缺O_2、低温和高CO_2对某些致喘介质致痉作用的影响

用20只成年豚鼠气管,制成多个“Z”形相连气管条,置入含Krebs-Henseleit液的器官浴中,以浴液温度为37℃,通5％CO_2和95％O_2为对照,观察缺O_2(通5％CO_2和95％N_2)、低温(浴液温度为12～15℃)或高CO_2(10％CO_2和90％O_2)对乙酰胆碱和组织胺致痉作用的影响并分析其机制。结果表明:缺O_2使平滑肌对乙酰胆碱和组织胺张力反应速度加快,总张力升高;低温使平滑肌对乙酰胆碱和组织胺张力反应速度减慢,总张力降低;高CO_2不影响平滑肌对组织胺或乙酰胆碱的反应;缺O_2、低温和高CO_2不影响异丙基肾上腺素对乙酰胆碱或组织胺所致痉挛的解痉作用。     

平滑肌BKCa通道在运动改变大鼠胸主动脉舒缩特性中的作用

背景：大电导钙激活钾通道(BK_Ca)是调节细胞兴奋性和血管张力的重要离子通道,有关大动脉平滑肌BK_Ca通道的作用机制鲜有报道。 目的：观察有氧运动对大鼠胸主动脉舒缩特性的影响,并探讨平滑肌BK_Ca通道在其中的作用。 方法：将20只Wistar大鼠随机分为安静对照组和有氧运动组,运动组进行12周跑台运动,坡度0°, 20 m/min, 60 min/d, 5 d/周。之后每组5只大鼠行股动静脉插管术。恢复1 d后,于在体、清醒状态下进行心血管功能监测。另各组5只大鼠,取胸主动脉制备去内皮血管环,进行体外血管收缩特性检测。 结果与结论：①有氧运动后静脉注射去甲肾上腺素引起的升压反应幅度下降。②静脉注射BK_Ca通道阻断剂Iberiotoxin可诱发升压反应,且运动组更显著。③ 120 mmol/L KCl在两组胸主动脉血管环均可诱发收缩,最大张力差异无显著性意义。④去甲肾上腺素(10^-9~10^-5 mol/L)诱发的血管收缩呈浓度依赖性,但运动组的最大张力显著低于安静组。⑤Iberiotoxin (3×10^-8 mol/L)预处理血管后,可增强去甲肾上腺素(10^-5 mol/L)诱发的张力增加,且运动组增加幅度显著大于安静组。⑥BKCa通道开放剂NS1619 (10^-10~10^-6 mol/L)可引起去甲肾上腺素诱发的血管收缩张力下降,且运动组对其敏感性(pD2)增加。提示,有氧运动可诱导大鼠心血管反应性和胸主动脉舒缩特性改变,其中平滑肌BKCa通道起着重要作用。     

小檗碱对卵白蛋白致敏豚鼠离体回肠平滑肌的影响

目的:研究小檗碱对卵白蛋白致敏的离体回肠平滑肌的影响。方法:采用体外离体器官实验法,观察小檗碱(20~100μg·ml-1)对卵白蛋白致敏豚鼠离体回肠平滑肌的影响,以及对磷酸组织胺(His)和氯化乙酰胆碱(Ach)所致豚鼠离体回肠收缩的影响。结果:小檗碱(20~100μg·ml-1)能明显抑制卵白蛋白致敏豚鼠离体回肠平滑肌收缩,对His和Ach所致的豚鼠离体回肠平滑肌收缩也有一定的抑制作用。结论:小檗碱对卵白蛋白致敏的豚鼠离体回肠平滑肌有明显的解痉作用。     

血管平滑肌钙激活钾通道及其在高血压发病中的功能异常

目的:血管平滑肌大电导钙激活钾通道(BKCa)是血管平滑肌细胞膜电位的主要调控器,它调节血管张力。研究表明高血压时出现脉管张力增高及对扩张的血管的缓冲能力下降等多种病理状态与血管平滑肌BKCa功能变化有关,包括与BKCa对Ca2 火花的调节反应发生变化相关。本文综述高血压时血管平滑肌BKCa功能和结构变化的研究报道。     

衰老大鼠动脉超微结构及平滑肌钾通道反应性变化

背景：K⁺通道是调节血管平滑肌的收缩性与舒张性的主要离子通道,与血管张力息息相关,但对K⁺通道在机体衰老过程中的作用鲜有报道。 目的：观察衰老对大鼠动脉超微结构和平滑肌钾通道反应性的影响及可能的作用机制。 方法：健康雄性Wistar大鼠16只,19月龄设为老年组(n=8),2月龄设为青年组(n=8)。两组各随机抽取6只大鼠进行胸主动脉血管环张力测定,分别给予钙激活钾通道特异性阻断剂TEA、电压依赖性钾通道特异性阻断剂4-AP、ATP敏感性钾通道特异性阻断剂glibenclamide、内向整流钾通道的特异性阻断剂BaCl₂等药物刺激,观察各阻断剂引起的动脉反应性变化。余下每组2只,取胸主动脉以透射电镜观察动脉超微结构的变化。 结果与结论：与青年组大鼠比较,老年组胸主动脉内皮细胞和平滑肌细胞等结构发生衰老性变化;KCl诱发大鼠胸主动脉达到最大收缩张力后恢复基础张力所需时间,老年组明显长于青年组;4种阻断剂均诱发血管张力增加,且TEA和4-AP诱发的胸主动脉收缩反应,老年组显著低于青年组;glibenclamide和BaCl₂诱发的血管收缩两组间无显著性差异。说明衰老可引起大鼠动脉超微结构发生改变,血管舒张能力下降,其中平滑肌钾通道尤其是钙激活钾通道和电压依赖性钾通道功能下降可能是其重要机制之一。     

用肺组织条作缺氧性肺血管收缩反应研究的探索

目的: 探索由急性缺氧所致肺组织条张力变化与肺动脉和气管张力变化的关系,以探讨用肺组织条研究缺氧性肺血管反应的可行性。方法:因为肺组织条中可收缩的部分主要是血管和气管,所以分别做肺组织条、肺动脉、气管的张力实验。纵向剪取Wistar大鼠肺组织条以及肺动脉环(肺动脉三级分支制成的肺动脉环)和肺内段气管条悬挂于张力传感器上,记录张力变化。结果:急性缺氧使肺组织条及肺动脉环张力增加,而气管条张力下降,在加入吲哚美辛阻断前列腺素生成后,肺组织条缺氧性收缩反应增强,肺血管环缺氧反应也增加,而对肺内气管条的缺氧反应无明显影响;在加入L-NAME阻断一氧化氮生成后,肺组织条和肺血管环缺氧性收缩反应均增强,而对肺内气管条的缺氧反应无明显影响;在加入4-AP阻断电压门控钾通道后,肺组织条与肺血管环缺氧性收缩反应均下降,而气管缺氧性舒张反应则减弱。 结论:必要时可用肺组织条作缺氧性肺血管反应性研究。     

β-肾上腺素能刺激促进离体小鼠心脏缺氧/复氧诱导的细胞凋亡

目的：观察β-肾上腺素能刺激与缺氧/复氧损伤对离体小鼠心脏细胞凋亡的影响。 方法： 逆行灌注离体小鼠心脏，观察不同剂量异丙基肾上腺素（Iso）和不同时间缺氧/复氧心肌细胞凋亡率的变化，并观察β1-肾上腺素能受体阻滞剂、caspase-拮抗剂、Bcl-2对其凋亡率的影响，以TUNEL法检测心肌细胞凋亡率。 结果： 单独Iso未引起心肌细胞凋亡率的变化，但可增加缺氧/复氧所诱导的细胞凋亡率；Bcl-2转基因鼠细胞凋亡率明显低于正常小鼠；β1-受体拮抗剂（美托洛尔）及caspase -拮抗剂（zVAD.fmk）可明显抑制Iso和缺氧/复氧所致细胞凋亡。 结论： β-肾上腺素能受体激动剂可促使缺氧/复氧所诱导心肌细胞凋亡，其诱导凋亡的作用主要通过β1-受体介导，β1-受体拮抗剂可抑制二者共同作用所诱导心肌细胞凋亡。     

少年红矾杏平喘糖浆镇咳、祛痰和平喘作用的实验研究

目的:观察少年红矾杏平喘糖浆(简称平喘糖浆)的止咳、祛痰和平喘作用。方法:采用氨水引起小鼠咳嗽实验观察平喘糖浆止咳作用;通过小鼠酚红祛痰实验观察平喘糖浆排痰作用,通过磷酸组胺所致豚鼠哮喘及离体豚鼠气管平滑肌实验观察平喘糖浆平喘作用。结果:平喘糖浆能明显延长引起半数小鼠咳嗽的氨水喷雾时间(EDT50),增加小鼠气管酚红的排出,显著延长豚鼠由磷酸组胺引起哮喘的潜伏期,明显抑制离体气管平滑肌的收缩。结论:平喘糖浆有祛痰、止咳和平喘作用。     

荷叶水煎剂对家兔小肠平滑肌的收缩效应及机制研究

目的:观察不同浓度的荷叶水煎剂对离体家兔小肠平滑肌收缩效应的影响及机制.方法:选用体重为2.0～2.5 kg的健康家兔20只,取其小肠平滑肌,置于恒温灌流槽中,用37℃的台氏液灌流,待小肠收缩波形稳定后,依次用含有不同浓度(0.1,0.2,0.4,0.6及0.8 g?kg-1)荷叶水煎剂的灌流液作用于小肠平滑肌,观察小肠平滑肌的收缩张力及收缩频率;并用阿托品(5 g?kg-1)、乙酰胆碱(0.5 g?kg-1)、维拉帕米(5 g?kg-1)、多巴胺(2 g?kg-1)等药物探讨荷叶水煎剂引起小肠平滑肌收缩张力变化的机制.结果:灌流浓度在0.2 g?kg-1至1g?kg-1范围内,小肠平滑肌的收缩张力增强,并有剂量依赖性;而收缩节律无明显变化;且荷叶水煎剂可改善阿托品对小肠平滑肌收缩的抑制作用.结论:荷叶水煎剂可兴奋小肠平滑肌,其作用机制可能主要与兴奋小肠平滑肌M受体有关.     

2.129 TNFα对结肠平滑肌细胞动力的影响及机制研究

目的近来的研究发现TNFαIL-1β等细胞因子可能参与胃肠动力障碍的发生.但在细胞水平,观测细胞因子对胃肠平滑肌细胞运动、细胞内钙水平影响,并探讨其作用机制的研究还鲜见报道.本工作旨在研究TNFα对结肠平滑肌细胞舒缩功能和细胞内钙水平的影响并探讨其发挥作用的可能的信号转导途径.方法分离游离家兔结肠环形平滑肌细胞,采用平滑肌细胞长度测定和激光扫描共聚焦显微镜钙测定技术观察1.不同浓度(1,5,10,50ng/mL)TNFα对平滑肌细胞长度和[Ca2+]i的影响,2. 10ng/mL TNFα与平滑肌细胞预先孵育30min后,观测平滑肌细胞对不同浓度KCl、乙酰胆碱作用后的反应,3.使用PD-98059(ERK MAPK抑制剂) 、manoalide(磷脂酶A2抑制剂)与平滑肌细胞孵育30min,再加入10ng/mL TNFα继续孵育30m in,观测平滑肌细胞对不同浓度KCl、乙酰胆碱作用后的反应.结果 TNFα不能直接收缩或舒张平滑肌细胞,对[Ca2+]i也没有影响.有无TNFα作用,KCl引起平滑肌细胞收缩和细胞内[Ca2+]i升高的差别无显著性(P＞0.05);乙酰胆碱引起的细胞内[Ca2+]i升高差别无显著性(P ＞0.05),但TNFα作用后,乙酰胆碱引起的平滑肌细胞收缩剂量-反应曲线左移,且浓度＞10-6mmol/L引起的平滑肌细胞收缩增加,差别具有显著性(P＜0.05).使用 PD-98059、manoalide后,TNFα引起的乙酰胆碱剂量-反应曲线左移被部分抑制.结论虽然TNFα对平滑肌细胞的收缩和[Ca2+]i没有直接影响, 但TNFα可增强G蛋白偶联的钙敏感性调节,促进平滑肌细胞的收缩.可能的信号转导途径是通过ERK MAPK激活磷脂酶A2,产生花生四烯酸,进而激活ROK,抑制肌球蛋白轻链磷酸酶 .     

Airway effects of slow reacting substance, prostaglandin F2alpha and histamine in the guinea-pig.

SRS, PGF2chi, and histamine were administered intravenously or as aerosols to artifically ventilated guinea-pigs in order to asses their capacity to affect tracheal insufflation pressure measured by means of Konzett-R?ssler technique, Independently of route of administration all three compounds increased tracheal insufflation pressure, SRS being the most potent one. Bilateral cervical vagotomy did not alter the effect. Relative to histamine SRS and PGF2chi were considerably more active by aerosol administration than by intranvenous injection. The aerosols had little or no effect on systemic blood pressure. On intravenous injection, histamine decreased and SRS and PGF2chi increased arterial blood pressure in a dose-dependent fashion. The airway effects of histamine were correlated to those on blood pressure whereas with SRS and PGF2chi this was not seen when the blood pressure effects were marked. Preadministration of adrenaline or isoprenaline as aerosols antagonized the increase in insufflation pressure, but not the effects on blood pressure, produced by intravenously injected histamine or PGF2chi. It is concluded that SRS, PGF2chi and histamine on intravenous or aerosol adminstration increase tracheal insufflation pressure in the guinea-pig mainly by an action on airway tone. The data emphasize that SRS is a potent bronchoconstricting agent, possibly of pathophysiological significance in guinea-pig anaphylaxis.     

Airway Effects of Slow Reacting Substance,Prostaglandin F2α and Histamine in the Guinea-Pig

SRS, PGF_2α, and histamine were administered intravenously or as aerosols to artificially ventilated guineapigs in order to assess their capacity to affect tracheal insufflation pressure measured by means of Konzett-Rössler technique. Independently of route of administration all three compounds increased tracheal insufflation pressure, SRS being the most potent one. Bilateral cervical vagotomy did not alter the effect. Relative to histamine SRS and PGF_2α were considerably more active by aerosol administration than by intravenous injection. The aerosols had little or no effect on systemic blood pressure. On intravenous injection, histamine decreased and SRS adn PGF_2α increased arterial blood pressure in a dose-dependent fashion. The airway effects of histamine were correlated to those on blood pressure whereas with SRS and PGF_2α this was not seen when the blood pressure effects were marked. Preadministration of adrenaline or isoprenaline as aerosols antagonized the increase in insufflation pressure, but not the effects on blood pressure, produced by intravenously injected histamine of PGF_2α. It is concluded that SRS, PGF_2α and histamine on intravenous or aerosol administration increase tracheal insufflation pressure in the guinea-pig mainly by an action on airway tone. The data emphasize that SRS is a potent bronchoconstricting agent, possibly of pathophysiological significance in guinea-pig anaphylaxis.     

Effects of histamine on slowly adapting pulmonary stretch receptor activities in vagotomized rabbits

Thirty-two SAR fibers located below the carina were used in 32 anesthetized, bilaterally vagotomized, and artificially ventilated rabbits. After intravenous administration of histamine (20, 40, and 80 micrograms/kg, n = 13) or ACh (10, 20, and 40 micrograms/kg, n = 13), SARs became active during expiration but decreased their inspiratory activity. The effects of both drugs were dose-dependent. The injection of histamine or ACh at all doses examined had no effect on tracheal pressure (PT). Atropine (3 mg/kg) and isoprenaline (100 micrograms/kg) blocked the responses of SAR activity to low doses of histamine (20 and 40 micrograms/kg) and to all doses of ACh. The response of SARs to 80 micrograms/kg of histamine was not altered by atropine (n = 10) nor by isoprenaline (n = 10). These results suggest that low-dose effects of histamine on SARs occur as the result of ACh release whereas with high doses the effect of histamine on the receptors is mainly independent of ACh released from the nerve endings. In another series of experiments (n = 6) where animals were treated with isoprenaline (100 micrograms/kg) and, subsequently, physostigmine (200 micrograms/kg), histamine (20 and 40 micrograms/kg) or ACh (10 and 20 micrograms/kg) increased the inspiratory discharge in SARs and the level of PT. From these results, it is assumed that the changes of SAR activity following histamine injection in vagotomized animals reflect a local bronchomotor effect which takes place in a peripheral bronchial tree that does not affect the level of PT. Histamine seems to release ACh and to elicit bronchoconstriction that can be manifested by physostigmine treatment.     

Thymoquinone-induced relaxation of guinea-pig isolated trachea

The effect of thymoquinone (TQ), the main constituent of the volatile oil of black seed (Nigella sativa), on the guinea-pig isolated tracheal zig-zag preparation was investigated. TQ caused a concentration-dependent decrease in the tension of the tracheal smooth muscle precontracted by carbachol. The effects of TQ were significantly potentiated by pretreatment of the tracheal preparations with quinacrine, a phospholipase A2 inhibitor, nordihydroguiaretic acid, a lipoxygenase inhibitor and by pretreatment with methylene blue, an inhibitor of soluble guanylyl cyclase. On the other hand, the effects of TQ were not influenced by pretreatment of the tracheal preparations with indomethacin, a cyclooxygenase inhibitor, propranolol, a non-selective beta-adrenoceptor blocker or by the pretreatment with theophylline, an adenosine receptors antagonist TQ totally abolished the pressor effects of histamine and serotonin on the guinea-pig isolated tracheal and ileum smooth muscles. The results of the present study suggest that TQ induced relaxation of precontracted tracheal preparation is probably mediated, at least in part, by inhibition of lipoxygenase products of arachidonic acid metabolism and possibly by non-selective blocking of the histamine and serotonin receptors. This relaxant effect of TQ, further support the traditional use of black seeds either alone or in combination with honey to treat bronchial asthma.     

Isoprenaline-stimulated differential adrenergic response of K+ channels in skeletal muscle under hypokalaemic conditions

The mechanism underlying the hyperpolarization induced by isoprenaline in mouse lumbrical muscle fibres was studied using cell-attached patch and intracellular membrane potential ( V(m)) recordings. Sarcolemmal inwardly rectifying K(+) channels (K(IR): 45 pS) and Ca(2+)-activated K(+) channels (BK: 181 pS) were identified. Exposure to isoprenaline closed K(IR) channels and increased BK channel activity. This increase was observed as a shift from 50 to -40 mV in the voltage dependence of channel activation. Isoprenaline prevented hysteresis of V(m) when the extracellular [K(+)] fell below 3.8 mM. This hysteresis was due to the properties of the K(IR). The effects of chloride transport and isoprenaline on V(m) did not interact purely competitively, but isoprenaline could prevent the depolarization induced by hyperosmotic media equally as well as bumetanide, which inhibits the Na(+)/K(+)/2Cl(-) cotransporter. In lumbrical muscle this leads to hyperpolarization, but this might vary among muscles. The switch from K(IR) to BK as the component of total K(+) conductance was due to isoprenaline.     

The effect of adrenaline on the contraction of human muscle

1. Infusions of adrenaline in physiological amounts alter human muscle contractions evoked by nerve stimulation.2. Adrenaline shortens the duration of the slow calf muscle twitch, but has no effect on the fast twitch of adductor pollicis.3. Adrenaline decreases unfused tetanic tension and increases the oscillation of tension in 10/sec tetani of calf muscle and adductor pollicis. The usual rise of tension and decrease in oscillation in unfused tetani (;ramp' phenomenon) is abolished.4. Adrenaline has no effect on maximal tetanic tension or maximal rate of rise of tension in a fused tetanus of adductor pollicis.5. The effects of adrenaline on human muscle are due to stimulation of beta-adrenotropic receptors, for they are abolished by the beta-adrenotropic antagonist DL-propranolol (but not by D-propranolol), and are mimicked by isoprenaline but not by noradrenaline.6. The effect of adrenaline on adductor pollicis is abolished by local beta-blockade of one arm with intra-arterial DL-propranolol, indicating that the responsible beta-receptors lie peripherally.7. The changes in muscle contraction observed cannot be explained by altered muscle temperature, for this falls during adrenaline infusion; nor are they due to an action on neuromuscular transmission, for these small doses of adrenaline do not affect the muscle action potential. The evidence points to a direct action of adrenaline on muscle.     

Identification of the tracheal and laryngeal afferent neurones mediating cough in anaesthetized guinea-pigs

We have identified the tracheal and laryngeal afferent nerves regulating cough in anaesthetized guinea-pigs. Cough was evoked by electrical or mechanical stimulation of the tracheal or laryngeal mucosa, or by citric acid applied topically to the trachea or larynx. By contrast, neither capsaicin nor bradykinin challenges to the trachea or larynx evoked cough. Bradykinin and histamine administered intravenously also failed to evoke cough. Electrophysiological studies revealed that the majority of capsaicin-sensitive afferent neurones (both Aδ- and C-fibres) innervating the rostral trachea and larynx have their cell bodies in the jugular ganglia and project to the airways via the superior laryngeal nerves. Capsaicin-insensitive afferent neurones with cell bodies in the nodose ganglia projected to the rostral trachea and larynx via the recurrent laryngeal nerves. Severing the recurrent nerves abolished coughing evoked from the trachea and larynx whereas severing the superior laryngeal nerves was without effect on coughing. The data indicate that the tracheal and laryngeal afferent neurones regulating cough are polymodal Aδ-fibres that arise from the nodose ganglia. These afferent neurones are activated by punctate mechanical stimulation and acid but are unresponsive to capsaicin, bradykinin, smooth muscle contraction, longitudinal or transverse stretching of the airways, or distension. Comparing these physiological properties with those of intrapulmonary mechanoreceptors indicates that the afferent neurones mediating cough are quite distinct from the well-defined rapidly and slowly adapting stretch receptors innervating the airways and lungs. We propose that these airway afferent neurones represent a distinct subtype and that their primary function is regulation of the cough reflex.     

The significance of liberated cyclooxygenase products for the pulmonary and cardiovascular actions of leukotriene C4 in the guinea pig depends upon the route of administration

Leukotriene C4 (LTC4), given as an aerosol or by the intravenous route, was at least 100 times more potent than histamine in causing an increase of the tracheal insufflation pressure in pentobarbital anaesthetized artificially ventilated guinea pigs. Indomethacin or meclofenamate enhanced the longlasting bronchoconstriction elicited with aerosols of LTC4, but antagonized the relatively short lived airway response to intravenously injected LTC4. However, by increasing the injected dose of LTC4, a slowly developing but maximal bronchoconstriction could be obtained in the presence of indomethacin. Indomethacin did not affect the airway response to histamine, administered by either route. Intravenous injection of LTC4 had little effect on the heart rate, but evoked a biphasic change of the systemic arterial blood pressure. An initial pressor response, which was attenuated but not abolished by indomethacin, was followed by a longlasting reduction of blood pressure. The hypotensive period evoked with higher doses of LTC4 occurred earlier and was of greater magnitude in indomethacin treated animals. Thus, LTC4 has a potent cyclooxygenase-independent bronchoconstrictor action in the intact guinea pig, which supports the possibility that LTC4 and its metabolites are important mediators of airway anaphylaxis in this animal. Depending upon the route of administration, secondarily released prostaglandins and/or thromboxanes may amplify or reduce the direct pulmonary effects of LTC4.(ABSTRACT TRUNCATED AT 250 WORDS)     

Histamine promotes excitability in bovine adrenal chromaffin cells by inhibiting an M-current

The current study has investigated the electrophysiological responses evoked by histamine in bovine adrenal chromaffin cells using perforated-patch techniques. Histamine caused a transient hyperpolarization followed by a sustained depolarization of 7.2 ± 1.4 mV associated with an increase in spontaneous action potential frequency. The hyperpolarization was abolished after depleting intracellular Ca²⁺ stores with thapsigargin (100 n m ), and was reduced by 40 % with apamin (100 n m ). Membrane resistance increased by about 60 % during the histamine-induced depolarization suggesting inhibition of a K⁺ channel. An inward current relaxation, typical of an M-current, was observed in response to negative voltage steps from a holding potential of −30 mV. This current reversed at −81.6 ± 1.8 mV and was abolished by the M-channel inhibitor linopirdine (100 μ m ). During application of histamine, the amplitude of M-currents recorded at a time corresponding with the sustained depolarization was reduced by 40 %. No inward current rectification was observed in the range −150 to −70 mV, and glibenclamide (10 μ m ) had no effect on either resting membrane potential or the response to histamine. The results show that an M-current is present in bovine chromaffin cells and that this current is inhibited during sustained application of histamine, resulting in membrane depolarization and increased discharge of action potentials. These results demonstrate for the first time a possible mechanism coupling histamine receptors to activation of voltage-operated Ca²⁺ channels in these cells.     

The actions of histamine in cat and rabbit superior cervical ganglia

Depolarization of the cat superior cervical ganglion (SCG) evoked by histamine was antagonized by mepyramine. Histamine-induced depolarization, indicated by changes in the negative and positive afterpotentials of ganglionic action potentials, was decreased by pretreatment with aminophylline. In the cat SCG, histamine evoked stimulus bound decremental oscillatory potentials (SBDOP). In the rabbit SCG, only depolarization and no SBDOP were observed after the administration of histamine. Histamine-induced SBDOP were increased by isoprenaline and decreased by Leu-enkephalin pretreatment. Our results indicate that histamine evokes depolarization and an increase in excitability of the cat SCG which seems to be mediated by H₁-receptors.