神经降压素的肝细胞保护作用与Ca~（2＋）的关系

观察了神经降压素（ＮＴ）的肝细胞保护作用与Ｃａ２＋的关系。结果显示，醋氨酚使肝细胞Ｃａ２＋内流和肝脏钙含量增加，但对于线粒体Ｃａ２＋摄取及其钙含量无明显影响，表明细胞可能出现胞质Ｃａ２＋超载。若在醋氨酚之前给予ＮＴ则使肝细胞Ｃａ２＋内流明显减少，肝脏Ｃａ２＋含量有降低趋势，但线粒体钙含量显著增加。这些结果提示，ＮＴ通过减少Ｃａ２＋内流，增强线粒体贮存Ｃａ２＋的能力，部分缓解醋氨酚所致胞质Ｃａ２＋超载从而减轻细胞损伤。     

Stimulation of phagocytic function in mouse macrophages by neurotensin and neuromedin N

The neuropeptides neurotensin and neuromedin N (from 10⁻¹² M to 10⁻⁹ M) have been showed in this study to stimulate significantly in vitro several steps of the phagocytic process: adherence to substrate, chemotaxis, ingestion of inert particles (latex beads) and production of superoxide anion measured by nitroblue tetrazolium reduction in resting peritoneal macrophages from BALB/c mice. A dose-response relationship was observed, with a maximal stimulation of the phagocytic process at 10⁻¹¹ M. The two neuropeptides induced no change of intracellular cyclic AMP in murine macrophages. Moreover, adherence and chemotaxis decreased significantly in the presence of EGTA (1 mM), a chelator of extracellular Ca²⁺, or ryanodine (0.5 mM), a blocker of a Ca²⁺-gated channel from the endoplasmic reticulum, in both controls and samples with the addition of neurotensin or neuromedin N. These results suggest that there is no relation between the cAMP messenger system and the phagocytic process stimulation in murine peritoneal macrophages by neurotensin or neuromedin N. In addition, the results observed with EGTA and ryanodine could indicate that these two neuropeptides produce their effects through an increase of intracellular Ca²⁺ concentration.     

下丘脑弓状核注射神经降压素的镇痛效应及机制探讨

采用微量注射法,对37只大鼠进行了实验观察.结果如下:①下丘脑弓状核(ARC)注射神经降压素(NT)可使甩尾反应潜伏期(TFL)或痛阈显著升高.对照组注射生理盐水,TFL无明显变化.②ARC先注射纳洛酮,再注射NT,TFL变化值与单纯注射NT组相比明显下降.③ARC注射β-内啡肽(β-End)抗血清,再注射NT,TFL显著下降.④ARC注射生理盐水不影响注射NT的镇痛效应.上述结果表明,大鼠ARC注射NT可产生明显的镇痛效应,该效应可被ARC预先注射纳洛酮或β-内啡肽抗血清翻转,提示NT在ARC的镇痛作用,部分是由β-End介导的.     

大鼠下丘脑内神经降压素对体温的影响

目的　探讨下丘脑内神经降压素 (Neurotensin ;NT)对体温的影响。方法　使用核团内微量注射的方法向大鼠双侧视前区 -下丘脑前部 (PO/AH)和下丘脑后部 (PH) )分别注射NT和抗NT血清 ,观察大鼠体温的变化。结果　双侧PO/AH注射NT后大鼠体温下降 (P <0 0 5 ) ,且呈明显的量效依赖关系 ,但注射抗NT血清不能引起体温变化 ;下丘脑后部 (PH )注射NT对体温无明显影响 (P >0 0 5 )。结论　下丘脑内外源性NT可能参与机体的体温调节过程 ,其作用部位在视前区 -下丘脑前部 ,内源性的NT对体温无明显影响。     

功能性消化不良患者胃排空障碍与胃肠激素的关系

目的 探讨功能性消化不良(FD)患者胃排空障碍与胃肠激素间的关系。方法 对54例四患者进行胃排空检查，根据结果将其分为胃排空延缓的FD组(FDD组)和胃排空正常的四组(FDN组)，另以17名正常人作为对照组。用放免法测定受试者血浆(空脂和餐后)、胃窦十二指肠粘膜组织的神经降压素(NT)和胃动宗(MTL)含量。结果 FDD组空脂和餐后血浆、胃窦和十二指肠粘膜组织的NT含量均明显高于对照组及FDN组。各组试餐前后血浆NT增幅差异无显著性。FDD组空脂和餐后血浆、胃窦和十二指肠粘膜组织的MIL含量均明显低于对照组及FDN组。各组十二指肠粘膜组织MTL含量均明显高于胃窦粘膜。结论 FD患者胃排空障碍与NT、MIL密切相关。NT、MIL在FD的发病机制中可能具有一定作用。     

下丘脑前部注射微量神经降压素对大鼠减压反应的影响

直接将神经降压素注射于大鼠下丘脑前部一侧减压区后,再以电刺激该区,观察其对减压反应的影响。结果表明,注射微量神经降压素后,可使电刺激该区所出现减压反应的最低值和持续时间,都比注射前明显增大。这证明,神经降压素参与电刺激大鼠下丘脑前部一侧减压区所出现的减压反应过程。     

大鼠孤束核含酪氨酸羟化酶、神经降压素和胆囊收缩素样神经元向伏核的投射—HRP和免疫细胞化学双重标记法的研究

本文应用HRP顺、逆行追踪法结合免疫细胞化学双重标记法,对大鼠孤束核向伏核的投射进行了研究。主要结果如下:1.WGA-HRP注入孤束核尾侧段,在伏核后部的腹、内侧区,出现较密集的标记纤维、终末和标记细胞;将HRP注入伏核后部的腹、内侧区,在孤束核尾侧段(主要在连合核和内侧亚核)出现大量的顺、逆行标记,以同侧为主。2.HRP注射到伏核并结合免疫细胞化学反应,在孤束核尾侧段发现HRP-TH,HRP-NT、HRP-CCK双重标记细胞。HRP-TH的数目最多,其次是HRP-NT双标细胞,HRP-CCK双标细胞最少。     

Characteristics of β-endorphin-induced histamine release from rat serosal mast cells Comparison with neurotensin,dynorphin and compound 48/80

Summary Rat peritoneal mast cells were exposed to the neurohormone and basic opioid peptide -endorphin. -Endorphin induced a dose-dependent release of histamine from the mast cells. A significant histamine release was found at 5 mol/l of -endorphin and maximal release (35% of total) at 20 mol/l. The histamine release process was very rapid and terminated within 30 s at 37°C, and in this sense is very similar to the histamine release induced by compound 48/80 or neurotensin. The histamine release was temperature-dependent showing an optimum release around 30°C, and it was independent of available extracellular calcium, but was inhibited in the presence of high extracellular calcium concentrations. Naloxone, only in very high concentrations (10 mmol/l), inhibited the release, and the very same concentration also inhibited the neurotensin — as well as the compound 48/80-induced histamine release. Cromoglycate and benzalkoniumchloride, a 48/80 antagonist, both produced a progressive dose-dependent inhibition of -endorphin-, neurotensin- as well as compound 48/80-induced histamine release. Taken together, the findings indicate that the opioid peptide -endorphin induces a selective, energy-dependent release of histamine from peritoneal rat mast cells. The pattern of release has much in common with that of compound 48/80 and other basic peptides, such as neurotensin and substance P. In addition this pattern of release is similar to that induced by dynorphin. Send offprint requests to Anita Sydbom at the above address     

Possible neuronal mechanisms involved in neurotensin-induced catalepsy in mice

The neuronal mechanisms of neurotensin (NT)-induced catalepsy were investigated in mice. NT administered intracerebroventricularly (ICV 0.5, 1.0 and 2.0 g) produced catalepsy in a dose-dependent fashion. A significant effect was observed at 2.0 g and a maximal effect 2–3 h after injection. The NT-induced catalepsy was inhibited by pretreatment with atropine, trihexyphenidyl or biperiden (each drug, 0.8–5.0 mg/kg, IP), anticholinergic drugs, and L-DOPA (100, 200 mg/kg, IP). However, the catalepsy was not significantly antagonized by p-chlorphenylalanine (300 mg/kg×3 days, IP) or methysergide (5, 10 mg/kg, IP), antiserotonergic drugs, and was not potentiated by the GABAergic drugs, aminooxyacetic acid (25 mg/kg, IP) or muscimol (1 mg/kg, IP). In addition, the NT-induced catalepsy was dose-dependently reduced by antihistamines, such as diphenhydramine (0.8–10 mg/kg, IP) and tripelennamine (0.4–5.0 mg/kg, IP) and was potentiated after treatment with histidine (250, 500 mg/kg, IP), a precursor of brain histamine. NT-induced catalepsy was also reduced by ICV pretreatment with diphenhydramine (1–5 g/rat), a H₁ antagonist, but not by cimetidine (5, 20 g/rat), a H₂ antagonist. These findings suggest that the catalepsy induced by NT may involve not only central cholinergic and dopaminergic mechanisms but also a histaminergic mechanism mediated via H₁-histamine receptors, and seems to differ from the catalepsy induced by neuroleptics.     

CCK and other peptides modulate hypothalamic norepinephrine release in the rat: Dependence on hunger or satiety

The purpose of this investigation was to determine the functional relationship between putative satiety peptides and endogenous norepinephrine (NE) activity in the hypothalamus. Permanent guide cannulae for push-pull perfusion were implanted stereotaxically in Sprague-Dawley rats so as to rest above the medial or lateral hypothalamus (LH). Post-operatively, the animals were either satiated with food and water, both available ad lib, or fasted for 18-22 hr prior to an experiment. To perfuse a site in the LH, paraventricular (PVN) or ventromedial nucleus (VMN), a concentric 29-23 ga push-pull cannula system was lowered to a pre-determined site, in most cases after catecholamine stores had been pre-labeled with [3H]-NE. During control tests, an artificial CSF was perfused at a rate of 20-25 microliter/min for 5-8 min with a 5 min interval between each sample. The addition of cholecystokinin (CCK) in a concentration of 2.0-6.0 ng/microliter to the CSF perfused in PVN or VMN of the satiated rat enhanced the efflux of NE; however, in the fasted animal CCK often suppressed the catecholamine's release. Perfused in the LH, CCK exerted opposite effects, typically augmenting NE output when the rat was fasted but not affecting the amine's activity during the sated condition. Proglumide (1.2 micrograms/microliter) attenuated CCK's effect in releasing NE when the antagonist was perfused in the PVN of the satiated rat. Similar experiments in which neurotensin (NT) was perfused in the LH, PVN and VMN revealed virtually the same inverse effects on NE release in the fasted and satiated rat, which again were anatomically specific. Finally, insulin and 2-deoxy-D-glucose (2-DG) exerted similar state-dependent effects on the release of NE within LH and PVN. Overall, the results suggest that CCK or other neuroactive peptide could serve as a "neuromodulator" of the pre-synaptic release of NE within classical hypothalamic structures which are thought to underlie both hunger and satiety. The state-dependent nature of the peptides' activity on the noradrenergic feeding mechanism implies that these substances constitute a pivotal portion of the profile of factors which impinge functionally upon the hypothalamic neurons responsible for the feeding response and its cessation.