猪胰细胞膜缩胆囊肽结合蛋白的纯化

从猪胰细胞膜提取、纯化得到一种缩胆囊肽（ＣＣＫ）结合蛋白，达电泳纯。经十二烷基硫酸钠聚丙烯酰胺凝胶电泳（ＳＤＳ－ＰＡＧＥ），其亚基分子量为４３．１×１０－２２ｋｇ。此结合蛋白与不同的ＣＣＫ－Ｓｅｐｈａｒｏｓｅ作用时显示，其与硫酸化ＣＣＫ－８、ＣＣＫ－８、硫酸化亮氨酸脑啡肽（Ｌｅｕ－ｅｎｋ）结合活性较大，而与ＣＣＫ－６、ＣＣＫ－４及Ｌｅｕ－ｅｎｋ结合活性较弱。说明ＣＣＫ羧基末端第七位上酪氨酸的硫酸化对ＣＣＫ结合活性有较大影响。并与ＣＣＫ肽链的长度有关。     

Interaction of cholecystokinin with vasoactive intestinal peptide in body shaking response to ice-water immersion in rats

Interaction of cholecystokinin (CCK) with vasoactive intestinal peptide (VIP) in body shaking response to ice-water immersion was observed in pentobarbital-anesthetized rats. Although CCK itself had no influence on the response, VIP suppressed it and this effect of VIP was antagonized by simultaneous administration of sulfated octapeptide of CCK, but not by non-sulfated CCK.     

Coexistence of somatostatin- and avian pancreatic polypeptide (APP)-like immunoreactivity in some forebrain neurons

The indirect immunofluorescence technique was used to demonstrate the coexistence of somatostatin together with avian pancreatic polypeptide-like immunoreactivity within certain neurons of the rat forebrain. Numerous neurons containing these peptides were observed in the neocortex, hippocampus, olfactory tubercle, striatum, nucleus accumbens and lateral septum. In studies of serial sections stained alternately for these two peptides, and in restaining experiments, It could be determined that in many neurons in these areas these two peptides coexisted. In other brain areas such as the anterior periventricular hypothalamus, somatostatin cells were never found to contain avian pancreatic polypeptide-like immunoreactivity. Also, within the pancreas these two peptides were never found to coexist in the same cells. The findings represent a further example of the coexistence of more than one neuropeptide within a single neuron.     

Types of nerves in the enteric nervous system

The enteric nervous system is one of the three divisions of the autonomic nervous system, the others being the sympathetic and parasympathetic. In contrast to the other divisions, it can perform many functions independently of the central nervous system. It consists of ganglionated plexuses, their connections with each other, and nerve fibres which arise from the plexuses and supply the muscle, blood vessels and mucosa of the gastrointestinal tract. The enteric nervous system contains a large number of neurons, approximately 10⁷ to 10⁸. About ten or more distinct types of enteric neurons have been distinguished on electrical, pharmacological, histochemical, biochemical and ultrastructural grounds as well as on the basis of their modes of action. Both excitatory and inhibitory nerves supply the muscle and there are inhibitory and excitatory interneurons within the enteric plexuses. There are also enteric nerves which supply intestinal glands and blood vessels, but these receive less emphasis in this commentary.Correlations between groups of neurons defined on different criteria are poor and in many cases the physiological roles of the nerves are not known. The functions of noradrenergic nerves which are of extrinsic origin are reasonably well understood, but cholinergic nerves in the intestine are the only intrinsic nerves for which both the transmitter and to some extent the functions are known. In the case of non-cholinergic, non-noradrenergic enteric inhibitory nerves, the functions are understood but the transmitter is yet to be determined, both adenosine 5′-triphosphate and vasoactive intestinal polypeptide having been proposed. Other nerves have been defined pharmacologically (non-cholinergic excitatory nerves to neurons and muscle, intrinsic inhibitory inputs to neurons, and enteric, non-cholinergic vasodilator nerves) and histochemically (intrinsic amine-handling neurons and separate neurons containing peptides: substance P, somatostatin, enkephalins, vasoactive intestinal polypeptide, gastrin cholecystokinin tetrapeptide, bombesin, neurotensin and probably other peptides). Little is known of the functions of these nerves, although a number of proposals which have been made are discussed.     

Intracerebroventricularly administered corticotropin-releasing factor releases somatostatin through a cholinergic,vagal pathway in freely fed rats

The aim of this study was to investigate whether corticotropin-releasing factor influences the plasma levels of somatostatin, gastrin or cholecystokinin when administered intracerebroventricularly to rats, and if such an effect could be vagally mediated, and dependent on the animals feeding states. Anaesthetized, freely fed rats were given 5 μl intracerebroventricular injections of corticotropin-releasing factor in four doses; 10 pmol-1.28 nmol. Immediately following death, trunk blood was collected for subsequent peptide analysis with radioimmunoassay (RIA). The three higher doses of corticotropin-releasing factor elevated the plasma levels of somatostatin (P < 0.01) after 20 min but left the plasma levels of gastrin and cholecystokinin unchanged. Intraperitoneal injections of 60 and 320 pmol of corticotropin-releasing factor did not influence the somatostatin levels. Further, intracerebroventricular injections of 60 pmol of corticotropin-releasing factor produced a peak increase in somatostatin after 20 min (P < 0.01). After 60 min the somatostatin levels were still increased (P < 0.05). Gastrin and cholecystokinin remained unaltered at these timepoints. Intracerebroventricular administration of 10 nmol of a-helical corticotropin-releasing factor 9–41 attenuated the basal levels of somatostatin and blocked the corticotropin-releasing factor-induced rise in somatostatin. Bilateral truncal vagotomy, as well as pretreatment with atropine (0.05 mg kg^-1, subcutaneously) abolished the effects of corticotropin-releasing factor on somatostatin. In animals which were food-deprived for 24 h, corticotropin-releasing factor did not influence somatostatin, gastrin or cholecystokinin. Pretreatment with cholecystokinin did not potentiate corticotropin-releasing factor-induced somatostatin release in food-deprived rats. These findings suggest that corticotropin-releasing factor acting within the central nervous system may regulate gastrointestinal functions partially through a cholinergic, vagally mediated release of somatostatin in freely fed, but not in food-deprived rats.     

脂多糖对胆汁分泌的影响

[目的 ]通过脂多糖对胆汁分泌的影响实验 ,初步探讨引起肝功能障碍及肝内结石形成的机理 .[方法 ]在麻醉状态下 ,直接往实验动物肝内注入脂多糖等实验药物 ,测定相关数据 .[结果 ]脂多糖对胆汁分泌有抑制作用 ,并对胆汁酸、磷脂浓度有降低作用 ,而对胆红素、钙的浓度无显著作用 .[结论 ]脂多糖对胆汁分泌有明显作用 ,对诱发肝功能障碍及形成肝内胆结石有一定的影响     

脾虚证大鼠胃、肠电—机械活动异常与CCK，SS含量变化的关系

目的：探讨脾虚证时胃肠激素改变与胃肠运动异常之间的关系,方法：采用放射免疫分析法测定实验性脾虚证大鼠不同造模时间（7d,14d),胃窦,十二指肠,空肠,下丘脑及血浆中生长抑素（SS）,缩胆囊素（CCK）含量并与正常对照组和四君子汤预防组比较,通过体内埋藏电极和传感器记录胃,肠电－机械活动进行造模前后自身比较,结果：脾虚早期（7d),SS在下丘脑,血浆中含量升高,外周组织中含量下降（P＜0．01）,CCK在组织和血浆中含量均升高（P＜0．01）,胃电一机械活动节律,振幅均下降（P＜0．01）,肠机械活动节律,振幅均升高（P＜0．01）,电慢波节律下降,振幅升高（P＜0．01）,脾虚晚期（14),SS在下丘脑,血浆中含量下降,外周组织中含量升高（Ｐ＜０．０１）,CCK参下丘脑及胃窦组织中含量升高（Ｐ＜０．０１）,在血浆和肠道组织中含量下降（Ｐ＜０．０１）,胃机械活动节律下降（Ｐ＜０．０１）,振幅改变不明显,电慢波节律,振幅均下降（Ｐ＜０．０１）,肠电一机械活动节律,振幅均下降（Ｐ＜０．０１）,经四君子汤预防性治疗的动物体内激素含量及胃,肠电一机械活动变化均无显著意义,结论：脾虚证时胃肠激素改变与胃肠运行异常之间存在内在联系,且随病程发展呈动态变化,四君子汤对此有纠正作用。     

Effect of CCK-4 on a 35% carbon dioxide challenge in healthy volunteers

1. 1. The purpose of this study was to determine whether a subthreshold dose of CCK-4 would enhance the vulnerability of healthy subjects to a 35% carbon dioxide challenge.

2. 2. 27 subjects, with no prior or present psychiatric disorder and in good physical condition were challenged with a vital capacity breath of a 35% carbon dioxide mixture, immediately after an intravenous injection of 5 μg CCK-4 or placebo, according to a random order double blind crossover design.

3. 3. Subjects reported significantly less panic symptoms upon carbon dioxide after premedication with CCK-4 than after placebo.

4. 4. Both CCK-4 and carbon dioxide may act on the same neuronal pathways, but seem to inhibit rather than potentiate each other effects.

     

中风始发态证候与血浆脑肠肽的相关性

目的探讨中风始发态中医证候与血浆脑肠肽CCK(cholecystokinin,CCK)水平的相关性。方法对确诊急性脑出血或急性脑梗死(发病时间<72h)患者采用RIA法检测血浆CCK-8水平,根据中医证候诊断标准对纳入患者进行证候辨证,分析不同证候间血浆CCK-8水平的差异。结果肝阳上亢证患者血浆CCK-8水平较非肝阳上亢证患者显著升高(P<0.01)。结论中风始发态中医证候与血浆CCK水平有相关性。     

缺锌大鼠海马胆囊收缩素和一氧化氮合酶阳性细胞数目的变化

目的　观察缺锌对海马胆囊收缩素 (CCK)和一氧化氮合酶 (NOS)阳性细胞数的影响及其与动物行为变化的关系 ,研究缺锌对学习记忆影响的机制。方法　通过管饲低锌液体饲料复制缺锌大鼠模型。二周后 ,使用Y 迷宫实验检测动物学习记忆能力 ;采用ABC免疫组化法和NADPH d组化检测海马各区CCK和NOS阳性细胞数目。结果　与对照组相比 ,缺锌大鼠学习记忆能力明显下降 (P <0 0 5 ) ;缺锌大鼠血清锌水平明显降低 (P <0 0 5 ) ,但海马锌含量未见明显改变 ;缺锌大鼠海马CA1区和CA3区CCK和NOS阳性细胞数目均明显减少。结论　缺锌导致海马CA1和CA3区CCK和NOS阳性细胞数目减少可能是缺锌影响脑学习记忆功能的重要机制之一