組織胺引起的胃分泌的反射抑制

(一)在慢性實驗中用備有小胃的狗,我們证明組織胺引起的胃分泌能反射地为皮膚電刺激及一些其他外界刺激所抑制。 (二)這抑制現象在除去胃的迷走神經支配相交或神經支配,並隔離腎上腺的神經聯系時,仍能出現。它似有某種可以反射地形成的抑制性體液變化為基礎。 (三)但在急性實驗中我們又證明大內臟神經和注射腎上腺素均能抑制組織胺引起的胃分泌,這指示在正常動物胃分泌的反射抑制仍可能通過交感神經-腎上腺系統而得實現。 (四)本文所述的胃分泌的反射抑制現象顯然包含複雜的神經-體液機制,並且是在高級神經中樞參加下產生的。     

中国协和医学院有关生理科学的研究工作情况简介

生理學方面:在乙醯胆鹼的研究方面,正以之作為中樞神經系統活動時的化學指標,來觀察中樞抑制、间生態及外傷性休克等情况下,乙醯胆鹼含量的改變。實驗內分泌學方面仍在進行機體內激素不平衡与腫瘤生長的關係,以及激素對神經過程活動的影響等研究工作。另外也進行了組織胺對胃液分泌及血壓的反射性作用,神經體液對腎臟活動的調節,實驗性神經     

植物性神經系統對血沉的作用

在前一篇文章中,我們報告電針刺激兩側坐骨神經能够引起紅血球沉降反應的加速並且在這個反射的基楚上還建立了條件反射,本文進一步報告有關交感神經和副交感神經對於血沉的作用的試驗。以前學者對植物性神經系統對血沉的作用,多用植物性神經系藥物來試驗。增原等報告腎上腺素使血沉變慢,而和則報告腎上腺素使血沉加速,阿託品使血沉變慢。利用毛香芸果鹼(pilocarpine)和腎上腺素     

麻醉劑(巴比妥類)對於鹽酸引起胰液分泌的影響

本實驗比較急性實驗狗、慢性胰瘻狗和經過麻醉的慢性胰屢狗對於鹽酸注入小腸所引起的胰液分泌量和潛伏期,結果證明: (1)在急性實驗情况下,狗胰腺對鹽酸刺激小腸所引起的胰液分泌量遠較在慢性實驗時為少,且潛伏期較長。 (2)巴比妥類麻醉劑:硫賁妥鈉(sodium pentothal)和戊烷巴比妥鈉(sodiumpentobarbital)對鹽酸所引起的胰液分泌量及潛伏期影響極微。 (3)在急性實驗情况下,由鹽酸所引起的胰液分泌量的減少和潛伏期的加長,似乎不是由於巴比妥類麻醉劑的作用,而可能是由於手術創傷的影響。 (4)注射阿托平後,胰腺對於鹽酸刺激小腸所引起的反應顯著减小,故推测在鹽酸引起胰液分泌的機制中可能有神經反射作用的參與。本工作在进行過程中,承蘇聯專家同志親切地給予指導,并承沈(?)淇、劉曾復二教授关懷和支持,(?)此誌謝。     

关於化學感受性反射後血壓的波浪性變化的問題

在以前的研究裏,我們曾觀察到在輕度麻醉的貓或狗,以游離腸段或後肢的灌注管中,注射適當劑量的二硝基酚、對硝基酚、乙酰胆鹼等藥物,反射地引起血壓升高和呼吸的變化。但在部分實驗中,每當血壓一度升高後,跟着出現一段時間的血壓的波浪性变化。當切斷四條緩衝神經,消除它們的抑制影響而使中樞神經系統處於興奮性提高的情况下,跟着化学感受性反射的增强,這種血壓的波浪性變化也相應地加大;與這一情况相反,如果在頸動脈寶内加壓而引起中樞抑制時,這種波浪性變化即减弱或者消失。 為了進一步瞭解這種波浪性變化產生的主要部位,我們繼續做以下兩组實驗。     

戊巴比妥鈉麻醉對於四氧嘧啶引起的初期血糖變化的影響

動物於注射四氧嘧啶(alloxan)後,產生初期高血糖和低血糖,最後形成永久性高血糖。一般認為初期高血糖的產生和腦下垂體,腎上腺及肝臟有關,低血糖係由胰島β細胞受損傷放出已形成的胰島素所引起。中樞神經機能活動的改變可以影響内外環境的各種動因對機體引起的反應,因此,中樞神經在戊巴比妥鈉麻醉下是否也能影響四氧嘧啶引起的初期血糖变化,是值得研究的。     

皮膚電刺激對胃分泌的抑制作用與神經型的關係

我們按小標準测定了實驗動物的神經型。基本上可將它們分成兩類:2只狗屬於强型;3只狗屬於弱型。在强型狗,皮膚電刺激對由組織胺所引起的胃液分泌有顯著的抑制作用,而在弱型狗則抑制作用不顯著。這些初步實驗結果說明,皮膚電刺激對胃液分泌抑制作用的個體差異与動物的神經型有着一定的關係。     

乙酰胆鹼和迷走神經对离体豚鼠心房的兴奋效应

乙酰胆鹼对心臟所表現的抑制作用是众所周知的事实。但在某些实驗条件下,也可观察到乙酰胆鹼对心臟功能具有兴奋效应。1945年以来,許多作者对这現象进行过仔细的研究,并提出不同的解釋。Hoffmann及其同事在阿托品化的离体心臟中,观察到乙酰胆鹼能加强心搏力量,并且發現此时灌流液中含有类腎上腺素物質。假如先以菸鹼或麦角毒素处理心臟,則乙酰胆鹼即不能再引起心肌收縮的增强。因此他們認为乙酰胆鹼能刺激心臟中交感神經节細胞或嗜鉻組織,使之釋放类腎上腺素物質,而后者則加强心臟     

卵巢瘤在中國地鼠的實驗發生

應用移植卵巢到阉割小鼠的脾臟或胰臟的方法,可以造成內分泌素的不平衡,引起移植的卵巢發生腫瘤。在對這些腫瘤的生長進行初步的研究後,作者於1946年曾就敍利亞地鼠(Cricetus auratus)作同樣的實驗,但因移植到脾臟的卵巢多有粘連現象,而且實驗的時間較短,雖個別移植的卵巢有增大的表現,未見有腫瘤的發生。近年     

磷脂類對於蟾蜍心臟的作用——Ⅳ.在鉀離子乙醯胆鹼抑制中磷脂的作用

(一)在高鉀抑制的心臟,大豆磷脂與油脂酸鈉和血清有恢復或增強心臟搏動的能力。 (二)磷脂在加強高鉀抑制中的機械反應同時,亦加強心肌的動作電流。 (三)腎上腺素亦有興奮高鉀與乙醯胆鹼抑制心臟的作用。與磷脂所表現有所不同,腎上腺素在高鉀任氏溶液中不出現房室阻滯;在乙醯胆鹼抑制下,則不但興奮心肌的機械反應且增加心搏的頻率。     

大鼠前庭内侧核在前庭—交感反应中的作用

实验在氯醛糖和尿酯混合麻醉的大鼠上进行。在内脏大神经上记录刺激同侧前庭神经进入脑干处的交感反应。电刺激前庭神经可在同侧内脏大神经引出—明确的叠加反应,其平均潜伏期为45.8±6.98ms,时程为55.21±5.35ms。增加刺激强度,反应幅度也增加,但潜伏期不变。用前庭内侧核(NVM)的片层场电位作为指标并选择其相位倒转处作刺激点,可在同侧内脏大神经记录到潜伏期为32ms 的叠加反应,而同一动物刺激前庭神经入脑处时内脏大神经反应的潜伏期为43ms。在 NVM 头端损毁后,此前庭-交感反应明显减小,再损毁尾端 NVM 后,此反应消失。损毁 Deiters 核对前庭-交感反应无影响。这些结果表明 NVM在内脏大神经记录到的前庭-交感反应中是一重要的中继站。     

刺激大鼠尾核对丘脑束旁核躯体-内脏会聚神经元放电的影响

实验记录大鼠丘脑束旁核躯体-内脏会聚(PfSV)神经元伤害性放电。观察刺激尾核(Cd)对 PfSV 神经元放电的影响。(1)Cd 对刺激内脏大神经诱发 PfSV 神经元伤害性放电有抑制作用(n=19)。(2)Cd 对刺激腓浅神经和内脏大神经诱发同一 PfSV 神经元伤害性放电均有抑制作用(n=11)。结果提示,躯体和内脏痛觉信息可会聚到丘脑束旁核同一神经元,Cd 可能不仅能抑制躯体痛也能抑制内脏痛。     

Blockade of reflex venous capacitance responses in liver and spleen by hexamethonium, atropine, and surgical section.

Since hexamethonium and surgical section have been used to prevent reflex splanchnic capacitance responses, we examined the effectiveness of these procedures in blocking responses to direct stimulation of preganglionic fibres in the splanchnic nerves. Liver blood volume was measured by plethysmography and splenic blood volume by weighing in cats anesthetized by pentobarbital. The cats were adrenalectomized to prevent adrenal catecholamine secretion in response to splanchnic nerve stimulation. Hexamethonium (10 and 20 mg/kg) alone or atropine (1 mg/kg) alone caused only a small variable block of the responses to preganglionic nerve stimulation. A combination of the two drugs essentially produced a complete block of the liver capacitance response, but a significant response still persisted in the spleen. Surgical section of the postganglionic nerve bundles around the hepatic and splenic arteries completely abolished the responses to preganglionic stimulation. It is concluded that a relatively complete block of reflex splanchnic capacitance responses requires either a combination of hexamethonium and atropine or surgical section of the postganglionic nerves.     

In vivo modulation by alpha 2-adrenoceptors of adrenal catecholamine release in the anaesthetized dog

In this study, the reversal of the potentiating effect of idazoxan, a selective alpha 2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective alpha 2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i.v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 micrograms/kg). The alpha 2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the alpha 2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of alpha 2-blockade can be reversed by activation of those receptors by a selective alpha 2-agonist.     

在不同的交感中枢活动水平时刺激腓深神经对肾神经发放的影响

本工作记录家免肾神经冲动和动脉血压,观察电刺激腓深神经的效应。在用减少通气量、切断双侧迷走神经、切断双侧缓冲神经等方法使交感中枢活动水平升高时,刺激腓深神经(3V、10Hz、0.3ms 持续15min)对血压无明显影响,但可以抑制肾神经的发放。相反,用过度通气或刺激一侧降压神经的方法使交感中枢活动水平降低时,同样的参数刺激腓深神经,则使肾神经发放增加。刺激腓深神经对肾神经发放的抑制效应,可为静脉注射纳洛酮阻断,而兴奋效应则被静脉注射东莨菪碱阻断。上述结果表明:低频低强度刺激腓深神经可引起肾神经发放的抑制或增强,其效应取决于交感中枢的活动状态。躯体传入对肾神经发放的抑制效应有内源性阿片样物质参与,而躯体传入对肾神经发放的兴奋效应则和中枢胆碱能系统的激活有关。     

兔腹部迷走神经、内脏大神经活动在孤束核中的相互作用

本实验在67只家兔身上分别观察了电解损毁孤束核(NTS)前后刺激腹迷走神经和内脏大神经中枢端对血压的影响,以及刺激这两种神经中枢端对 NTS 神经元放电活动的影响。结果表明:来自腹迷走神经和内脏大神经的感觉冲动不仅都可以投射至 NTS,而且这两种传入冲动在 NTS 还存在着会聚现象。一种传入神经的阈下刺激(背景刺激)可以削弱另一传入神经的血压效应,一种传入神经的(背景刺激)可以抑制另一种神经元引起的 NTS 神经元电活动。本文对这两种传入冲动之间存在的相互作用关系的可能机制及意义进行了讨论。     

PACAP-(1-38) as neurotransmitter in the porcine adrenal glands

The concentration of pituitary adenylyl cyclase-activating polypeptide [PACAP-(1-38)] in porcine adrenal glands amounted to 14 +/- 3 pmol/g tissue. PACAP immunoreactive (PACAP-IR) fibers innervated adrenal chromaffin cells (often co-localized with choline acetyltransferase). Subcapsular fibers traversed the cortex-innervating endocrine cells and blood vessels [some co-storing mainly calcitonin gene-related peptide but also vasoactive intestinal polypeptide (VIP)]. PACAP-IR fibers were demonstrated in the splanchnic nerves, whereas IR adrenal nerve cell bodies were absent. In isolated, vascularly perfused adrenal gland, splanchnic nerve stimulation (16 Hz) and capsaicin (10(-5) M) increased PACAP-(1-38) release (1.6-fold and 6-fold respectively, P = 0.02). PACAP-(1-38) dose-dependently stimulated cortisol (2 x 10(-10) M; 24-fold increase, P = 0.02) and chromogranin A fragment (2 x 10(-9) M; 15-fold increase, P = 0.05) secretion. Both were strongly inhibited by the PAC(1)/VPAC(2) receptor antagonist PACAP-(6-38) (10(-7) M). PACAP-(6-38) also inhibited splanchnic nerve (10 Hz)-induced cortisol secretion but lacked any effect on splanchnic nerve-induced pancreastatin secretion. PACAP-(1-38) (2 x 10(-10) M) decreased vascular resistance from 5.5 +/- 0.6 to 4.6 +/- 0.4 mmHg. min. ml(-1). PACAP-(6-38) had no effect on this response. We conclude that PACAP-(1-38) may play a role in splanchnic nerve-induced adrenal secretion and in afferent reflex pathways.     

Effect of adrenalin and adrenal desympathization on brain-seizure activity

The effect of adrenalin and bilateral adrenal desympathization on brain-seizure activity evoked by electrical stimulation of the dorsal hippocampus was studied in adult cats. A few days after bilateral adrenal desympathization the threshold of epileptogenic hippocampal stimulation was lowered and the duration of the evoked seizure response increased. Intravenously injected adrenalin raised the threshold of epileptogenic hippocampal stimulation. After injection of small doses of adrenalin directly into the mesencephalic reticular formation the evoked seizure activity was inhibited: The threshold of epileptogenic hippocampal stimulation was raised and the total duration of the seizure discharges reduced. It is postulated that one of the important factors limiting brain-seizure activity is an increase in the circulating blood adrenalin level.     

Functional Aspects of Calcium Channels of Splanchnic Neurons and Chromaffin Cells of the Rat Adrenal Medulla

Effects of the inorganic calcium channel blockers zinc, manganese, cadmium, and nickel on secretion of catecholamines from the perfused adrenal gland of the rat were investigated. Secretion of catecholamines evoked by splanchnic nerve stimulation (1 and 10 Hz) was not affected by nickel (100 microM), partially blocked (50%) by cadmium (100 microM), and almost completely blocked (90%) by zinc (1 mM) or manganese (2 mM). A combination of nickel and cadmium inhibited nerve stimulation-evoked secretion by 80-90%. Catecholamine secretion evoked by direct stimulation of chromaffin cells by acetylcholine (50 micrograms), nicotine (5 microM), muscarine (50 micrograms), and K+ (17.5 mM) was not blocked by either cadmium, nickel, or their combination. However, zinc and manganese almost abolished nicotine- and K(+)-evoked secretion of catecholamines. None of the above agents had any effect on the secretion evoked by muscarine. Acetylcholine-evoked secretion of catecholamines was only partially reduced (50%) by zinc and manganese. We draw the following conclusions from the above findings: (a) cadmium plus nickel selectively blocks the calcium channels of splanchnic neurons but has no effect on calcium channels of the chromaffin cells; (b) zinc and manganese do not discriminate between calcium channels of neurons and calcium channels of chromaffin cells; (c) partial inhibition of acetylcholine-evoked secretion by inorganic calcium channel blockers is consistent with the idea that activation of nicotinic receptors increases Ca2+ influx, and activation of muscarinic receptors mobilizes intracellularly bound Ca2+, which is not affected by calcium channel blockers.     

Effects of clentiazem (TA-3090) and nifedipine on basal circulating catecholamine levels and on stimulation-evoked adrenal catecholamine secretion in anesthetized dogs.

The effects of TA-3090 (clentiazem) and nifedipine on basal sympathoadrenal activity and on the adrenal medullary response during splanchnic nerve stimulation were studied in dogs anesthetized with sodium pentobarbital. Plasma concentrations of epinephrine and norepinephrine were measured in aortic and adrenal venous blood before and after acute administration of the drugs, as well as during left splanchnic nerve stimulation before and after administration of drugs. Following intravenous injections, TA-3090 (30, 100, and 300 micrograms/kg) did not affect basal circulating catecholamine levels, whereas nifedipine (10, 30, and 100 micrograms/kg) markedly increased aortic epinephrine and norepinephrine concentrations in a dose-dependent manner in correlation with progressive decreases in mean arterial pressure. The changes in aortic epinephrine and norepinephrine concentrations were inversely related to those in mean arterial pressure (r = 0.603, p < 0.01; r = 0.536, p < 0.01; respectively). In response to direct splanchnic nerve stimulation (2 Hz, 2 ms, 1 min, 12 V), adrenal venous epinephrine and norepinephrine concentrations significantly increased, with a high degree of reproducibility. The catecholamine responses to splanchnic nerve stimulation were not affected by either TA-3090 or nifedipine at any dose tested. The present results suggest that the increases in circulating catecholamine levels following nifedipine administration are due to baroreflex activation secondary to the drug-induced hypotension. The study indicates that both TA-3090 and nifedipine did not significantly affect L-type Ca2+ channels related to catecholamine release in the adrenal medulla under the present experimental conditions.