的　研究大豆苷元对小鼠的耐缺氧作用。方法　常压耐缺氧法、对抗异丙肾上腺素法、断头喘息法、结扎双侧颈总动脉法及游泳实验法。结果　大豆苷元能显著延长常压耐缺氧条件下小鼠的存活时间;显著延长皮下注射异丙肾上腺素的小鼠在常压缺氧条件下的生存时间;显著性延长断头小鼠的喘息时间;显著延长脑缺氧时间和游泳时间。结论　大豆苷元具有显著的耐缺氧作用。     

Anti-hypoxic effect of piracetam and its interaction with prostacyclin

The anti-hypoxic effect of piracetam was studied using the following experimental methods: hypobaric and anoxic hypoxia in mice, complete ischemia by decapitation in mice, incomplete ischemia by bilateral carotid occlusion in rats and hemic hypoxia in rats. Cinnarizine and vinpocetine were used as reference drugs. In hypobaric hypoxia, anoxic hypoxia, and complete ischemia by decapitation the interaction of piracetam with the effect of prostacyclin (PGI2) was investigated. Piracetam showed anti-hypoxic effect in all the methods used. Its effect was greater than that of cinnarizine and similar to that of vinpocetine. Piracetam potentiated the effect of PGI2 shifting the anti-hypoxic dose-response curve of PGI2 to the left.     

羌活不同提取物对小鼠脑缺血缺氧的保护作用

目的:探讨羌活不同溶剂提取物对小鼠急性脑缺血缺氧损伤的保护作用。方法:制备羌活水提取物和75%乙醇提取物,通过常压耐缺氧实验、亚硝酸钠中毒性缺氧实验,饱和氯化镁溶液致小鼠急性脑缺血实验和小鼠断头实验复制小鼠急性脑缺血缺氧模型,检测急性全脑缺血缺氧小鼠脑组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果:与正常对照组相比较:在饱和氯化镁溶液致小鼠急性脑缺血实验、常压耐缺氧实验和断头实验中各给药组小鼠的存活时间均显著延长(P<0.05,P<0.01);尼莫地平和羌活水提取物均能显著延长NaNO₂所致小鼠中毒性缺氧的存活时间(P<0.01),羌活醇提取物有延长存活时间的趋势(P>0.05);各给药组脑指数和MDA含量均显著降低(P<0.05,P<0.01),SOD活性显著增高(P<0.05,P<0.01)。结论:羌活水提取物和醇提取物对脑缺血缺氧损伤有一定的保护作用。     

The response of diterpene sclareol glycol to acute hypoxia in mice

The effects of a reversible activator of adenylate cyclase sclareol glycol (SG), a semisynthetic diterpene of the labdane family, on acute hypoxia (asphyctic, hemic-induced by 300 mg/kg of sodium nitrite injected subcutaneously, and histotoxic-induced by 20 mg/kg sodium nitroprusside injected intraperitoneally) in mice were studied. SG was applied at doses well below the lethal dose. SG increased the latency to convulsions and the survival time to death. It is suggested that the antihypoxic effects of SG on these three models of acute hypoxia are induced mainly via its effects on adenylate cyclase and perhaps its involvement in synaptic transmitter action.     

Dissociation of the anti-amnesic and antihypoxic effects of nootropic and antihypoxic preparations

In experimental studies on mice it was shown that piracetam, Cleregil, centrophenoxine, pyritinol possessed the most pronounced anti-amnestic activity. A close effect was noted with Euclidan, 3-hydroxypyridine and ionol. GABAergic agents (sodium oxybutyrate, phenibut, pantogam), gutimine, nicotinoyl-GABA eliminated amnesia to a lesser extent. The antihypoxic effect on the model of hypobaric hypoxia was exerted by typical antihypoxic agents (gutimine, sodium oxybutyrate, 3-hydroxypyridine). The antihypoxic activity of nootropic drugs (centrophenoxine, pyritinol, phenibut) could be determined only at a significant increase of doses. No interrelationship and the presence of dissociation in manifestation of anti-amnestic and antihypoxic effects were revealed.     

Study on the cerebral effects of sabeluzole

The cerebral effects of subeluzole have been studied using the following methods: hypobaric hypoxia in mice, complete ischemia by decapitation in mice, anoxic hypoxia in mice, hemic hypoxia in rats, incomplete ischemia by bilateral carotid ligation in rats, anoxic hypoxia in rats and asphyxic hypoxia in cats. Sabeluzole was active in all the models used: it increased the survival time in hypobaric hypoxia (maximum at 40 mg/kg--by 92.0%, p less than 0.001), survival time in anoxic hypoxia in mice (maximum at 40 mg/kg--by 27.2%, p less than 0.001), gasping in decapitation model (maximum at 20 mg/kg--by 155.4%, p less than 0.001) and survival in hemic hypoxia (maximum at 2.5 mg/kg--by 21.1%, p less than 0.05). The duration of the effect as evaluated in the decapitation model was about 6 h. In incomplete ischemia in rats, however, it showed a weak effect. In anoxic hypoxia in rats, sabeluzole (5 mg/kg i.v.) increased the time latency between onset of anoxia and negative DC-shift by 20.5% and the K+e-threshold by 25.7%. In asphyxic hypoxia in cats, sabeluzole (0.5 mg/kg i.v.) counteracted the hypoxia-induced decrease of the fast-wave amplitudes during the cortical resistance period and the hypoxia-induced decrease of the slow-wave and increase of the fast wave amplitudes during the cortical recovery period.     

蜕皮甾酮对小鼠脑缺氧的保护作用

目的研究蜕皮甾酮对小鼠脑缺氧的影响。方法利用亚硝酸钠和氰化钾造成急性脑缺氧模型,考察蜕皮甾酮的抗脑缺氧作用,并观察蜕皮甾酮对氰化钾引起的脑组织过氧化脂质生成的影响和亚硝酸钠致小鼠脑缺氧引起的记忆巩固障碍的影响。结果蜕皮甾酮ｉｇ１４４ｍｇ·ｋｇ－１能明显对抗小鼠急性脑缺氧,在体内和体外实验中均能抑制小鼠脑缺氧引起的脑组织过氧化脂质的生成,改善脑缺氧引起的记忆巩固障碍。结论蜕皮甾酮对小鼠脑缺氧有保护作用。     

脑心舒胶囊抗脑缺血作用研究

目的:研究脑心舒胶囊抗脑缺血的作用。方法:四血管阻断法复制大鼠脑缺血模型并复制小鼠断头完全性脑缺血模型,测定脑心舒胶囊对模型大鼠三磷酸腺苷(ATP)及超氧化物歧化酶(SOD)活力的影响,并测定大鼠脑指数、脑含水量及小鼠张口喘气时间。结果:脑心舒胶囊能提高模型大鼠的ATP及SOD活力,对脑缺血模型大鼠脑指数和脑含水量有显著的改善作用,并能明显延长断头完全性脑缺血模型小鼠张口喘气时间。结论:脑心舒胶囊有一定的抗脑缺血作用。