胆碱能神经对人餐后神经降压素释放的影响

本文比较了6名健康成人进食、餐前肌注阿托品以及单纯咀嚼食物后的血浆神经降压素样免疫活性物质(NTLI)水平的变化,以探讨胆碱能神经对神经降压素释放的影响。用放射免疫测定法分别测定NTLI和胰多肽(PP)的含量,以便同时比较两者释放的状态。6人的基础血浆NTLI和PP的水平平均分别为15.7±2.4和16.6±9 7pmol/L。进食后,血浆NTLI和PP水平均显著增高,并呈双相反应。第一个血浆NTLI高峰平均为60.7±13.2pmol/L,出现于餐后的20min。餐后90min,又出现另一个高峰,其平均水平为58.8±8.2pmol/L。在进食前肌注阿托品1mg,餐后的第一个血浆NTLI高峰消失,而第二个高峰仍存在。单纯咀嚼食物后,血浆PP水平明显增高,而对NTLI的释放无刺激作用。本文结果提示,餐后早期的神经降压素释放的调节是由非迷走胆碱能神经参与的,而后期的释放不受胆碱能神经的影响。     

电刺激兔延髓腹侧化学敏感区和压力敏感区对呼吸、血压,的影响及其中枢递质机制

电刺激麻醉兔延髓腹侧化学敏感区头端区引起潮气量(V_T)增加,呼吸频率(f)增快;电刺激压力敏感区(中间区)则使V_T减小,f亦增快。弱刺激时,两者均产生降压反应;刺激增强可诱发双相或升压反应。在出现周期性呼吸时,电刺激化学敏感区可使呼吸节律正常化、V_T增大,而电刺激压力敏感区则导致呼吸暂停。电刺激压力敏感区时,吸气时间(TI)和呼气时间(T_E)均缩短,以T_E变化更明显;由于V_T减小和T_I缩短,V_T/T_I保持相对不变,提示吸气终止的中枢阈值降低。在准备刺激的相应局部预先应用阿托品,可使电刺激化学敏感区产生的通气增强效应翻转,而对电刺激压力敏感区引起的通气抑制无明显影响;用印防己毒素则可选择性消除电刺激压力敏感区的通气抑制和降压效应。本工作表明延髓腹侧存在两个不同的中枢机制,其中化学敏感区产生的通气增强与胆碱能系统有关;压力敏感区产生的通气减弱效应与GABA系统有关。     

Effect of atropine on plasma gastrin and somatostatin concentrations during sham feeding in man

The purpose of these studies was to measure circulating gastrin and somatostatin concentrations during sham feeding in humans and to evaluate the effect of two doses of intravenous atropine on circulating concentrations of these peptides. Gastric acid and bicarbonate secretion and pulse rate were also measured. Sham feeding increased plasma gastrin concentrations by approximately 15 pg/ml but had no effect on plasma somatostatin-like immunoreactivity (SLI). A small dose of atropine (5 micrograms/kg) augmented plasma gastrin concentrations during sham feeding significantly (P less than 0.01), but did not affect plasma SLI. Atropine also significantly inhibited gastric acid secretion and gastric bicarbonate secretion (by 62% and 52%, respectively), but pulse rate was not affected. A larger dose of atropine (15 micrograms/kg intravenously) suppressed plasma gastrin concentrations significantly compared to the smaller 5 micrograms/kg atropine dose (P less than 0.02), so that plasma gastrin concentrations when 15 micrograms/kg atropine was given were not significantly different from those during the control study. 15 micrograms/kg atropine reduced gastric acid and bicarbonate secretion by 81% and 66%, respectively, and also increased pulse rate by 15 min-1. These studies indicate that small doses of atropine enhance vagally mediated gastrin release in humans, probably by blocking a cholinergic inhibitory pathway for gastrin release. Although the nature of this cholinergic inhibitory mechanism is unclear, we found no evidence to incriminate somatostatin. Our finding that the larger dose of atropine reduced serum gastrin concentrations compared with the smaller dose suggests that certain vagal-cholinergic pathways may facilitate gastrin release.     

家兔脊髓蛛网膜下腔注射乙酰胆碱对血压和心率的影响

将乙酰胆碱(ACh)注入麻醉家兔脊髓蛛网膜下腔,观察其对心血管活动的影响。结果表明:(1)脊髓蛛网膜下腔注射50～100μg ACh可使血压下降,心率减慢;(2)预先由脊髓蛛网膜下腔注射阿托品,可阻断ACh引起的降压和降心率作用;(3)脊髓蛛网膜下腔注射六甲双铵、酚妥拉明或心得安均不能阻断上述ACh的心血管反应;(4)切断两侧颈部迷走神经,ACh不再使心率减慢,但其降低血压的作用不受到任何影响。 脊髓中ACh水平升高可通过激活胆碱能M-受体引起血压下降和心率减慢。ACh的这种降压作用既没有中枢肾上腺素能受体活动参与,也不是通过迷走神经实现的,可能是由于脊髓交感血管中枢紧张性降低所造成的。     

Microwave influence on the isolated heart function: II. Combined effect of radiation and some drugs

The combined effects of microwave radiation and some drugs were studied in an isolated frog auricle preparation. The experiments established that exposure to pulse-modulated 915 MHz microwaves for up to 40 min had no effect on either the rate or the amplitude of spontaneous auricle twitches, unless the average absorbed power was high enough to produce preparation heating. Treatment of the preparation with saline containing (0.6–3.0) 10^?5 M of propranolol or (0.5–1.5) 10^?7 M of atropine altered neither its pacemaker nor its contractile functions; these drugs also had no effect when they were combined with nonthermal microwave irradiation. Caffeine (1 mM) strongly increased the average heart power, which was calculated as the product of twitch rate and amplitude. The caffeine effect appeared to be significantly augmented (by about 15%, P<0.02) under exposure to burst-type pulsed microwaves (pulse width, 1.5 msec; pause, 2.5 msec; 8 pulses/burst, 16 bursts/s; average SAR, 8–10 W/kg). By itself, this modulation was not effective; the heating of the preparation and saline during exposure was approximately 0.1°C, which could not account for the detected changes. The experimental results demonstrate that caffeine treatment increases the microwave sensitivity of the frog auricle preparation and reveals primarily subthreshold, nonthermal microwave effect. © 1995 Wiley-Liss, Inc.     

缩胆囊素和促胰液素对豚鼠离体胃平滑肌运动的影响

用８个肌槽同时记录豚鼠胃不同部位肌条的收缩活动,以观察八肽缩胆囊素（ＣＣＫ－８）和促胰液素的影响。结果表明：ＣＣＫ－８能（１）增高各部位纵行肌和环行肌的张力;（２）加快胃体纵行肌,胃窦纵行肌、环行肌和幽门环行肌的收缩频率;（３）增大胃窦环行肌收缩波平均振幅和（４）增加幽门环行肌收缩波运动指数,但减少胃体和胃窦纵行肌收缩波平均振幅。上述作用均不能被阿托品和消炎病所阻断。而促胰液素对各部位肌条的收缩活动没有明显的影响。     

The effect of atropine and vagal stimulation on the release of neurotensin-like immunoreactivity in man

This study investigated the food stimulated release of neurotensin-like immunoreactivity (NTLI) in man with and without the administration of atropine, and the influence of vagal stimulation by modified sham feeding and insulin hypoglycaemia. NTLI was measured, after ethanol extraction, by specific C- and N-terminally directed antisera. With both a liquid fat meal and a mixed meal an early peak of NTLI occurred. The mixed meal also produced a second sustained rise in plasma NTLI. An intramuscular injection of 0.6 mg atropine sulphate abolished the early peak, but had no effect on the late peak. Modified sham feeding and insulin hypoglycaemia did not release NTLI. We conclude that it is possible that a cholinergic non-vagal mechanism is responsible for the early phase of food stimulated release of NTLI in man, and that the second sustained rise may be cholinergically independent.     

刺激迷走神经和酸化十二指肠对狗胰液分泌的相互影响

用5条制备有 Thomas 胰瘘和胃瘘的狗作慢性麻醉实验,观察刺激迷走神经和酸化十二指肠对胰液分泌的相互影响,结果如下:1.在酸化肠的情况下,刺激迷走神经所引起的胰蛋白质和碳酸氢盐的排出量显著增多,其效应超过单独刺激迷走神经和酸化肠所产生效应之和。2.在酸化肠引起胰分泌停止后的短时间内,再刺激迷走神经,胰液分泌的潜伏期缩短,蛋白质和碳酸氢盐排出量增多。3.阻断迷走冲动或注射阿托品后,酸化肠所引起胰液的分泌明显减少。4.用利多卡因麻痹肠粘膜后,酸化肠所引起胰液的分泌也明显降低。这些结果提示,在酸化十二指肠引起胰液分泌的机制中,有迷走神经和局部神经参与,迷走冲动和促胰液素及促胰酶素共同作用靶器官时,有相互加强作用,一旦迷走冲动被阻断,这两种激素的作用即明显降低。     

梭曼对大鼠摄食中枢的抑制作用

采用双侧下丘脑外例区（摄食中枢）局部给药的方法,观察梭曼对大鼠摄食中枢的作用。实验结果表明,双侧下丘脑摄食中枢各注入梭曼３μｇ,给药当日大鼠平均摄食量下降６０．９％,抑制作用持续３ｄ,与给药前比较,差别显著（Ｐ＜０．０１或０．０５）;各注入阿托品０．１ｍｇ,平均摄食量下降４１．０％,第２天后恢复正常。胆碱酪酶重活化剂ＨＩ－６与梭曼同时注入下丘脑摄食中枢,或者中枢注入梭曼后立即肌注阿托品、美加明,均可部分对抗梭曼引起的中枢性摄食抑制。说明梭曼抑制大鼠摄食中枢与乙酰胆碱酯酶及乙酰胆碱受体确实有密切关系。     

Different modes of action of substance P in the motor control of the feline stomach and pylorus

In an experimental in vivo model to study gastropyloric motility in the cat a contraction of the stomach and the pyloric sphincter was regularly obtained in animals subjected to electrical vagal nerve stimulation or local intraarterial (i.a.) injection of substance P (SP). Much more infrequently contractile motor responses were recorded at splanchnic nerve stimulation. The contractile effects of SP were sensitive to atropine or local infusion of a SP analogue, (d-Pro²,d-Trp^7,9)-SP, indicating that SP activated a final common cholinergic neuron in both stomach and pylorus. However, there seemed to be separate transmission mechanisms in these two regions based on the results of the physiological studies. The vagally induced pyloric contraction was noncholinergic, nonadrenergic, but sensitive to ganglionic blockade (hexamethonium) or the SP analogue, indicating involvement of SP in a peptidergic pathway to the sphincter. The infrequent splanchnically induced pyloric contraction was sensitive to atropine, the SP analogue or ganglionic blockade (hexamethonium) in favour of SP acting on a final cholinergic neuron in this system. On the other hand the gastric contraction, obtained at either extrinsic nerve stimulations or local i.a. injection of SP, was sensitive to atropine or the SP analogue but hexamethonium resistant. These findings suggest antidromic activation of SP-containing axon collaterals of the extrinsic nerves terminating on cholinergic neurons of the gastric wall. When afferent C-fibres of the vagal nerve were selectively activated by local heating, pyloric contraction and gastric relaxation were obtained via vago-vagal reflexes. After cervical vagotomy heating of the distal end of the vagal nerve elicited a gastric contraction, previously demonstrated to be atropine sensitive and hexamethonium resistant, but no pyloric motor response. This suggests that the antidromic activation mechanism was present only in the stomach, not in the pylorus.