辛夷挥发油的抗炎、抗过敏作用

辛夷挥发油腹腔注射(50,100mg/kg)能明显对抗二甲苯所致小鼠耳廓肿和蛋清所致的大鼠足跖肿。辛夷挥发油(20,30,40mg/ml)能对抗SRS-A、HA所致的豚鼠离体回肠的收缩作用,并能对抗致敏豚鼠回肠的过敏性收缩,这证明辛夷挥发油具有明显的抗炎、抗过敏作用。     

辛夷挥发油的抗炎、抗过敏作用

辛夷挥发油腹腔注射(50,100mg/kg)能明显对抗二甲苯所致小鼠耳廓肿和蛋清所致的大鼠足跖肿。辛夷挥发油(20,30,40mg/ml)能对抗SRS-A、HA所致的豚鼠离体回肠的收缩作用,并能对抗致敏豚鼠回肠的过敏性收缩,这证明辛夷挥发油具有明显的抗炎、抗过敏作用。     

柴胡皂甙抗炎作用机制初探

本文对柴胡粗皂甙的抗炎作用进行了研究,肌肉注射柴胡粗皂甙50mg/kg 能明显抑制由右旋糖酐引起的大鼠足浮肿。切除大鼠双侧肾上腺后,该作用消失。腹腔注射柴胡粗皂甙100mg/kg,能抑制由醋酸引起的小鼠腹液的渗出。     

两面针结晶8的解痉和镇痛作用研究

结晶-8,是从两面针提出的一种单体。当浓度为1×10^-6～1×10^-4g/ml对正常离体豚鼠回肠活动无影响,但对乙酰胆硷、匹鲁卡品、氯化钡及组织胺所致肠肌收缩有明显的松弛作用;结晶-8腹腔注射10 mg/kg有明显抑制小鼠扭体反应;8～20 mg/kg明显提高家兔及大鼠痛阈,200μg/kg脑室注射亦有明显提高大鼠痛阈。其镇痛作用不被丙烯吗啡(5 mg/kg)所拮抗,而被利血平(4 mg/kg)所对抗。表明结晶-8的解痉作用直接作用于肠平滑肌。而镇痛作用具有中枢性,与吗啡受体无直接关系,但与脑内单胺类介质有关。     

碘化二甲基木防己碱对实验性心律失常及心肌电活动的作用

静脉注射碘化二甲基木防己碱(DMT)1mg/kg,有对抗乌头碱诱发大鼠心律失常的作用。腹腔注射DMT0.25mg/kg,有对抗氯仿-肾上腺素诱发家兔心律失常的作用。腹腔注射DMT1.5mg/kg,对抗哇巴因诱发豚鼠心律失常,使豚鼠心室肌细胞动作电位平台期延长。DMT3.0×10^-6使家兔离体心房肌功能不应期延长。     

连钱草乙醇提取物对豚鼠离体肠平滑肌和小鼠肠运动功能的影响

目的:观察连钱草乙醇提取物对小鼠小肠推进运动、药物性腹泻小鼠模型和豚鼠离体回肠平滑肌收缩的影响,探讨其作用机理.方法:采用在体方法观察连钱草乙醇提取物对小鼠小肠推进功能的影响,采用离体方法观察连钱草乙醇提取物对豚鼠回肠平滑肌运动功能的影响.结果:连钱草乙醇提取物能够显著抑制小鼠小肠炭末推进率(P＜0.01),缓解大黄所致小鼠腹泻 (P＜0.01),对抗新斯的明所致的肠蠕动亢进 (P＜0.01).抑制豚鼠离体回肠平滑肌收缩(P＜0.01),拮抗乙酰胆碱、组胺、氯化钡对离体豚鼠回肠平滑肌的激动作用(P＜0.01).结论:连钱草乙醇提取物具有抑制肠蠕动作用,这种作用可能由胃肠道的胆碱能受体和组胺受体介导,或直接作用于回肠平滑肌细胞.     

氯哌胺对15-甲基前列腺素F_(2α)致泻和兴奋子宫作用的影响

氯哌胺(Loperamide)是一种新型止泻药,能拮抗15-M-PGF_(2α)引起的小鼠小肠内碳粉推进加速和腹泻,作用比吗啡和阿托品强,对离体大鼠回肠的抑制作用也比吗啡、阿托品强。氯哌胺能降低肠平滑肌张力,抑制离体大鼠回肠对15-M-PGF_(2α)的反应性,但却增强子宫平滑肌对15-M-PGF_(2α)的反应性。氯哌胺对离体大鼠子宫自发收缩活动低浓度兴奋、高浓度抑制。氯哌胺对15-M-PGF_(2α)促进大鼠空肠水和钠离子分泌也有拮抗作用,此作用不能被纳洛酮翻转。氯哌胺在小鼠的急性半数致死量为77.9 mg/kg。     

辣椒提取物的健胃和消食作用研究

目的探讨辣椒提取物的健胃消食作用。方法采用小鼠小肠推进试验和胃排空试验、对大鼠胃酸和胃蛋白酶分泌的影响以及对豚鼠离体回肠的影响等进行健胃消食试验。结果小鼠灌服低（0．025g·kg^-1）、中（0．05g·kg^—1）、高（0．1g·kg^—1）剂量的辣椒提取物后,可显著促进小鼠胃排空和小肠推进的作用,且中剂量的辣椒提取物对小鼠的胃排空作用更强,高剂量的辣椒提取物反而起到抑制小鼠胃排空的作用;随着剂量的增大,对小鼠小肠的推进作用也逐步地减小。在阿托品对豚鼠离体回肠抑制后加入辣椒提取物能使抑制后的回肠开始兴奋。对大鼠灌服低（0．075g·kg^-1）、中（0．15g·kg^—1）、高（0．3g·kg^-1）剂量的辣椒提取物,发现辣椒提取物有促进大鼠胃酸和胃蛋白酶分泌的作用。结论辣椒提取物有健胃     

蛇床子素抗变态反应的研究

蛇床子素能较强地抑制小鼠被动皮肤过敏(PCA)反应,对整体豚鼠组胺性喘息具有保护作用,对慢反应物质(SRS-A)引起的豚鼠离体回肠收缩以及豚鼠离体回肠的Schultz-Dzle反应呈明显的拮抗和阻断作用,并能抑制大鼠腹腔肥大细胞脱颗粒。上述作用均呈一定的剂量依赖关系。     

中华眼镜蛇毒口服给药镇痛作用的研究

目的：研究中华眼镜蛇毒灌服给药对小鼠的镇痛作用。方法：将ICR和昆明种小鼠,采用3种致疼痛模型,即冰醋酸所致扭体反应、小鼠热板法致痛实验和甲醛致炎性疼痛反应;中华眼镜蛇毒经热变性复性处理,将其灌胃给药30-270μg／kg。结果：中华眼镜蛇毒粗毒灌服给药能减少腹腔注射醋酸引起的扭体次数,延长热引起的疼痛反应潜伏期和减少甲醛引起的舔足反应。结论：中华眼镜蛇毒灌服给药具有良好的镇痛作用,且给药途径方便、安全范围大,具有进一步开发成新型镇痛药的潜力。     

Some pharmacological effects of the nematocide, morantel

1. In isolated nerve-muscle preparations as well as in nerve-muscle preparations in intact anaesthetized animals, morantel exhibited neuromuscular blocking properties similar to those of depolarizing blockers. The drug also caused spastic paralysis of 3 day-old chicks and contracture of the isolated toad rectus abdominis muscle.

2. Morantel caused contraction of the guinea-pig and rabbit isolated small intestine. This effect was antagonized by atropine and hexamethonium.

3. Morantel caused an increase in the blood pressure of the anaesthetized rat and cat and contraction of the nictitating membrane of the anaesthetized cat. These effects were antagonized by hexamethonium.

4. It was concluded that morantel (like the related compound pyrantel) has acetylcholine-like action and that its structure is consistent with such action.

     

Some pharmacological properties of the alpha-toxin of staphylococcus pyogenes

The alpha-toxin of Staphylococcus pyogenes produced a slowly developing contracture of isolated preparations of rabbit jejunum and of guinea-pig ileum which persisted after thorough washing and left the gut unresponsive to further doses of alpha-toxin or of acetylcholine. After incubation with antitoxin, the alpha-toxin no longer produced a contracture. Antitoxin only prevented the alpha-toxin response if added to the bath fluid before but not after the alpha-toxin. Certain drugs reduced the alpha-toxin contracture when added to the bath fluid before or after the alpha-toxin, but the contracture reappeared on washing. Papaverine abolished the contracture and pethidine was only slightly less active. Mepyramine, amyl nitrite, caffeine, aminophylline, adrenaline and ephedrine partly reduced the contracture. Hexamethonium, cocaine, tubocurarine and gallamine had no effect. The effect of atropine was only small. The gut-stimulant activity/haemolytic unit of two alpha-toxin samples differed greatly; this difference did not appear to be due to activity of impurities. The implications of these observations are discussed.     

Some pharmacodynamic effects of the babesicidal agents quinuronium and amicarbalide

The intravenous injection of a therapeutic dose of quinuronium methylsulphate (1 mg/kg) causes a fall in blood pressure in sheep, which is partly prevented by mepyramine and abolished by atropine. Larger doses of quinuronium cause more marked hypotension and inhibition of respiratory movement, which are not affected by atropine. Quinuronium strongly increases the amplitude of contraction of the isolated rabbit heart. This effect is not antagonized by atropine or mepyramine. Contractions of plain muscle in the guinea-pig and sheep, and hypersecretion of gastric acid in the rat and of saliva in the sheep were all produced by quinuronium. The responses to acetylcholine were potentiated by quinuronium, an effect which was abolished by atropine. Amicarbalide isethionate by comparison was weakly active. The drug causes no change in blood pressure, smooth muscle contraction or salivary secretion, but stimulates gastric secretion and partially inhibits the actions of acetylcholine in these preparations.     

Contraction induced by (-)-tartaric acid on rat isolated gastric fundus and its inhibition with indomethacin

Tartaric acid-evoked contractions of the rat isolated fundus could not be antagonized by atropine sulphate or methysergide hydrogen maleate, but were partially reduced by mepyramine hydrochloride. The contractions were prevented by indomethacin (25 micrograms ml-1) although the tissue remained sensitive to PGE2.     

Acetylcholine inhibition in the intact and chronically isolated cerebral cortex

1. Some spontaneously firing cells in the cerebral cortex of cats can be depressed by iontophoretically applied acetylcholine or acetyl-beta-methylcholine, and this depression is antagonized by atropine. Thirteen per cent of 101 spontaneously active neurones tested were depressed by cholinergic agents and 64% were excited.2. Single stimuli applied to the adjacent cortical surface excited 132 neurones orthodromically. Acetylcholine or acetyl-beta-methylcholine depressed this synaptic firing in 18% of the cells. The depression was blocked by atropine.3. The population of neurones in which cholinergic agents depressed spontaneous or synaptic firing was located within the superficial half of the cortex.4. Glutamate-induced firing was depressed by cholinergic agents in 41% of 211 cells tested; atropine and strychnine strongly antagonized this depressant action, while dihydro-beta-erythroidine was a weaker antagonist.5. Long duration inhibition of glutamate-induced firing evoked by repetitive stimulation of the cortical surface could be blocked by atropine or strychnine in both the intact and chronically isolated cortex. This provides strong evidence for a system of intracortical cholinergic neurones which make direct inhibitory contacts with neurones in the superficial layers of the cortex.     

Antagonism of acetylcholine by adrenaline antagonists

Phenoxybenzamine antagonized the inhibitory action of acetylcholine on the guinea-pig isolated atrium. The antagonism was slow in onset, very slowly reversible, and could be overcome by increased concentrations of acetylcholine. In contrast, atropine inhibited the action of acetylcholine quickly, and the effect disappeared soon after withdrawal. The pA₁₀ of phenoxybenzamine (2 hr of contact) was 6.8, and that of atropine (30 min of contact) was 8.4. In the presence of atropine phenoxybenzamine did not exert a slowly reversible antagonism, and the dose-ratio of acetylcholine returned to normal soon after withdrawal of both drugs. Phenoxybenzamine also antagonized acetylcholine in the guinea-pig isolated ileum, but with higher concentrations acetylcholine did not overcome the antagonism. The pA₁₀ (60 min of contact) was 6.6. The pA₁₀ of chlorpromazine in the atrium (2 hr of contact) and ileum (60 min of contact) was 5.9. Phentolamine, 2-diethylaminomethylbenzo-1,4-dioxan hydrochloride (883 F), and yohimbine antagonized acetylcholine in the atrium and ileum but required higher concentrations than chlorpromazine.     

Some pharmacological properties of the α-toxin of staphylococcus pyogenes

The α-toxin of Staphylococcus pyogenes produced a slowly developing contracture of isolated preparations of rabbit jejunum and of guinea-pig ileum which persisted after thorough washing and left the gut unresponsive to further doses of α-toxin or of acetylcholine. After incubation with antitoxin, the α-toxin no longer produced a contracture. Antitoxin only prevented the α-toxin response if added to the bath fluid before but not after the α-toxin. Certain drugs reduced the α-toxin contracture when added to the bath fluid before or after the α-toxin, but the contracture reappeared on washing. Papaverine abolished the contracture and pethidine was only slightly less active. Mepyramine, amyl nitrite, caffeine, aminophylline, adrenaline and ephedrine partly reduced the contracture. Hexamethonium, cocaine, tubocurarine and gallamine had no effect. The effect of atropine was only small. The gut-stimulant activity/haemolytic unit of two α-toxin samples differed greatly; this difference did not appear to be due to activity of impurities. The implications of these observations are discussed.     

Studies on antinephritic effects of plant components in rats (1). Effects of saikosaponins original-type anti-GBM nephritis in rats and its mechanisms

This study was designed to clarify the anti-nephritic effects of the saikosaponins that are contained in Bupleurum falcatum L. crude saikosaponin at 1.0 mg and 5.0 mg/kg, i.p. prevented urinary protein excretion and elevation of serum cholesterol content on the 10th day after the injection of anti-GBM serum. Moreover, crude saikosaponin at 1.0 mg and 5.0 mg/kg, i.p. significantly inhibited histopathological changes such as hypercellularity and adhesion. On the other hand, saikosaponin a (5.0 mg/kg, i.p.) and d (1.0 mg and 5.0 mg/kg, i.p.) also prevented urinary protein excretion, elevation of serum cholesterol content, and histopathological changes. In the second study, to clarify the anti-nephritic mechanisms of saikosaponins on this model, we investigated the effect of saikosaponins on platelet aggregation, release of corticosterone and reactive oxygen species scavengers activity. Crude saikosaponin and saikosaponin d significantly inhibited the increase in platelet aggregation, and saikosaponin d enhanced the serum and intra-adrenal corticosterone levels. Crude saikosaponin and saikosaponin a inhibited the decrease in activity of scavengers (SOD, catalase, glutathione peroxidase). These results indicate that saikosaponins were effective on this model, and anti-nephritic mechanisms of saikosaponins were party due to anti-platelet, corticosterone releasing and enhancing action on the activity of reactive oxygen species scavengers.     

Effects of atropine on responses to directly and indirectly acting cholinomimetics

In the isolated guinea-pig ileum atropine delayed the onset and slowed the rate of contraction of responses to indirectly acting cholinomimetics (nicotine, dimethylphenylpipezinium, dimethlaminoethanol, dimethylaminopropanol and supinidine), while response heights were little affected. In contrast, atropine had little effect on the time taken for acetylcholine to produce its peak response, while contraction height was reduced.The competitive action of atropine on concentration-effect curves to acetycholine was not apparent with indirectly acting cholinomimetics. Nevertheless analysis of time-effect rather than concentration-effect curves showed that atropine competitively antagonized responses to acetylcholine released by the latter agonists. Atropine antagonism of exogenously administered and endogenously released acetylcholine was similar. The extent and offset of acetylcholine antagonism by atropine was unaffected by indirectly acting compounds.With indirectly acting cholinomimetics, the atropine resistance may be explained on the basis of the differing mechanisms by which exogenous and endogenous acetylcholine elicit responses, rather than a difference in the receptors involved or limited access of atropine to endogenous sites.     

Ca antagonistic and non-specific effects of diltiazem on the rat phrenic nerve diaphragm preparation

The calcium antagonist diltiazem (2.8 X 10(-4) M) blocked the twitches of a rat phrenic nerve diaphragm preparation after a period of twitch potentiation. Its ability to block twitches was greater during indirect than direct stimulation. Experiments on the isolated phrenic nerve indicated that the excitability of the nerve was blocked. Diltiazem (2.3-9.0 X 10(-5) M) caused a similar inhibition of indirectly and directly elicited tetanic contractions and EMG. Experiments with d-tubocurarine and lowered temperature disclosed a separate inhibition at the neuromuscular junction. High Ca2+ did not reverse the diltiazem-affected twitch or tetanic contractions, which suggests that they are non-specific effects. KCl (100 mM)-induced contractures were antagonized at low (2.3-4.5 X 10(-5) M) but not at high (1 mM) concentrations of diltiazem. Diltiazem depressed the initial phase of the two-phasic caffeine (10 mM) contracture and increased and accelerated the slow phase. Diltiazem greatly reduced the amplitude and duration of the caffeine-potentiated KCl contracture, and reduced and delayed the slow phase of the KCl-potentiated caffeine contracture. The effects on the combined contractures (caffeine-induced, KCl-potentiated) were partly antagonized by a high Ca2+ (2.2 X 10(-5) M) solution, which suggests that diltiazem has calcium antagonistic effects.