促甲状腺素释放激素类似物YM14673对小鼠学习记忆的影响

采用小鼠跳台法评价促甲状腺素释放激素类似物YM14673(ip 1 mg·kg^-1) 对正常成年小鼠被动回避学习记忆成绩的影响. 结果表明YM14673对东莨菪碱， 氯霉素和乙醇造成的小鼠记忆获得,巩固及再现障碍均有明显的改善作用.     

促甲状腺素释放激素(TRH)类似物YM14673对大鼠脑损伤并发脑水肿的作用

用雄性Wistar大鼠,采用Feeney等的落体撞击法造成左顶颅脑挫伤。动物随机分组,给于TRH类似物YM14673(0.1 mg·kg^-1或1.0 mg.kg^-1,ip)或等体积生理盐水。治疗组可明显地减轻脑水肿。     

促甲状腺素释放激素类似物YM—14673对脑出血大鼠的治疗作用

近年研究发现,促甲状腺素释放激素(TRH)及其类似物具有神经递质的某些特征,能改善外伤性脊髓损伤的神经缺失,具有较广泛的生物效应。我们用胶原酶和肝素诱导大鼠脑出血,用一种新的TRH类似物YM-14673对其进行治疗,观察YM-14673对脑出血的疗效和作用。 材料与方法 1.材料 雄性Wistar大鼠(250±30)g60只。(1)行为观察组20只(治疗组与对照组各10只)。(2)实验组40只:分为正常组5只,对照组18只(24     

促甲状腺素释放激素类似物YM14673对大鼠脑缺血再灌注致学习记忆功能障碍的作用

目的观察促甲状腺素释放激素类似物ＹＭ１４６７３对大鼠脑缺血再灌注损伤致学习记忆功能障碍的作用及其对脑脂质过氧化物的影响。方法用双侧颈总动脉反复短暂夹闭法造成大鼠脑缺血再灌注模型,通过跳台和Ｍｏｒｉｓ水迷津实验观察促甲状腺素释放激素类似物ＹＭ１４６７３对大鼠学习记忆功能障碍的作用,用ＴＢＡ法了解ＹＭ１４６７３对大鼠脑脂质过氧化作用的影响。结果ＹＭ１４６７３（１ｍｇ·ｋｇ－１,ｉｐ）明显地改善了脑缺血再灌注所致的大鼠学习记忆功能障碍。实验表明ＹＭ１４６７３（１ｍｇ·ｋｇ－１,ｉｐ）能抑制体内氧自由基的大量生成,但体外实验ＹＭ１４６７３（００１～１０μｍｏｌ·Ｌ－１）却没有表现出清除羟自由基的能力。结论ＹＭ１４６７３对大鼠脑缺血再灌注致学习记忆障碍有明显的改善作用,但这不是ＹＭ１４６７３直接清除氧自由基的结果     

促甲状腺素释放激素对应激小鼠免疫功能的影响

促甲状腺素释放激素对应激小鼠免疫功能的影响吴敏毓，汤斌，曲卫敏（皖南医学院微生物学教研室，芜湖２４１００１）促甲状腺素释放激素（ＴＲＨ）是丘脑下部分泌的三肽激素，能刺激垂体释放促甲状腺素（ＴＳＨ），进而促使甲状腺合成与分泌三碘甲状腺原氨酸（Ｔ３）和甲...     

促甲状腺素释放激素对失血性休克犬心血管功能的影响

本文证明失血性休克大iv TRH后心血管功能有明显改善,表现为CI,SVI,LVSWI,RVSWI及RP都明显增加,其中以LVSWI增加最明显,眼球结膜微循环观察发现细静脉扩张,微循环血流速度加快,红细胞聚集减轻。此外尚有减轻休克酸中毒、提高24h存活率及延长存活时间的效应。但对溶酶体酶的影响不明显,伍用地塞米松未见明显优点。     

促甲状腺素释放激素对创伤休克大鼠肝线粒体呼吸功能的影响

采用大鼠单侧股骨粉碎性骨折伴15％体重失血的模型,观察动物存活率,肝脏线粒体呼吸控制率(RCR),ADP/O值的变化以及ia TRH 5 mg·kg~(-1)对肝线枉体呼吸功能的保护作用,创伤休克时,肝脏线粒体RCR,ADP/O值显著降低,24 h大鼠存活率明显减少,TRH能明显提高肝线粒体RCR,ADP/O值以及休克动物存活率,提示TRH有明显改善休克大鼠肝线粒体氧化磷酸化功能的作用。     

促甲状腺素释放激素对失血性休克大鼠脑μ,δ和κ阿…

本用放射相对选择性配体初步研究了促甲状腺素释放素（ＴＲＨ）对失血性休克大鼠脑μ、δ和κ阿片受体的影响，结果提示ＴＲＨ减数调节失血性休克动物脑阿片受体数量可能是ＴＲＨ拮抗内阿片肽的心血管抑制作用，发挥抗休克作用的重要机理。     

促甲状腺素释放激素对失血性休克大鼠脑μ、δ和K阿片受体的影响

本文用放射性相对选择性配体初步研究了促甲状腺素释放素（ＴＲＨ）对失血性休克大鼠脑μ、δ和Ｋ阿片受体的影响。结果显示失血性休克大鼠δ和ｋ阿片受体最大结合数（Ｂｍａｘ）显著升高，亲和力变化不大，μ阿片受体Ｂｍａｘ和亲和力无明显变化。ＴＲＨ（５ｍｇ·ｋｇ￣（－１））可使休克大鼠脑δ阿片受体Ｂｍａｘ降低，对其亲和力影响不大，对μ和ｋ受体无明显影响。这一结果提示ＴＲＨ减数调节失血性休克动物脑阿片受体数量可能是ＴＲＨ拮抗内阿片肽的心血管抑制作用，发挥抗休克作用的重要机理。     

促黄体释放素类似物和促甲状腺激素释放激素对青少年型日本血吸虫病性侏儒症的促生长发育作用

为了观察在杀虫治疗后使用国产促黄体释放素类似物D一丙~6-LRH和促甲状腺激素释放激素对青少年型日本血吸虫病性侏儒症患者促生长发育作用的远期效果,作者对19例已作治疗的患者进行了连续3-4yr的随访观察。结果发现身高、体重和性发育情况均有明显改善,并以2药合用为优。不论近期或远期效果均甚满意,值得临床进一步研究。     

促甲状腺素释放素增敏失血性休克大鼠心脏肾上腺素受体及其机理

采用失血性休克大鼠离体心脏观察了促甲状腺素释放素（ＴＲＨ）对肾上腺素受体激动剂正性肌力作用的影响及对肾上腺素受体数量和亲和力的影响，并用全细胞记录式膜片钳技术研究了ＴＲＨ对豚鼠单一心肌细胞慢钙内流及其对肾上腺素受体激动剂促钙内流作用的影响。结果表明，ＴＲＨ可上调失血性休克大鼠β肾上腺素和多巴胺受体数量，并增加β肾上腺素受体的亲和力。ＴＲＨ可延长心肌细胞膜钙通道开放时间，增加异丙肾上腺素和多巴胶的促钙内流作用，ＴＲＨ的这一作用可能是其增敏心脏肾上腺素受体，增强其激动剂正性肌力作用的重要原因。     

Acute effects of high-dose thyrotropin releasing hormone infusions in Alzheimer's disease

Thyrotropin releasing hormone (TRH) was administered intravenously to ten patients with Alzheimer's Disease (AD) in a high-dose paradigm, thought to maximize central nervous system effects and potentially produce facilitation of cholinergic function, a known property of the neuropeptide. Acute effects of TRH on behavioral, cognitive and physiologic measures were assessed after patients received 0.1 mg/kg TRH, 0.3 mg/kg TRH and placebo, the higher TRH dose and placebo being given in a randomized, double-blind fashion. Patients showed statistically significant increases in arousal and improvement in affect, as well as a modest improvement in semantic memory, all after receiving the higher TRH dose. Both TRH doses produced transient rises in systolic blood pressure, with no effect on diastolic blood pressure, heart rate or temperature. This study suggests that high-dose TRH can be safely administered to AD patients and is neurobehaviorally active; further studies are needed to determine the extent and mechanism of the cognitive and psychobiological properties of this peptide in AD and other neuropsychiatric disorders.     

Thyrotropin releasing hormone, cholecystokinin and endogenous opioids in the modulation of spinal reflexes in the rabbit

Electrical stimulation of the sural nerve of the rabbit evokes reflexes in the ipsilateral ankle extensor gastrocnemius medialis and in the knee flexor semitendinosus which are differentially modulated by endogenous opioids. Intravenous injection of the putative functional opioid antagonist, thyrotropin releasing hormone (TRH) or its analogue RX77368, caused the extensor response to double in size and the flexor reflex to increase to 1.5–1.7 times pre-drug controls. The opioid RX77368 had no effect on the naloxone-reversible inhibition of the gastrocnemius reflex which followed tetanic stimulation of the fine afferent fibres of the common peroneal or sural nerves. The cholecystokinin antagonist proglumide, which has been shown to enhance the actions of endogenous opioids in some species, had no effects on either reflex. It is possible that TRH acts as an excitatory neurotransmitter or modulator in the spinal cord of the rabbit opposing, but not blocking, the actions of endogenous opioids.     

Jumping behavior induced by thyrotropin releasing hormone in combination with apomorphine in mice

Neuronal mechanisms involved in the jumping produced by thyrotropin releasing hormone (TRH) plus apomorphine were studied in mice. TRH (5–20 mg/kg IP) administered after apomorphine (0.25–2.0 mg/kg IP) elicited jumping behavior, the frequency of jumping being proportional to the dose of TRH but inversely related to the dose of apomorphine. Jumping behavior was also induced by TRH (20 mg/kg IP) administered after atropine (5 mg/kg IP) or clonidine (0.5 mg/kg IP). The jumping elicited by TRH (20 mg/kg IP) in combination with apomorphine (0.25 mg/kg IP) was decreased by pretreatment with haloperidol (1 mg/kg IP), physostigmine (0.2 mg/kg IP) or phentolamine (10 mg/kg IP), unaffected by propranolol (10 mg/kg IP), and markedly increased by atropine (5 mg/kg IP) or clonidine (0.5 mg/kg IP). The results suggest that TRH in combination with apomorphine, atropine or clonidine elicits jumping in which dopaminergic, cholinergic and noradrenergic functions are concomitantly involved.