景蜂胶囊对小鼠的耐缺氧作用

目的研究景蜂胶囊对小鼠耐缺氧作用的影响。方法连续给予小鼠不同剂量的景蜂胶囊10 d,末次给药1 h后,进行密闭缺氧、亚硝酸钠中毒缺氧和急性脑缺血性缺氧实验。以存活时间、血红蛋白(Hb)、丙二醛(MDA)的含量和超氧化物歧化酶(SOD)的活性为指标,观察景蜂胶囊对小鼠耐缺氧作用的影响。结果景蜂胶囊可延长小鼠在不同缺氧条件下的存活时间,增加小鼠Hb的含量,抑制脂质过氧化反应并增加血清中SOD活性。结论景蜂胶囊具有提高小鼠耐缺氧能力的作用。     

穿山龙水提物对小鼠耐缺氧及抗疲劳的作用

目的:观察穿山龙水提物对小鼠耐缺氧及抗疲劳作用的影响。方法:采用常压耐缺氧法和负重游泳法观察穿山龙水提物对小鼠耐缺氧和抗疲劳作用的影响。结果:与生理盐水组比较,穿山龙水提物治疗组能明显延长缺氧小鼠的存活时间(P<0.05或P<0.01),并能明显延长小鼠的负重游泳时间(P<0.01)。结论:穿山龙具有明显的耐缺氧及抗疲劳的作用。     

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。     

大苞雪莲有效成分的抗缺氧药效学研究

目的 研究大苞雪莲有效成分（石油醚活性部位及其主要单体成分二十八烷）的抗缺氧药效学。方法 首先采用常压密闭缺氧耐受力实验和急性减压缺氧耐受力实验联合评价大苞雪莲石油醚部位和二十八烷的抗缺氧活性,然后采用3种化学中毒缺氧模型（氰化钾、亚硝酸钠、盐酸异丙肾上腺素）进行其抗化学中毒缺氧活性的药效学评估。结果 大苞雪莲石油醚部位和二十八烷可以有效延长常压密闭缺氧小鼠的存活时间（P<0.01）,降低急性减压缺氧小鼠的死亡率（P<0.01）,且具有剂量依赖关系;化学中毒缺氧药效学研究表明,石油醚部位和二十八烷在化学中毒缺氧实验中的小鼠存活时间均明显大于乙酰唑胺（P<0.05）。结论 大苞雪莲石油醚部位和二十八烷具有良好的抗缺氧活性。     

5-甲基-7,4’-二羟基异黄酮水溶性衍生物的合成及其抗缺氧活性

目的5-甲基-7,4’-二羟基异黄酮水溶性衍生物的合成及其抗缺氧活性的比较。方法三氟化硼-乙醚催化的“一锅法”工艺制备母体化合物1,并通过甲基化和磺化反应合成衍生物2～4,常压耐缺氧试验评价其活性。结果化合物3和4水溶性强,且抗缺氧作用等价于母体化合物。结论新合成的水溶性化合物3和4具有明显的抗缺氧活性。     

综合评判人参根皂甙抗低压缺氧作用

本文利用模糊数学中综合评判法对人参根皂甙(GRS)抗低压缺氧作用进行了考察。结果表明,腹腔注射GRS(70-200mg/kg)可明显延长小鼠在不同低压缺氧环境(205-235mm Hg)的存活时间。采用综合评判处理可提高实验结果的准确性和可靠性,并得到满意的结果。     

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。     

圣脑康丸与3种中药复方制剂耐缺氧作用比较研究

目的比较圣脑康丸与几种中药复方制剂对缺氧小鼠的保护作用。方法采用小鼠常压密闭缺氧、急性脑缺氧和亚硝酸钠(NaNO2)中毒缺氧实验,观察圣脑康丸与几种中药复方制剂(红景天胶囊,复方党参片,速效救心丸)对缺氧小鼠存活时间的影响。结果与几种中药复方制剂比较,圣脑康丸能显著延长小鼠常压密闭缺氧存活时间、急性脑缺氧存活时间及NaNO2中毒小鼠的存活时间。结论圣脑康丸具有显著的耐缺氧作用。     

The usefulness of a model of acute hypoxia for the testing of cerebroprotective drugs

The aim of this study was to find out whether the mouse in acute normobaric hypoxia (3.5% O2) may be appropriate as a screening model for testing cerebroprotective drugs. The survival time of the mice in hypoxia was used to determine drug effects. 39 agents with various pharmacological and toxicological properties were investigated. Cerebroprotective, centrally depressant and stimulating as well as cardiovascular drugs were included. Only 6 out of 16 cerebroprotective drugs used therapeutically prolonged the survival time of mice in acute hypoxia. However, a positive effect was demonstrable especially for those cerebroprotective drugs (extractum Ginkgo bilobae, meclofenoxate, naftidrofuryl, pentoxifylline and pyritinol), which are generally accepted to be active. On the other hand, 12 out of 23 drugs which are therapeutically used as cardiovascular drugs, central stimulants or depressants or have known toxicological effects also prolonged the survival time of mice in hypoxia. Thus, it became clear that the result of this hypoxia test may be influenced by various pharmacological actions. Especially drugs stimulating the cardiovascular system or depressing CNS activity could prolong the survival time of mice in hypoxia, whereas drugs with vasodilating effects could even shorten it. Opposite effects could superpose or neutralize each other. Therefore, the mouse in acute hypoxia seems to be of limited value as a screening model for testing cerebroprotective drugs.     

Survival time in hypoxic mice: differentiation between apomorphine-induced hypothermia and antihypoxic properties

The effects of apomorphine on survival time of mice during lethal anoxic hypoxia were studied. Apomorphine induced hypothermia and an increase in survival time. Both these effects were mediated by cerebral dopamine receptors, however with different affinity for the neuroleptics haloperidol and sulpiride. These data suggest that apomorphine's antihypoxic effect is not only mediated by the classical effect of hypothermia but also by slowing of oxydative metabolism.     

新型双靶标化合物的合成与其抗高原缺氧损伤活性研究

目的：根据“双靶标药物设计原理”,设计合成出一种兼具自由基清除活性和碳酸酐酶抑制活性的新型双靶标化合物,并研究其抗高原缺氧活性。方法将乙酰唑胺（碳酸酐酶抑制剂）与氮氧自由基（新型自由基清除剂）通过桥联基结合,设计具有双靶标联合作用的目标化合物,并经过小鼠常压密闭、急性减压和化学性中毒3种缺氧耐受力实验评价其抗缺氧活性。结果所合成的化合物结构经过电子顺磁共振、ESI-MS 和元素分析进行确认。与缺氧模型组、乙酰唑胺组和氮氧自由基组相比,目标化合物组可以明显延长小鼠在常压密闭缺氧环境中的存活时间（ P ﹤0.05,P ﹤0.01）,降低急性减压缺氧小鼠1 h 内死亡率（P ﹤0.01）,延长氰化钾、亚硝酸钠和盐酸异丙肾上腺素3种化学性中毒缺氧小鼠的存活时间（P ﹤0.05,P ﹤0.01）。结论新型双靶标抗缺氧损伤化合物合成方法简便,产率较高,并且表现出了较好的抗缺氧活性。     

Dopamine receptor-mediated hypothermia induced in rats by (+)-, but not by (-)-3-PPP

The novel dopaminergic agents (+)- and (-)-3-PPP were evaluated for their effects upon thermoregulation in rats maintained at room temperature (approximately 22 degrees C). Although approximately 30 times less potent than apomorphine, (+)-3-PPP induced a clearcut, dose-dependent and haloperidol/pimozide-reversible hypothermia. In contrast, the (-)-enantiomer per se lacked a significant effect upon rat body temperature. However, (-)-3-PPP clearly attenuated apomorphine-induced hypothermia. Simultaneous biochemical investigations confirmed the presence of central dopamine (DA) agonist and antagonist properties for (+)- and (-)-3-PPP, respectively, at the doses employed. The results are compared to the agonist and antagonist effects of the 3-PPP enantiomers in various other central DA receptors systems. Particular reference is made to the recent hypothesis by Carlsson (J. Neural Transm. 57 (1983) 309, relating agonist intrinsic activity to the DA receptor responsiveness state, in turn determined by the endogenous tone. Based on the findings with (+)- and (-)-3-PPP it is suggested that DA receptors mediating hypothermia in the rat may be more akin to 'normosensitive' postsynaptic than to highly 'agonist-responsive' autoreceptors.     

Is taurine-induced hypothermia in the rat mediated by 5-HT?

Summary Intraventricular administration of taurine in the rat caused hypothermia, the extent of which was directly dependent upon the thermal gradient between the body and the environment.Pre-treatment of animals with p-chlorophenylalanine, which depleted most of the brain serotonin, strongly reduced the hypothermia induced by taurine.Pre-treatment with -methyltyrosine induced hypothermia and sedation in animals. When this was followed by a taurine injection, they exhibited a decrease in body temperature which fitted the curve relating thermal gradients to hypothermic responses.It is suggested that taurine induced hypothermia in rat is mediated in part by central 5-HT systems.     

半乳糖苷三氮唑鹰嘴豆芽素A的合成与抗缺氧活性研究

目的设计合成半乳糖苷三氮唑鹰嘴豆芽素A并研究其抗缺氧活性。方法以半乳糖叠氮化物、炔丙基溴和鹰嘴豆芽素A为原料,利用＂Click＂化学方法将糖基化三氮唑药效基团引入鹰嘴豆芽素A分子结构中得到一种衍生物——半乳糖苷三氮唑鹰嘴豆芽素A,并通过小鼠常压密闭耐缺氧实验和化学物质中毒实验对其抗缺氧活性进行评价。结果产物结构经1H-NMR、IR、EI-MS和元素分析确认,半乳糖苷三氮唑鹰嘴豆芽素A能够显著延长不同缺氧状态下小鼠的存活时间,且活性优于乙酰唑胺（P〈0.05,P〈0.01）。结论本研究采取的合成半乳糖苷三氮唑鹰嘴豆芽素A的方法操作简便、条件温和、产率较高,而且该化合物表现出较高的抗缺氧活性。     

Are ascending noradrenergic and serotonergic pathways necessary for effects of electroconvulsive treatment? Clonidine hypothermia and forced swim study

Are ascending noradrenergic and serotonergic pathways necessary for effects of electroconvulsive treatment? Clonidine hypothermia and forced swim study. W. DANYSZ , W. KOSTOWSKI, M. HAUPTMANN, A. BIDZINSKI. Pol. J. Pharmacol. Pharm., 1989, 41, 15-22. Influence of chemical lesions to the noradrenergic locus coeruleus (intracerebral 6-OHDA injection, systemic administration of DSP-4) and serotonergic raphe system (intracerebral 5,7-DHT) on some effects produced by electroconvulsive shock (ECS) was studied. Administration of ECS slightly but significantly attenuated clonidine (CLO)-induced hypothermia and reduced rats immobility in forced swim test. DSP-4 reduced ECS action on CLO hypothermia remaining without effect upon ECS action in the second test. Other lesions were ineffective in both tests. This finding is in contrast to results obtained previously in animals receiving desipramine. The possible difference between ECS and antidepressant drugs action is discussed.     

Effects of neutral aminoacids injected into cerebrospinal fluid space on glucose metabolism in the rat brain

In order to ascertain whether the hypothermia induced by neutral aminoacids could depend upon a reduced oxygen supply to the brain, rats received, through a cannula chronically implanted into the lateral ventricle, glycine, GABA and taurine (20 $\text{μmol}\text{250}$ g body weight). The brain levels of glucose, lactate, pyruvate and glycogen and those of glucose and lactate in the blood were determined during hypothermia.The concentration of these metabolites and the brain blood volume of cannulated animals were similar to those of unoperated controls.No consistent biochemical evidence of brain hypoxia was found after glycine, taurine and GABA administration.It is concluded that the effect exerted by the injection of neutral aminoacids into the CSF on thermoregulation is dependent on their direct action on nervous centres.     

A comparison of the effects of morphine and pethidine upon body temperature and the reversal of reserpine's effects upon body temperature in the mouse.

The effects of morphine and pethidine upon body temperature and upon the reversal of reserpine hypothermia in the mouse were investigated. Both morphine and pethidine produced a dose-dependent fall in body temperature, that of morphine being totally antagonized by nalorphine and partially by naloxone, while that of pethidine was antagonised by naloxone and enhanced by nalorphine. Both drugs reversed reserpine-induced hypothermia. The reversal by morphine, but not by pethidine, was partially antagonized by naloxone. Adrenalectomy prevented the reversal of reserpine hypothermia by pethidine but morphine produced a partial reversal. Ganglion blockade and alpha-and beta-blockade all prevented reversal of reserpine hypothermia by both drugs. The results are discussed with regard to differences between pethidine and morphine and possible involvement of opiate receptors.     

Differential effects of morphine on core temperature in stressed and non-stressed rats

The effects of morphine on body temperature were studied in rats in two different states - stressed and non-stressed. Morphine injected subcutaneously (s.c.) produced a dual action on body temperature in non-stressed rats. Hyperthermia occurred at lower doses (2.5-10 mg/kg) while hypothermia was produced with a higher dose (20 mg/kg). Both of these effects of morphine were reversed by naloxone (0.1-5.0 mg/kg). Stressing the rats (immobilization with wire mesh) produced slight hypothermia which was markedly potentiated by morphine (5-20 mg/kg) in a dose-dependent manner. Enhancement of hypothermia by morphine in the stressed animals was antagonized by pretreatment with naloxone (0.1-5.0 mg/kg). When rats were treated with morphine (10 mg/kg) 1 h before stress, and were then exposed to immobilization stress, the hyperthermia exhibited in the non-stressed state changed to hypothermia in the stressed state. When the rats which were treated with morphine and then stressed for 1 h were released from stress, the hypothermia observed in the stressed state progressively changed to hyperthermia. Furthermore, these morphine effects, i.e. hyper- and hypothermia in the non-stressed and stressed states, respectively, were reversed but not eliminated by naloxone. These results suggest that the effects of morphine on core temperature in rats are altered depending upon the state of the animals. That is, morphine appears to have a dual action, hyperthermia in the non-stressed state and hypothermia in the stressed state. It also appears that these actions are mediated via opiate receptors.     

蜂斗菜总内酯对动物高原缺氧保护作用的研究

目的 探讨蜂斗菜总内酯对动物高原缺氧的保护作用。方法 通过建立小鼠急性密闭缺氧模型、小鼠急性减压缺氧模型以及大鼠减压缺氧模型,观察蜂斗菜总内酯对实验动物存活时间及死亡率的影响,并检测动物血糖、不同脏器中糖原、三磷酸腺苷（adenosine triphosphate,ATP）、乳酸（lactic acid,LD）、乳酸脱氢酶（lactic dehydrogenase,LDH）的含量。结果 蜂斗菜总内酯能够明显延长小鼠急性密闭缺氧的存活时间,提高存活时间增加率;能显著降低小鼠急性减压缺氧的死亡率;对于减压缺氧大鼠,能显著降低血糖含量,显著增加肝脏、骨骼肌、心肌中的糖原含量以及脑、肝脏、骨骼肌、心肌中的ATP含量,并能显著降低血浆、骨骼肌和心肌中的LD含量,降低心肌中的LDH含量。结论 蜂斗菜总内酯对小鼠急性密闭缺氧、小鼠急性减压缺氧和大鼠减压缺氧均具有明显的保护作用,其抗高原缺氧作用与其降低血糖含量,提高脏器中糖原含量、ATP含量,降低脏器中LD及LDH含量有关。     

提高2,3-BPG水平对组织氧气供应的影响及其药物研究进展

初次进入高原的人由于环境氧分压降低,机体易产生一系列急性高原反应(acute mountain sickness,AMS).国内对于抗缺氧药物的研究大多以改善AMS症状为主,从氧气利用解决缺氧问题的研究甚少.因此以释氧源头红细胞为着手点,通过增加红细胞中的2,3-二-磷酸甘油酸(2,3-diphosphoglycera...