兔右房超速驱动后阻抑机制的初步探讨

本文用微电极技术,在20份离体兔心窦房结标本上观察了不同驱动频率和驱动时程对窦房结超速驱动后阻抑的影响。结果表明,在一定范围内右房超速驱动后阻抑及驱动后的负性变速效应,随驱动频率和驱动时程增加而加强。高频驱动期间和驱动停止后,优势起搏细胞跨膜电位幅度减小。驱动停止后第一个窦性动作电位4相自动去极化斜率和0相上升速率均降低,与驱动前相比有非常显著的差异(P<0.01)。毒扁豆碱可加强驱动后阻抑及驱动后的负性变速效应,阿托品不能完全阻断驱动后阻抑。我们初步认为:右房超速驱动后阻抑效应可能是内源性乙酰胆碱的释放和[Na~ ]_i 及[Ca~2 ]_i 的增加等多种因素作用的结果。     

吗啡和纳洛酮对豚鼠离体胆囊肌条活动的作用

5种浓度的吗啡对胆囊肌条的自动节律性收缩,均有明显加强作用。阿片受体拮抗剂——纳洛酮可阻断和翻转吗啡对胆囊肌条的作用,说明豚鼠的胆囊壁有阿片受体。乙酰胆碱显著地加强胆囊肌条的收缩,此效应可被阿托品阻断,而且阿托品也使吗啡对胆囊肌条的作用明显减弱。异丙肾上腺素和去甲肾上腺素分别抑制和加强胆囊肌条的运动,前者的效应可被心得宁阻断,后者则被酚妥拉明阻断,但两者的效应均不受纳洛酮的影响。而心得宁和酚妥拉明不影响吗啡对胆囊肌条的作用。本实验似能表明,吗啡对胆囊肌条运动的调节是通过阿片受体而起作用的。但吗啡对胆囊肌条的作用与肾上腺素能α和β受体无关。     

侧脑室内注射微量五肽胃泌素对大鼠胃肠推进运动的影响

以炭粉混悬液在大鼠小肠内推进距离占小肠全长的百分数,作为胃肠推进运动的指标,观察了侧脑室内注射微量五肽胃泌素(G_5)对这一推进运动的影响。结果如下:(1)侧脑室内(ICV)注射c_5(1μg/10μl、2μg/10μl 或4μg/10μl)可显著增强胃肠推进运动(P<0.01—0.001)。切断两侧膈下迷走神经、阿托品皮下(0.2mg/kg)或侧脑室内(5μg/10μl)注射均可完全阻断这一增强效应(P<0.001)。(2)肌注较大剂量G_5(20μg/100g)可显著增强胃肠推进运动(P<0.001),这一效应亦可为皮下注射阿托品(0.2mg/kg)所完全阻断(P<0.001)。(3)酚妥拉明(2.5mg/kg im或50g/10μl ICV)或心得安(5mg/kgim或50μg/50μl ICV)对侧脑室内注射G_5增强胃肠推进运动的作用均无影响(P>0.05)。上述结果表明侧脑室内注射G_5后,可能激活中枢胆硷能系统,通过迷走神经而使胃肠推进运动增强。     

大鼠侧脑室注射神经降压素对血压的作用

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠,用乌拉坦腹腔麻醉,在侧脑室注射神经降压素（ＮＴ）（１０,２０μｇ）可引起血压升高或降低,心率减慢,预先ｉｃｖ ａ１受体阻断剂哌唑嗪,可阻断ＮＴ的中枢升压反应,预先ｉｃｖ Ｍ受体阻断剂硫酸阿托品,可阻断ＮＴ的中枢降压反应,预先ｉｃｖ Ｈ１受体阻断剂扑尔敏或Ｈ２受体阻断剂甲氰咪胍,对ＮＴ的中枢心血管效应均无明显影响。实验结果表明：脑中ＮＴ升高可使血压升高或降低;在     

Effects of atropine on the release of newly synthesized acetylcholine from rat striatal slices at various concentrations of calcium ions

The release of acetylcholine (ACh) from brain tissue is known to be inhibited by muscarinic autoreceptors on cholinergic nerve terminals but the mechanism of the inhibition is not understood. Atropine brings about an increase of ACh release by removing the inhibitory action of autoreceptors. We investigated whether the effect of atropine on the release of [¹⁴C]ACh newly synthesized during incubations from [U-¹⁴C] glucose depends on the concentration of Ca²⁺ in the medium. In rat striatal slices incubated in the presence of an inhibitor of cholinesterases and of 30 mmol/l K⁺, significant increases in the release of [¹⁴C]ACh elicited by atropine were only observed during incubations with very low concentrations of Ca²⁺. This finding supports the view that the activation of presynaptic muscarinic autoreceptors in the brain affects the release of ACh by reducing the availability of Ca²⁺ that is required for transmitter liberation.     

Biosynthesis of tropic acid: Feeding experiments with cinnamoyltropine and littorine

The administration of cinnamoyl-[2-¹⁴C]-tropine-[N-methyl-¹⁴C] to Datura stramonium plants resulted in the formation of labeled atropine and scopolamine. However the atropine was found to have almost all its radioactivity located on the N-methyl group of the alkaloid, indicating that the administered ester had undergone hydrolysis in the plant affording tropine and cinnamic acid, the latter not being utilized for the biosynthesis of tropic acid. Dual labeled RS-littorine (3β-(2-hydroxy-3-phenylpropionyloxy-[1-¹⁴C]-tropane-[3β-³H]) was also fed to D. stramonium and radioactive atropine was obtained. However the drastic change in the ³H:¹⁴C ratio found in the atropine indicated that the littorine was not converted directly to the alkaloid, and it is suggested that the littorine is hydrolysed _{in vivo} to tropine and phenyl-lactic acid, the latter undergoing rearrangement to tropic acid prior to esterification with tropine.     

Deterrence of feeding and oviposition responses of adult Heliothis virescens by some compounds bitter-tasting to humans

Some compounds that are bitter-tasting to humans, both alkaloidal (quinine, quinidine, atropine, caffeine) and non-alkaloidal (denatonium benzoate, sucrose octaacetate, naringin), deterred feeding and oviposition by Heliothis virescens (F.) in laboratory and field cage experiments. Preliminary electrophysiological studies of gustatory sensilla on the ovipositor of H. virescens provided evidence of 3 neurons, one of which is responsive to sucrose. Preliminary indications are that responses of this neuron may be inhibited by quinine and denatonium benzoate.     

顶核—延髓头端腹外侧区系统参与前庭降压降心率反应

实验用乌拉坦麻醉、箭毒化、人工呼吸的大鼠。将神经元胞体兴奋剂L-谷氨酸钠(Glu)微量注入顶核或前庭上核均引起血压下降;心率减慢。该顶核-和前庭上核-降压降心率反应均可被延髓头端腹外侧区内注射GABA受体阻断剂荷包牡丹碱阻断。顶核内注射普鲁卡因也能阻断Glu兴奋前庭上核的心血管反应。以上结果提示前庭-降压降心率反应可能通过顶核-延髓头端腹外侧区系统实现。静脉注射甲基阿托品也能衰减Glu兴奋顶核的心血管反应,显示迷走神经也参与前庭-顶核降压降心率反应。     

Fe3O4 and bimetal–organic framework Zn/Mg composite peroxide-like catalyze luminol chemiluminescence for specific measurement of atropine in Datura plant

Atropine (AT) is an anticholinergic drug. AT is abundantly in Datura plant seeds. Fe₃O₄@Zn/Mg MOF (Fe₃O₄@MOF) composite was synthesized. The compound had a high peroxidase-like activity in a chemiluminescence (CL) reaction. Addition of AT quenched CL. The linear range and limit of detection were 5–600 μg L⁻¹ and 2 × 10⁻² μg L⁻¹. This method is fast, reversible, and selective, without biodegradability effects, high accuracy, and precision for measuring AT in the Datura plant.     

缰核内注射Ca^2＋拮抗电针镇痛的作用可被三碘季铵酚翻转

通过埋植套管向大鼠双侧缰核分别注射0.1mol/L CaCl_2 0.5μl,0.06mol/L ACh0.5μl,5.4×10~(-3)mol/L三碘季铵酚0.5μl和14.4×10~(-3)mol/L阿托品0.5μl后观察到,Ca~(2 )降低基础痛阈并拮抗电针镇痛效应;ACh拮抗电针镇痛;Ca~(2 )拮抗电针镇痛的作用可被胆碱能N受体阻断剂三碘季铵酚完全翻转。提示缰核内的Ca~(2 )可能通过ACh实现其拮抗电针镇痛的效应。