五味清热饮预防发热药效学研究

目的:研究五味清热饮在大鼠的预防发热作用.方法:大鼠口服正柴胡饮及高、中、低剂量五味清热饮30分钟后,皮下注射2,4-二硝基苯酚30 mg/kg致大鼠发热,观察0.5、1.0、1.5、2.0、2.5、3.0、4.0及5.0 h大鼠体温变化.结果:与对照组比较,五味清热饮高、中、低剂量组于给药后0.5、1.0、1.5、2.0、2.5及3.0 h对大鼠体温均具有非常显著的降低作用(P＜0.01).结论:五味清热饮对2,4-二硝基苯酚致大鼠发热有明显的预防作用.     

藏药经典验方玛奴西汤颗粒解热作用的实验研究

目的 观察藏药玛奴西汤颗粒的解热作用.方法 建立干酵母和2,4-二硝基苯酚致大鼠发热模型,观察灌胃给药玛奴西汤颗粒高、中、低剂量与阿司匹林后,1、2、3和4h内的体温变化.结果 与干酵母致热模型组相比,玛奴西汤颗粒高、中剂量组给药后2～4 h大鼠体温显著下降(P＜0.05),阿司匹林阳性对照组给药后1～4 h大鼠体温显著降低(P＜0.01);与 2,4-二硝基苯酚致热模型组相比,玛奴西汤高、中和低剂量组给药后2h大鼠体温显著下降(P＜0.05),阿司匹林阳性对照组给药后1～4 h大鼠体温与模型组无显著差异(P＞0.05).结论 玛奴西汤颗粒对干酵母和2,4-二硝基苯酚所致大鼠发热模型均有一定的解热作用.     

双黄连口服液解热抗炎作用的实验研究

目的 探讨双黄连口服液的解热抗炎作用.方法 采用2,4-二硝基苯酚致大鼠发热法研究双黄连口服液的解热作用,采用二甲苯致小鼠耳肿胀法和角叉菜胶致大鼠足肿胀法研究双黄连口服液的抗炎作用.结果 与空白对照组比较,双黄连口服液能显著降低2,4-二硝基苯酚致大鼠发热模型的体温(P＜0.05),并能显著抑制二甲苯致小鼠耳肿胀及角叉菜胶致大鼠足肿胀的炎症反应(P＜0.05).结论 双黄连口服液具有显著的解热、抗炎作用.     

清热糖浆的药理作用研究

目的观察清热糖浆的抗菌、抗炎、解热、镇痛和镇咳作用。方法试管法观察抗菌作用,醋酸法考察小鼠毛细血管通透性;2,4-二硝基苯酚致热法观察对大鼠的解热作用;扭体法和甲醛致痛法观察镇痛作用;氨水刺激法考察镇咳作用。结果清热糖浆对4株临床分离菌株均有抑制作用;能降低小鼠毛细血管通透性;对2,4- 二硝基苯酚致热大鼠有明显退热作用;明显减少醋酸致小鼠扭体次数,减少甲醛所致大鼠疼痛反应次数;减少氨水致咳嗽次数。结论清热糖浆有抗茵、抗炎、解热、镇痛和镇咳作用。     

三叶青提取物抗炎、镇痛及解热作用的实验研究

目的:探讨三叶青提取物(ERT)的抗炎、镇痛及解热作用,并验证其相关功效.方法:以小鼠腹腔毛细血管通透法、小鼠耳肿胀法及大鼠足肿胀法观察其抗炎作用;以小鼠扭体法、热板法观察其镇痛作用;以干酵母致热法及2,4-二硝基苯酚致热法观察其解热作用.结果:三叶青提取物能明显抑制小鼠腹腔毛细血管炎性渗出,抑制二甲苯所致小鼠耳廓肿胀及10%蛋清致大鼠足跖肿胀;减少醋酸致小鼠扭体次数,提高热板法小鼠痛阈值;并降低干酵母和2,4-二硝基苯酚致大鼠发热模型的体温.结论:三叶青提取物具有较好的抗炎、镇痛及解热作用,与其相关的中医临床功效及主治相符.     

柴胡静脉乳剂的解热、镇痛作用

目的研究柴胡静脉乳剂的解热、镇痛作用。方法分别采用2,4-二硝基苯酚致热大鼠模型、醋酸致小鼠扭体反应及小鼠热板致痛模型,研究柴胡静脉乳剂的解热、镇痛作用。结果柴胡静脉乳剂可以降低由2,4-二硝基苯酚引起的大鼠体温升高,减少醋酸致小鼠扭体反应次数及提高小鼠热板试验痛阈值。结论柴胡静脉乳剂具有解热、镇痛作用。     

芩术颗粒对发热和疼痛模型鼠的解热镇痛作用

目的:研究芩术颗粒的解热镇痛作用。方法:采用干酵母或2,4-二硝基苯酚致大鼠发热模型,观察芩术颗粒对模型大鼠的解热作用;通过热板法及小鼠醋酸致扭体反应,观察芩术颗粒对模型小鼠疼痛的影响。结果:40、20、10 g/kg芩术颗粒对模型大鼠体温有降低作用;40、20 g/kg芩术颗粒可明显延长模型小鼠疼痛潜伏期及减少其扭体反应次数。结论:芩术颗粒具有一定的解热镇痛作用。     

风热流浸膏解热镇痛和抗炎作用的实验研究

目的观察风热流浸膏的抗炎、镇痛和解热作用。方法采用二甲苯致小鼠耳肿胀、角叉菜胶致大鼠足趾肿胀的模型观察抗炎作用;采用乙酸和热刺激致小鼠疼痛的模型观察镇痛作用;采用2,4-二硝基酚和酵母粉致大鼠发热的模型观察解热作用。结果风热流浸膏能减轻小鼠耳肿胀和大鼠足趾肿胀炎症反应,缓解乙酸和热刺激所致疼痛,降低2,4-二硝基酚和酵母粉致大鼠发热的体温。结论风热流浸膏具有显著的抗炎、镇痛和解热作用。     

抗感灵片的解热镇痛及抗炎作用

目的：探讨抗感灵片的解热、抗炎、镇痛作用。方法：大鼠背部皮下注射1％二硝基苯酚造发热模型,观察抗感灵片对体温的影响;制备小鼠耳廓炎症以及大鼠蛋清性足肿胀模型,观察对炎症的影响;采用醋酸扭体实验研究镇痛作用。结果：抗感灵片对2,4-二硝基苯酚引起的大鼠体温升高及二甲苯和蛋清引起的炎性反应均有显著性抑制作用,能明显抑制醋酸引起的小鼠扭体反应,具有显著镇痛作用。结论：抗感灵片具有解热镇痛抗炎作用。     

银胡感冒海绵剂解热、抗炎、镇痛作用的实验研究

目的：研究银胡感冒海绵剂在解热、镇痛、抗炎等方面的作用,为临床用药提供实验依据。方法：采用2,4-二硝基苯酚致大鼠发热法观察银胡感冒海绵剂的解热作用,小鼠耳肿胀法、大鼠足跖肿胀法观察银胡感冒海绵剂的抗炎作用,小鼠扭体法、小鼠热板法、观察银胡感冒海绵剂的镇痛作用。结果：银胡感冒海绵剂对2,4-二硝基苯酚所致大鼠的发热反应有明显的解热作用;对巴豆油所致小鼠耳壳肿胀和对角又菜胶所致大鼠足跖肿胀均有显著的抑制作用;能显著抑制醋酸所致的小鼠扭体反应次数并能显著提高小鼠热板痛阈值。结论：银胡感冒海绵剂具有显著的解热、抗炎和镇痛作用。     

牛黄解毒滴丸解热镇痛和抗炎作用实验

目的：观察牛黄解毒滴丸的解热镇痛和抗炎作用。方法：采用2,4-二硝基酚大鼠致热法观察其解热作用;小鼠扭体法、热板刺激法观察其镇痛作用;小鼠耳部肿胀法、大鼠蛋清足肿胀法观察其抗炎作用。结果：牛黄解毒滴丸显著降低2,4-二硝基酚所致大鼠升高的体温;明显减轻和抑制热板所致的小鼠疼痛及醋酸所致的小鼠扭体反应;抑制二甲苯所致的小鼠耳肿胀和蛋清所致的大鼠足肿胀。结论：牛黄解毒滴丸对实验大鼠、小鼠具有良好的解热、镇痛和抗炎作用。     

Peripheral and central components in the hyperthermic effect of desipramine in reserpinized rats

Pithed rats show a decrease of body temperature which is not affected by reserpine, cocaine or desipramine. Noradrenaline decreases the rate of fall of body temperature and this effect is enhanced by pretreatment with cocaine or desipramine. Reserpine with desipramine or with cocaine also produces a decreased rate of fall of body temperature. But if reserpine is given 18 hr before pithing, desipramine is without effect although noradrenaline and 2,4-dinitrophenol produce a calorigenic response. The hyperthermic effect of desipramine in reserpinized rats is also decreased by spinal transection. Lumbar transection is less effective than cervical transection. It is concluded that the integrity of the central nervous system is required for the development of the hyperthermic effect of desipramine in previously reserpinized rats.     

芦竹根中双吲哚生物碱的分离鉴定及药效研究

目的 分离、鉴定芦竹根中的生物碱,并对其进行药效试验.方法 采用柱层析法从国产芦竹根中分离得一种生物碱,用NMR、HR-EIMS、IR和UV等分析方法测定其波谱数据和理化常数,鉴定其化学结构;考察其对2,4-二硝基酚所致大鼠发热和角叉菜致炎大鼠足跖肿胀的作用.结果 该化合物为3-(N,N-二甲氨基乙基)-4-(3-甲氨基乙基-吲哚-1-)-5-羟基吲哚(arundamine,芦竹胺),对2,4-二硝基酚致热大鼠有明显解热作用,对角叉菜致炎大鼠足跖肿胀有明显抑制作用.结论 芦竹胺系首次从中国芦竹根中分离得到,为芦竹根的有效成分.     

Comparative study of toxicity of 4-nitrophenol and 2,4-dinitrophenol in newborn and young rats

The toxicities of 4-nitrophenol and 2,4-dinitrophenol in newborn and young rats was examined and the susceptibility of newborn rats was analyzed in terms of presumed unequivocally toxic and no observed adverse effect levels (NOAELs). In the 18-day repeated dose newborn rat study, 4-nitrophenol was orally given from Day 4 to Day 21 after birth but did not induce any toxicity up to 160 mg/kg in the main study, although it induced death in one of six males at 160 mg/kg, and three of six males and one of six females at 230 mg/kg in a prior dose-finding study. In the 28-day repeated dose oral toxicity study starting at 6 weeks of age, 4-nitrophenol caused the death of most males and females at 1,000 mg/kg but was not toxic at 400 mg/kg except for male rat-specific renal toxicity. As unequivocally toxic levels were considered to be 230 mg/kg/day in newborn rats and 600 to 800 mg/kg/day in young rats, and NOAELs were 110 mg/kg/day in newborn rats and 400 mg/kg/day in young rats, the susceptibility of the newborn to 4-nitrophenol appears to be 2.5 to 4 times higher than that of young animals. In the newborn rat study of 2,4-dinitrophenol, animals died at 30 mg/kg in the dose-finding study and significant lowering of body and organ weights was observed at 20 mg/kg in the main study. In the 28-day young rat study, clear toxic signs followed by death occurred at 80 mg/kg but there was no definitive toxicity at 20 mg/kg. As unequivocally toxic levels and NOAELs were considered to be 30 and 10 mg/kg/day in newborn rats and 80 and 20 mg/kg/day in young rats, respectively, the toxicity of 2,4-dinitrophenol in newborns again seems to be 2 to 3 times stronger than in young rats. Abnormalities of external development and reflex ontogeny in the newborn were not observed with either chemical. Based on these results, it can be concluded that the toxic response in newborn rats is at most 4 times higher than that in young rats, at least in the cases of 4-nitrophenol and 2,4-dinitrophenol.     

Abolition of the morphine effect on body temperature in midbrain raphe lesioned rats

The hyperthermia and the hypothermia elicited by 5 mg/kg, i.p. or 30 mg/kg i.p. of morphine in rats are abolished by a previous lesion of the midbrain raphe resulting in a lowering of forebrain 5-HT and 5-hydroxyindolacetic acid. Lesions lateral to the midbrain raphe which do not modify brain 5-HT are without effect on body temperature changes induced by morphine. Animals lesioned in the midbrain raphe are still able to respond with a hyperthermia or with a hypothermia when they are treated respectively with 2,4-dinitrophenol or phentolamine.     

Hypothermia produced by tributyl S,S,S-phosphorotrithioate (DEF)

Tributyl S,S,S-phosphorotrithioate (DEF) produces profound hypothermia in rats, mice and guinea pigs by inhibition of thermogenesis. Its actions on heat conservation and motor control are, however, minimal. It is effective against both shivering and non-shivering thermogenesis and completely blocks the increase in body temperature evoked by anterior hypothalamic stimulation. A number of other measures indicated that this is unlikely to be due to a lack of peripheral thermogenic capacity: thus plasma concentrations of glucose, free fatty acids, and ketone bodies remained normal or rose after DEF, and in vitro noradrenaline-stimulated lipolysis was normal in the presence of DEF. The metabolic response to the uncoupler, 2,4-dinitrophenol was unchanged by DEF, and the increase in temperature of brown fat evoked in vivo by nerve stimulation or noradrenaline was also unaffected. It is suggested that DEF (or more likely a DEF metabolite) acts selectively on a central thermogenic control process.