中保牌健生胶囊的耐缺氧作用

目的研究中保牌健生胶囊的作用。方法采用常压耐缺氧试验、亚硝酸钠中毒存活试验和急性脑缺血性缺氧试验对小鼠进行耐缺氧功能试验。结果经口给予小鼠中保牌健生胶囊0．05、0．50、1．50g／kgBW,连续灌胃30d,高剂量组能延长常压缺氧小鼠缺氧存活时间;中、高剂量能延长亚硝酸钠中毒后存活时间;中剂量组能延长急性脑缺血性缺氧张口喘气时间。结论中保牌健生胶囊在一定剂量范围内具有提高小鼠缺氧耐氧的能力。     

蝙蝠葛苏林碱对小鼠和大鼠脑缺血的保护作用

目的研究蝙蝠葛苏林碱对小鼠缺氧、急性脑缺血和大鼠局灶性脑缺血的保护作用。方法采用小鼠常压密闭缺氧实验，观察了蝙蝠葛苏林碱对小鼠耗氧量和存活时间的影响；结扎小鼠双侧颈总动脉造成急性全脑缺血模型，观察了蝙蝠葛苏林碱对急性脑缺血小鼠死亡率的影响；电凝阻断大鼠一侧大脑中动脉造成大鼠局灶性脑缺血模型，观察了蝙蝠葛苏林碱对局灶性脑缺血大鼠梗塞面积和行为障碍的影响。结果蝙蝠葛苏林碱能明显降低常压密闭缺氧小鼠整体耗氧速度，延长缺氧小鼠的存活时间；明显降低急性脑缺血小鼠２ｈ死亡率；显著降低局灶性脑缺血大鼠梗塞范围，明显改善行为障碍。结论蝙蝠葛苏林碱具有抗缺氧、抗脑缺血作用。     

刺五加注射液对小鼠急性心肌缺氧的保护作用

目的 :观察刺五加对小鼠急性心肌缺氧的保护作用。方法 :常压和低压缺氧条件下分别观察小鼠平均存活时间和心肌耗氧量。结果 :刺五加注射液高低剂量组均可使小鼠常压和低压条件下平均存活时间延长 ;降低常压、低压条件下心肌耗氧量。结论 :刺五加注射液能明显降低小鼠心肌氧耗 ,提高小鼠抗应激能力 ,保护缺氧心肌     

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。     

醒脑康冲剂对动物机体缺氧的影响

不同剂量醒脑康冲剂灌胃小鼠，能显著延长常压、减压环境下及ＮａＮＯ２、ＫＣＮ中毒引起小鼠机体缺氧的存活时间。对夹闭小鼠气管后的心电活动时间亦有延长作用。表明，醒脑康冲剂具有提高机体耐缺氧能力和降低心肌耗氧作用。阳性对照药脑复康亦具有相似作用。     

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.     

四君子汤加味对小鼠抗缺氧作用的研究

目的观察四君子汤加味在不同缺氧状况下的抗缺氧作用。方法采用小鼠动物实验,观察四君子汤加味在常压缺氧情况下和高压缺氧情况下对小鼠存活时间的影响。实验分组采用实验动物随机分组法,统计分析采用SPSS16.0软件。结果 (1)四君子汤加味在常压缺氧情况下对小鼠存活时间的影响,根据统计结果可知四君子汤加味低剂量组和高剂量组均可显著延长常压缺氧情况下小鼠存活时间,和0.9%NaCl溶液对照组相比较,差异有统计学意义(P<0.05);(2)四君子汤加味在高压缺氧情况下对小鼠存活率的影响,根据统计结果可知四君子汤加味低剂量组和高剂量组小鼠存活率分别为70.0%、85.0%,与0.9%NaCl溶液组比较,均差异有统计学意义(P<0.05)。这说明四君子汤加味不仅在常压缺氧情况下可明显延长小鼠存活时间,而且在高压缺氧情况下提高了小鼠的存活率。结论四君子汤加味明显提高缺氧条件下小鼠存活时间和存活率,具有明显的抗缺氧作用。     

苁蓉益肾颗粒对小鼠实验性缺氧的保护作用

目的观察苁蓉益肾颗粒对小鼠实验性缺氧的保护作用.方法采用常压和低压缺氧条件下分别观察小鼠平均存活时间和心肌耗氧量.结果苁蓉益肾颗粒高低剂量组均可使常压和低压缺氧条件下小鼠平均存活时间延长;降低常压条件下心肌耗氧量.结论苁蓉益肾颗粒能明显降低小鼠氧耗,保护缺氧心肌.     

益气健身方抗疲劳和耐缺氧作用实验研究

目的研究益气健身方对小鼠的耐缺氧和抗疲劳作用。方法采用灌胃法给予小鼠不同剂量的益气健身方,分别测定小鼠的转棒时间、负重游泳时间及常压耐缺氧时间。结果益气健身方高、中、低剂量组(0.5、1.0、2.0g/kg)小鼠转棒时间较对照组显著延长(P<0.01),高、中剂量组负重游泳时间较对照组显著延长(P<0.05,P<0.01),高剂量组常压耐缺氧生存时间较对照组显著延长(P<0.05)。结论益气健身方具有一定的耐缺氧和抗疲劳作用。     

西红花酸对小鼠缺氧损伤的保护作用

目的:研究西红花酸对小鼠缺氧损伤的保护作用。方法:观察不同缺氧模型小鼠的存活时间或存活率,测定大鼠局灶性脑缺血再灌注后血氧分压及血红蛋白含量。结果:西红花酸50和100 mg·kg~(-1)能显著延长常压缺氧、sc异丙肾上腺素、ip亚硝酸钠小鼠的存活时间及断头小鼠的张口喘气时间、提高双侧颈总动脉结扎小鼠30 min内的存活率;明显提高脑缺血再灌注大鼠血氧分压,而对血红蛋白含量无影响。结论:西红花酸能够提高小鼠耐缺氧能力,其作用可能与增加血氧分压有关。     

Influence of different anesthetics on skin oxygenation studied by electron paramagnetic resonance in vivo

The effects of two general anesthetics on skin oxygenation in mice are evaluated by electron paramagnetic resonance oximetry. Up to now no data on the effects of different anesthetics on skin oxygenation could be found. In this study animals were anesthetized with ketamine/xylazine or isoflurane, and partial pressure of oxygen (pO(2)) in the skin, heart rate and hemoglobin oxygen saturation were followed as a function of time and inhaled oxygen concentration. The skin pO(2) significantly increased continuously for about 60 min in mice anesthetized with isoflurane and remained constant after that. During ketamine/xylazine anesthesia, the pO(2) in the skin only slightly decreased. The skin pO(2) increased with higher inspired oxygen concentrations for both anesthetics groups. When breathing 21% oxygen, mice anesthetized with isoflurane had two-fold higher pO(2) in the skin compared to mice anesthetized with ketamine/xylazine. The heart rate was significantly lower in animals anesthetized with ketamine/xylazine, while hemoglobin saturation was almost the same in both groups at all inhaled oxygen concentrations. These results show that the type of anesthesia is an important parameter that needs to be considered in experiments where skin pO(2) is followed.     

蝙蝠葛碱对动物耐缺氧及实验性心肌缺血和梗塞的影响

本文报道蝙蝠葛碱(Dau)对小白鼠耐缺氧和大鼠实验性心肌缺血及梗塞的影响。异丙肾上腺素(Iso)诱发耗氧量增加后,Dau,维拉帕米(Ver)和普萘洛尔(Pro)均能提高小鼠常压耐缺氧能力、延长存活时间、降低耗氧速率.Dau和Ver延长存活时间与其降低耗氧速率有关,而Pro的这一作用可能与降低耗氧速率和提高对氧的利用能力有关。 Dau明显降低iv垂体后叶素(Pit)所致的大白鼠心电图L—Ⅱ的J点和T波抬高幅度,降低大鼠冠脉结扎所致的心电图L—Ⅱ的J点抬高幅度和病理性Q波的出现率,明显缩小结扎24小时后心肌梗塞范围,提示Dau对实验性心肌缺血和梗塞具有保护作用。     

黄芪提取物对大鼠全脑缺血再灌注和小鼠缺氧性损伤的保护作用

目的　研究黄芪提取物 (EA)对大鼠全脑缺血再灌注和小鼠缺氧性损伤的保护作用。方法　采用小鼠常压耐缺氧实验和小鼠断头实验 ,观察EA对小鼠耐缺氧能力的影响 ;采用大鼠四动脉结扎模型 ,观察EA对缺血再灌注大鼠脑水肿 ,脑组织中超氧化物歧化酶 (SOD)活性、丙二醛(MDA)含量 ,血浆和海马内皮素 (ET)及病理性改变的影响。结果　EA能延长常压耐缺氧实验小鼠的存活时间及快速断头后小鼠的张口喘气时间 ;EA能减轻缺血再灌注大鼠脑组织的水肿程度 ,提高SOD活性、降低MDA含量 ,降低血浆和海马ET的含量 ,减轻病理性损伤。结论　EA对脑缺血再灌注和缺氧性损伤有明显的保护作用 ,减轻全脑缺血模型大鼠的脑水肿和病理性损伤 ,其作用机制可能与EA抗氧化、降低ET含量有关     

Toxicity and blood concentrations of xylazine and its metabolite, 2,6-dimethylaniline, in rats after single or continuous oral administrations

To cast light on whether the carcinogenic risk of 2,6-dimethylaniline (DMA), a metabolite of xylazine, may increase by ingestion of edible tissues from domestic animals treated with xylazine, the following studies of xylazine and DMA were performed. In Experiment I, male F344 rats received a single oral administration of 150 mg/kg of xylazine hydrochloride. Rats showed symptoms suggesting loss of sensation and pain immediately after the treatment. These signs had disappeared after 3 hr, but the animals died of hydrothorax and pulmonary edema by 9 hr. The plasma concentration of xylazine was 2.88 +/- 0.95 micrograms/ml at 15 min, and then decreased to 0.10 +/- 0.01 microgram/ml at 6 hr. The plasma level of DMA remained at 0.03 to 0.04 microgram/ml during the measurement period. In Experiment II, male F344 rats were fed a diet containing 1000 ppm of xylazine hydrochloride, regarded as the maximum tolerated dose, for 4 weeks. No clear clinical signs were evident and the plasma levels of xylazine and DMA were at the detection limit (0.02 microgram/ml) or less, although follicular cell hypertrophy of the thyroid was observed in all the treated animals. In Experiment III, male F344 rats were fed a diet containing 3000 ppm or 300 ppm of DMA for 4 weeks. Histological changes, such as atrophy of Bowman's gland and irregular arrangement of olfactory epithelial cells, were only observed in the olfactory epithelium of the 3000 ppm group. The plasma levels of DMA were 0.20 to 0.36 microgram/ml in the 3000 ppm group, but under the detection limit in the 300 ppm group. These results suggest that the probability of nasal carcinogenic effects of DNA on consumers via ingestion of edible tissues from food-producing animals treated with xylazine is extremely low, since DMA levels in the blood of rats subjected to continuous administration of high doses of xylazine remained under the detection limit.     

Antagonism of the antinociceptive action of xylazine, an alpha-sympathomimetic agent, by adrenoceptor and cholinoceptor blocking agents

The potency of adrenoceptor and cholinoceptor agents to antagonize the antinociceptive action of xylazine, an α-sympathomimetic agent, was studied.Yohimbine (1–2 mg/kg) and piperoxan (2.5–10 mg/kg) antagonized very effectively the antinociceptive effects of xylazine in two tests: electrical stimulation of the rat's tail and the hot plate test in mice.2-Diethylaminomethyl-1,4-benzodioxane (883 F), dibozane, ethomoxane, tolazoline and dibenamine were much less effective in rats. Azapetine, moxisylyte and phenoxybenzamine were as ineffective as propranolol, but Kö 1366, a potent β-adrenoceptor blocking agent was effective in high doses. Prindolol, another potent β-adrenoceptor blocking agent, only decreased the effect of xylazine on the startle. Atropine and mecamylamine did not change the effect of xylazine in rats.On the hot plate test in mice, dibozane, ethomoxane, tolazoline, phentolamine, dibenamine, chlorpromazine, clomipramine, pindolol, Kö 1366, atropine and atropine methyl nitrate were very effective in antagonizing the effect of xylazine, when both drugs were given intraperitoneally, but were less active when xylazine was given intracerebroventricularly. When the potential antagonist and xylazine were both administered into the cerebral ventricle of the brain, only piperoxan, yohimbine, tolazoline, clomipramine, Kö 1366, atropine and atropine methyl nitrate were effective. Phenoxybenzamine, azapetine, moxisylyte, propranolol and mecamylamine were ineffective by all routes of administration.These results suggest the involvement of receptors with properties in common with classical α-adrenoceptors in the antinociceptive action of xylazine, but these receptors seem to be distinct. In addition, in the hot plate test central cholinergic mechanisms could be involved as well as peripheral mechanisms.     

注射用尼莫地平脂质体对大鼠全脑缺血再灌注和小鼠缺氧性损伤的保护作用

目的：研究注射用尼莫地平脂质体（NDLI）对大鼠全脑缺血再灌注和小鼠缺氧性损伤的保护作用。方法：采用小鼠常压耐缺氧实验和小鼠断头实验，观察NDLI对小鼠耐缺氧能力的影响；采用Pulsinelli四动脉结扎法略加改良制作全脑缺血模型，记录对脑电图（EEG）及翻正反射的恢复时间、脑组织匀浆伊文思蓝含量的影响。结果：NDLI能显著延长小鼠的存活时间及断头后喘气持续时间，缩短大鼠脑电图及翻正反射的恢复时间，降低脑匀浆伊文思蓝的含量。结论：NDLI对全脑缺血再灌注和缺氧性损伤有明显的保护作用。     

果糖二磷酸钠对动物缺氧及急性脑缺血的保护作用

研究口服果糖二磷酸钠（ＦＤＰ）对动物缺氧及急性脑缺血的作用。方法：采用密闭、断头、结扎双侧带迷走神经颈总动脉等方法,观察ＦＤＰ对缺氧及急性脑缺血小鼠的影响;采用结扎双侧颈总动脉的方法,观察ＦＤＰ对急性脑缺血大鼠的影响。结果：ＦＤＰ可显著延长密闭、断头、结扎双侧带迷走神经颈总动脉后小鼠的死亡时间;可明显抑制结扎双侧颈总动脉大鼠的脑指数、脑含水量和血清磷酸肌酸激酶的增高,对脑血管通透性和血清乳酸脱氢酶的增高有抑制趋势,但作用不明显。结论：口服ＦＤＰ对动物缺氧及急性脑缺血有保护作用。     

Effect of yohimbine on xylazine-induced diuresis in rats

Intraperitoneal (ip) administration of xylazine (1-6 mg/kg) in male rats significantly increased urine flow over a 2-hr period in a dose-dependent manner, while urine osmolality was significantly decreased. Xylazine at 4.5 and 6 mg/kg significantly increased sodium excretion, whereas the 3 and 6 mg/kg doses of xylazine significantly increased potassium excretion. Yohimbine injected ip at 0.5 or 1 mg/kg 15 min before xylazine (6 mg/kg, ip) significantly decreased urine flow by 44% and 64% respectively. Yohimbine also prevented the increase in sodium and potassium excretion induced by xylazine. The data indicate that yohimbine is of value in controlling the diuretic effect of xylazine in rats.     

原儿茶酸衍生物的化学结构与冠脉流量、心肌耗氧量关系的探讨

本文研究原儿茶酸的三类衍生物,(1)原儿茶酸的四甲基吡嗪盐,(2)原儿茶酸与β-阻断剂有效基团相结合的衍生物,(3)原儿茶酸的同分异构物。利用测定猫冠状窦流量、心肌耗氧量、动静脉氧差、血压、心率等指标以及大、小鼠整体耐缺氧以探讨改变原儿茶酸的化学结构与药理作用间的关系。适量的吡嗪原儿茶酸在轻度增加冠脉流量的同时能较明显降低心肌耗氧量,而同剂量的四甲基吡嗪则明显增加心肌耗氧量,吡嗪原儿茶酸降低心肌耗氧量的程度较单用原儿茶酸约强14倍。四甲基吡嗪增强了原儿茶酸降低心肌耗氧量的作用。而原儿茶酸又能使四甲基吡嗪从增加心肌耗氧量反转为降低心肌耗氧量。原儿茶酸与β-阻断剂有效基团相结合合成的7704(异)、7704(叔)的作用基本上与β-阻断剂相似,但作用强度较心得宁弱。原儿茶酸同分异构物2,5-二羟基苯甲酸与2,6-二羟基苯甲酸虽能明显延长整体动物耐缺氧,但对猫心肌耗氧量则无明显作用。     

益气复脉合剂抗心律失常的实验研究

目的:证实益气复脉合剂的药理作用.方法:采用标准小鼠和健康大鼠,用氯仿、氯化钙、乌头碱造成动物心律失常模型,口服该合剂80 g.kg-1,观察动物的心律抑制或对抗作用.结果:益气复脉合剂对氯化钡、肾上腺引起的心律失常有明显的对抗作用,对氯仿、氯化钙引起心室纤颤致死有一定的保护作用.结论:该合剂为一个较好的抗心律失常新药.