共查询到19条相似文献,搜索用时 187 毫秒
1.
《中国老年学杂志》2019,(12)
目的研究麦冬皂苷(OP)D对兔离体十二指肠平滑肌的舒张作用及其机制。方法采用经典的家兔离体十二指肠平滑肌试验,应用BL-420F生物机能实验系统,累积加入0.65×10~(-6)、1.30×10~(-6)、1.95×10~(-6) mol/L的OPD溶液作用于家兔离体十二指肠平滑肌,观察记录家兔离体十二指肠平滑肌的平均收缩力、收缩振幅和收缩频率。应用工具药钌红(RR)、肝素(HP)、左旋硝基精氨酸甲酯(L-NAME)、维拉帕米研究OPD舒张十二指肠平滑肌作用的机制。结果加药后与加药前比较,低、中、高浓度组平均收缩力,中、高浓度组振幅均显著降低(P0.05,P0.01)。OPD 1.30×10~(-6) mol/L及OPD 1.95×10~(-6) mol/L时,与对照组比较,L-NAME组平滑肌收缩力均显著升高(P0.05,P0.01);OPD 0.65×10~(-6)、1.30×10~(-6)、1.95×10~(-6) mol/L浓度时,与对照组比较,维拉帕米组平滑肌收缩力显著降低(P0.01)。结论 OPD可浓度依赖性地抑制家兔离体十二指肠平滑肌的收缩活动,其机制可能与抑制外钙内流和增加十二指肠平滑肌的一氧化氮(NO)浓度有关,但对肌浆网Ryanodine受体途径和三磷酸肌醇(IP3)受体途径介导的内钙释放无明显影响。 相似文献
2.
目的观察胡椒碱对槟榔碱促进家兔离体小肠平滑肌运动的影响及其作用机制.方法采用离体平滑肌恒温灌流的方法,取家兔离体小肠,通过BL-420生物机能实验系统测定其张力的变化,观察不同浓度(0.06 g/L、0.6 g/L、6 g/L)胡椒碱溶液对正常状态下家兔离体小肠平滑肌自发性收缩的影响;先观察胡椒碱对家兔离体小肠平滑肌自发性收缩的影响,随后观察加入槟榔碱后对家兔离体小肠平滑肌自发性收缩的影响;为研究胡椒碱抑制家兔离体小肠平滑肌收缩的作用机制,应用IP3受体(inositol 1, 4, 5-trisphosphate, IP3)阻断剂肝素(Heparin,HP)、肌浆网ryanodine受体阻断剂钌红(ruthenium red,RR)和一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(N'-nitro-L-arginine-methylesterhydrochloride,L-NAME),共同阐明胡椒碱对家兔离体小肠平滑肌作用的机制.结果胡椒碱抑制家兔离体小肠平滑肌自发性收缩,药物浓度在6 g/L时可显著抑制家兔离体小肠平滑肌收缩的振幅(P0.01);在此基础上加入0.006 g/L槟榔碱溶液促进家兔离体小肠平滑肌收缩的振幅(P0.05)且升高小肠收缩幅度小于单个槟榔碱促进家兔离体小肠平滑肌的收缩振幅(P0.05); IP3受体HP能增强胡椒碱舒张家兔离体小肠平滑肌收缩的作用(P0.05),而肌浆网ryanodine受体阻断剂钌红对胡椒碱舒张家兔小肠平滑肌的作用无明显影响(P0.05); L-NAME能够部分阻断胡椒碱舒张家兔离体小肠平滑肌收缩的作用(P0.05).结论胡椒碱可显著抑制家兔离体小肠平滑肌收缩的振幅;抑制单个槟榔碱促进家兔离体小肠平滑肌的收缩振幅;其机制可能与增加一氧化氮浓度,抑制IP3受体介导的内钙释放有关,但对肌浆网ryanodine受体途径引起的内钙释放无关. 相似文献
3.
目的 观察替米沙坦对大鼠离体胸主动脉环张力的影响,并探讨其作用机制.方法 采用离体血管张力实验方法 .观察替米沙坦在1×10-9 mol/L,1×10-8 mol/L,1×10-7 mol/L,1×10-6 mol/L,1×10-5 mol/L浓度时,对去甲肾上腺素(NE,1×10-6 mol/L)、氯化钾(KCl,60 mmol/L)诱发大鼠离体胸主动脉环收缩的影响.观察Na+/Ca2+交换体阻断剂KB-R7943(1×10-6 mol/L)、KV通道阻断剂四胺基吡啶(4-AP,1×10-3 mol/L)、KATP通道阻断剂格列苯脲(Gli,1×10-5 mol/L)、KCa通道阻断剂四乙胺(TEA,1×10-2 mol/L)、KiR通道阻断剂氯化钡(BaCl2,1×10-3 mol/L)对替米沙坦作用的影响.结果替米沙坦对KCl(60 mmol/L) 预收缩的离体胸主动脉环张力无影响,对NE(1×10-6 mol/L) 预收缩的离体胸主动脉环产生浓度依赖性的舒张作用.用KB-R7943、4-AP、Gli预处理的血管环对替米沙坦的舒张反应与未经处理时比较无统计学意义(P>0.05).TEA及BaCl2可减弱替米沙坦对血管环的舒张作用(P<0.05).结论 替米沙坦对NE预收缩的大鼠胸主动脉环具有浓度依赖性的舒张作用,其舒张反应与Na+/Ca2+交换体、KV通道和KATP通道无关,可能与KCa通道及KiR通道有关. 相似文献
4.
AIM:To investigate the relaxant effect of chromane HEF-19 on colonic smooth muscles isolated from rabbits,and the underlying mechanisms.METHODS:The relaxant effect and action mechanisms of HEF-19 were investigated using descending colon smooth muscle of the rabbits.Preparations 1 cm long were mounted in 15-mL tissue baths containing Tyrode’s solution,maintained at 37±0.5℃and aerated with a mixture of 5%CO2in oxygen(Carbogen).The tension and amplitude of the smooth muscle strips were recorded after adding HEF-19(10-6,10-5and 10-4mol/L).After cumulative administration of four antispasmodic agents,including acetylcholine chloride(Ach)(10-4mol/L),histamine(10-4mol/L),high-K+(60 mmol/L)and BaCl2(8.2 mmol/L),HEF-19(3×10-7-3×10-4mol/L)was added to investigate the relaxant effect of HEF-19.CaCl2(10-4-2.5×10-3mol/L)was added cumulatively to the smooth muscle preparations pretreated with and without HEF-19(1×10-6or 3×10-6mol/L)and verapamil(1×10-7mol/L)to study the mechanisms involved.Finally,phasic contraction was induced with ACh(15×10-6mol/L),and CaCl2(4×10-3mol/L)was added to the smooth muscle preparations pretreated with and without HEF-19(3×10-6mol/L or 1×10-5mol/L)and verapamil(1×10-7mol/L)in calcium-free medium to further study the underlying mechanisms.RESULTS:HEF-19(1×10-6,1×10-5and 1×10-4mol/L)suppressed spontaneous contraction of rabbit colonic smooth muscles.HEF-19(3×10-7-3×10-4mol/L)relaxed in a concentration-dependent manner colonic smooth muscle preparations pre-contracted with BaCl2,high-K+solution,Ach or histamine with respective EC50values of 5.15±0.05,5.12±0.08,5.58±0.16and 5.25±0.24,thus showing a spasmolytic activity.HEF-19(1×10-6mol/L and 3×10-6mol/L)shifted the concentration-response curves of CaCl2to the right and depressed the maximum response to CaCl2.The two components contracted by Ach were attenuated with HEF-19(3×10-6mol/L or 10-5mol/L)in calcium-free medium.CONCLUSION:HEF-19 inhibited rabbit colonic smooth muscle contraction,probably through inhibiting opening of 相似文献
5.
目的 观察咪达唑仑对大鼠离体胸主动脉环张力的影响,并探讨其作用机制.方法 采用离体血管张力试验方法.观察咪达唑仑在3×10-6t mol/L、1×10-5 mol/L,3×10-5 mol/L、1×10-4 mol/L浓度时,对去甲肾上腺素(NE,1×10-6 mol/L)、氯化钾(KCI,60mmol/L)诱发大鼠离体胸主动脉环收缩的影响.观察Na+/Ca2+交换体阻断荆KB-R7943(1×10-5 mol/L)、Kv通道阻断剂4-AP(4-AP,1×10-3 mol/L)、KATP通道阻断剂格列苯脲(Gli,1×10-5 mol/L)、KCa通道阻断剂四乙胺(TEA,1×10-2 mol/L)、K1R通道阻断剂氯化钡(BaCl2,1×10-3 mol/L)对咪达唑仑作用的影响.结果 各浓度咪达唑仑对预收缩的大鼠离体胸主动脉环有舒张作用.用KB-R7943、4-AP、TEA及BaCl2预处理的血管环对咪达唑仑的舒张反应与未经处理时比较无统计学意义(P>0.05).Gli可减弱咪达唑仑对血管环的舒张作用(P<0.05).结论 咪这唑仑对大鼠胸主动脉环具有浓度依赖性的舒张作用,其舒张反应与Na+/Ca2+交换体、Kv通道、KCa通道和K1R通道无关,可能与KATP通道有关. 相似文献
6.
目的观察芒柄花素对兔离体肠平滑肌肌张力的影响并探讨其作用机制。方法采用经典的离体小肠灌流技术,观察芒柄花素对肠平滑肌收缩活动以及乙酰胆碱(Ach)、氯化钡(BaCl2)及组胺(HA)所致痉挛性收缩肠平滑肌的影响。应用L型钙通道开放剂Bay K8644、肌浆网ryanodine受体阻断剂钌红(RR)和一氧化氮(NO)合酶抑制剂左旋硝基精氨酸甲酯(L-NAME),研究芒柄花素舒张肠平滑肌的作用机制。结果芒柄花素(10、20、40、60、80、100μmol/L)能剂量依赖性的抑制家兔离体小肠平滑肌自发性收缩,对Ach,HA和BaCl2所致的兔离体肠痉挛性收缩也具有剂量依赖性抑制作用,且与无刺激肠平滑肌比较有显著性差异(P<0.05或P<0.01)。芒柄花素可明显抑制Bay K8644(0.5μmol/L),阻断RR引起肠平滑肌舒张作用,但L-NAME不能够抑制芒柄花素舒张肠平滑肌作用。结论芒柄花素显著抑制家兔小肠平滑肌的收缩活动,其抑制可能与抑制细胞外钙内流和内钙释放,从而使细胞内钙浓度降低有关,但与小肠平滑肌一氧化氮(NO)浓度无关。 相似文献
7.
目的 研究吲哚布芬对去甲肾上腺素(NE)预收缩大鼠主动脉血管环的效应及其可能的机制.方法 记录NE预收缩的离体大鼠主动脉环张力变化,观察吲哚布芬对大鼠主动脉血管环的作用及不同工具药对吲哚布芬的影响.结果 吲哚布芬(1×10-7 mol/L~3×10-5 mol/L)对NE引起的大鼠主动脉血管环的张力变化有浓度依赖性的舒张作用.在NE预收缩的血管环上,四乙胺(10-2 mol/L)、4-氨基吡啶(10-3 mol/L)和格列苯脲(10-5 mol/L)可抑制吲哚布芬的舒张血管作用.结论 吲哚布芬对NA引起的血管收缩有浓度依赖行的舒张作用,吲哚布芬可能通过开放Kca通道、Kv通道和KATP通道参与了吲哚布芬的舒血管作用. 相似文献
8.
钾通道参与牛磺酸对猪冠状动脉的舒张作用的影响 总被引:1,自引:1,他引:0
目的 研究牛磺酸舒张猪冠状动脉血管作用及其可能机制.方法 用Powerlab离体血管环实验系统,记录KCl、组胺、5-羟色胺及细胞外Ca2+所引起的离体猪冠状动脉环的收缩,观察牛磺酸预孵对这些收缩的影响,或观察急性加入牛磺酸对持续收缩的舒张作用;观察不同药物对牛磺酸的舒血管作用的影响.结果 牛磺酸(20.0 mmol/L、39.2 mmol/L、76.8 mmol/L)预孵浓度依赖性拮抗组胺(0.1 mmol/L)、5-羟色胺(10 μmol/L)及细胞外Ca2+引起的猪冠状动脉环收缩.牛磺酸(20.0 mmol/L~107.6 mmol/L)对KCl(30 mmol/L)所致的收缩呈现出浓度依赖性地舒张作用.去内皮和NO合成酶抑制剂L-NAME(0.1 mmol/L)对其舒张作用无影响.KCa通道抑制药四乙胺(10 mmol/L)、KATP通道抑制药格列苯脲(10 μmol/L)和KIR通道抑制药氯化钡(1 mmol/L)明显抑制牛磺酸的舒血管作用,而KV通道抑制药4-氨基吡啶(1 mmol/L)无明显影响.结论 在离体猪冠状动脉环,牛磺酸浓度依赖性抑制多种致痉剂引起的收缩;对持续收缩有舒张作用,该舒张作用为非内皮依赖性,可能与激动KCa、KATP和KIR通道有关. 相似文献
9.
目的:研究利拉鲁肽对离体大鼠胸主动脉环的血管舒张效应及其作用机制。
方法:分离32只SD雄性大鼠的胸主动脉环,分成去内皮组(n=16)和内皮完整组(n=16)。采用离体血管环实验方法,经生物信号采集与分析系统测定血管环张力的变化,观察利拉鲁肽(1×10-5 mol/L)对去甲肾上腺素(1×10-6 mol/L)预收缩的胸主动脉环的舒张作用。随后内皮完整组又分为左旋硝基精氨酸甲酯干预亚组(n=8)和格列苯脲干预亚组(n=8),分别接受一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(1×10-4 mol/L)和非特异性ATP敏感性钾通道(KATP)抑制剂格列苯脲(1×10-5 mol/L)的预处理,预处理后利拉鲁肽分别作用于预处理过的去甲肾上腺素预收缩的胸主动脉环,观察利拉鲁肽对离体大鼠胸主动脉环作用的影响。
结果:利拉鲁肽对基础状态的胸主动脉环无作用。去甲肾上腺素预收缩胸主动脉环后,当利拉鲁肽浓度达到1×10-5 mol/L时,利拉鲁肽对去内皮组和内皮完整组胸主动脉环均有舒张作用,但对内皮完整组舒张作用更强,胸主动脉环最大舒张幅度达17%(P<0.05),差异有统计学意义。经左旋硝基精氨酸甲酯和格列苯脲预处理后,左旋硝基精氨酸甲酯干预亚组利拉鲁肽对胸主动脉环舒张幅度为4%(P<0.05),与预处理前相比差异有统计学意义。格列苯脲干预亚组利拉鲁肽对胸主动脉环舒张幅度为14%(P>0.05),与预处理前相比差异无统计学意义。
结论:利拉鲁肽对去甲肾上腺素预收缩的胸主动脉环有明显的舒张作用,其机制与内皮细胞一氧化氮合酶有关。而KATP未能阻断利拉鲁肽的血管舒张作用。 相似文献
方法:分离32只SD雄性大鼠的胸主动脉环,分成去内皮组(n=16)和内皮完整组(n=16)。采用离体血管环实验方法,经生物信号采集与分析系统测定血管环张力的变化,观察利拉鲁肽(1×10-5 mol/L)对去甲肾上腺素(1×10-6 mol/L)预收缩的胸主动脉环的舒张作用。随后内皮完整组又分为左旋硝基精氨酸甲酯干预亚组(n=8)和格列苯脲干预亚组(n=8),分别接受一氧化氮合酶抑制剂左旋硝基精氨酸甲酯(1×10-4 mol/L)和非特异性ATP敏感性钾通道(KATP)抑制剂格列苯脲(1×10-5 mol/L)的预处理,预处理后利拉鲁肽分别作用于预处理过的去甲肾上腺素预收缩的胸主动脉环,观察利拉鲁肽对离体大鼠胸主动脉环作用的影响。
结果:利拉鲁肽对基础状态的胸主动脉环无作用。去甲肾上腺素预收缩胸主动脉环后,当利拉鲁肽浓度达到1×10-5 mol/L时,利拉鲁肽对去内皮组和内皮完整组胸主动脉环均有舒张作用,但对内皮完整组舒张作用更强,胸主动脉环最大舒张幅度达17%(P<0.05),差异有统计学意义。经左旋硝基精氨酸甲酯和格列苯脲预处理后,左旋硝基精氨酸甲酯干预亚组利拉鲁肽对胸主动脉环舒张幅度为4%(P<0.05),与预处理前相比差异有统计学意义。格列苯脲干预亚组利拉鲁肽对胸主动脉环舒张幅度为14%(P>0.05),与预处理前相比差异无统计学意义。
结论:利拉鲁肽对去甲肾上腺素预收缩的胸主动脉环有明显的舒张作用,其机制与内皮细胞一氧化氮合酶有关。而KATP未能阻断利拉鲁肽的血管舒张作用。 相似文献
10.
雌酚酮衍生物EA303对小鼠腹泻的抑制作用 总被引:1,自引:0,他引:1
目的:研究雌酚酮衍生物EA303对小鼠腹泻的抑制作用及机制.方法:采用小鼠的蓖麻油、硫酸钠、液体石蜡等腹泻模型及炭末推进法观察低、中、高剂量(14.87 mg/kg、29.74 mg/kg、59.48 mg/kg)的EA303对小鼠在体内胃肠道的作用.通过离体运动实验法分析不同浓度(10-5mol/L、3 × 10-5mol/L、10-4 mol/L)的EA303对家兔离体肠道平滑肌的作用.结果:EA303高、中、低3个剂量组灌胃给药后在不同时间段与生理盐水组相比可明显降低蓖麻油、硫酸钠、液体石蜡所致的小鼠腹泻的腹泻指数;高剂量组与生理盐水组相比可明显降低正常小鼠的小肠推进率(58.53%±14.12% vs 78.41%±15.91%,P<0.01);高、中、低剂量组与生理盐水组相比均可明显延缓正常小鼠的排便时间(116.40±17.69 min,114.40±45.76 min,101.50±50.02 min vs 78.10±15.98min,均P<0.01);中、高剂量的EA303与未给药前相比能显著降低小肠平滑肌自主活动的振幅(43.26%±14.83%,16.70%±10.89%vs 100.00%±0.00%,均P<0.01),高剂量组与未给药前相比还显著降低小肠平滑肌自主活动的张力(58.94%±7.16% vs 100.00%±0.00%,P<0.01).结论:EA303具有抑制肠运动和抗腹泻作用,其作用机制可能是降低肠管平滑肌振幅和张力. 相似文献
11.
Koyuncu A Bagcivan I Sarac B Aydin C Yildirim S Sarioglu Y 《World journal of gastroenterology : WJG》2008,14(29):4667-4671
AIM: To investigate the tolerance development against the relaxant effect of nitric oxide donating drug isosorbide dinitrate (ISDN) and sodium nitropruside (SNP) in internal anal sphincter (IAS) smooth muscle. METHODS: Relaxation responses of ISDN, and electrical fi eld stimulation (EFS) were obtained before and after tolerance induction by ISDN incubation. RESULTS: ISDN (10-7-10-4 mol/L) and SNP (10-8-10-4 mol/L) caused a concentration-dependent relaxation on the basal tonus of the isolated rabbit IAS strips. After a period of 2 h incubation of the 6 x 10-4 mol/L ISDN the relaxation effects of ISDN and SNP did not change compared to control strips. EFS evoked frequency-dependent relaxation in internal anal sphincter smooth muscle and Emax obtained from control strips were not changed in ISDN tolerance-inducing condition. In this study nitrate tolerance was not observed in rabbit IAS smooth muscle. CONCLUSION: This result shows that nitric oxide donating drugs relaxes the internal anal sphincter of the rabbits without the development of tolerance. 相似文献
12.
AIM: To investigate the effect and the possible mechanism of ginsenoside Rb1 on small intestinal smooth muscle motility in mice. METHODS: Intestinal smooth muscle strips were isolated from male ICR mice (5 wk old), and the effect of ginsenoside Rb1 on spontaneous contraction was recorded with an electrophysiolograph. The effect of ginsenoside Rb1 on ion channel currents, including the voltage-gated K + channel current (IK V ), calcium-activated potassium channel currents (IK Ca ), spontaneous transient outward currents and ATP-sensitive potassium channel current (IK ATP ), was recorded on freshly isolated single cells using the whole-cell patch clamp technique. RESULTS: Ginsenoside Rb1 dose-dependently inhibited the spontaneous contraction of intestinal smooth muscle by 21.15% ± 3.31%, 42.03% ± 8.23% and 67.23% ± 5.63% at concentrations of 25 μmol/L, 50 μmol/L and 100 μmol/L, respectively (n=5,P0.05). The inhibitory effect of ginsenoside Rb1 on spontaneous contraction was significantly but incompletely blocked by 10 mmol/L tetraethylammonium or 0.5 mmol/L 4-aminopyridine, respectively (n=5, P0.05). However, the inhibitory effect of ginsenoside Rb1 on spontaneous contraction was not affected by 10 μmol/L glibenclamide or 0.4 μmol/L tetrodotoxin. At the cell level, ginsenoside Rb1 increased outward potassium currents, and IK V was enhanced from 1137.71 ± 171.62 pA to 1449.73 ± 162.39 pA by 50 μmol/L Rb1 at +60 mV (n=6, P0.05). Ginsenoside Rb1 increased IK Ca and enhanced the amplitudes of spontaneous transient outward currents from 582.77 ± 179.09 mV to 788.12 ± 278.34 mV (n=5, P0.05). However, ginsenoside Rb1 (50 μmol/L) had no significant effect on IK ATP (n=3, P0.05). CONCLUSION: These results suggest that ginsenoside Rb1 has an inhibitory effect on the spontaneous contraction of mouse intestinal smooth muscle mediated by the activation of IK V and IK Ca , but the K ATP channel was not involved in this effect. 相似文献
13.
Effects of magnolol and honokiol derived from traditional Chinese herbal remedies on gastrointestinal movement 总被引:5,自引:0,他引:5
Zhang WW Li Y Wang XQ Tian F Cao H Wang MW Sun QS 《World journal of gastroenterology : WJG》2005,11(28):4414-4418
AIM: To study the effects of magnolol and honokiol on isolated smooth muscle of gastrointestinal tract and their relationship with Ca2+, and on the gastric emptying and the intestinal propulsive activity in mice. METHODS: Routine experimental methods using isolated gastric fundus strips of rats and isolated ileum segments of guinea pigs were adopted to measure the smooth muscle tension. The effects of magnolol 10-3,10-4,10-5 mol/L, and honokiol 10-4, 10-5,10-6 mol/L on the contractility of gastric fundus strips of rats and ileum of guinea pigs induced by acetylcholine (Ach) and 5-hydroxvtryptamine (5-HT) was assessed respectively. The method using nuclein and pigment methylene blue was adopted to measure the gastric retention rate of nuclein and the intestinal propulsive ratio of a nutritional semi-solid meal for assessing the effect of magnolol and honokiol (0.5, 2, 20 mg/kg) on gastric emptying and intestinal propulsion. RESULTS: Magnolol and honokiol significantly inhibited the contractility of isolated gastric fundus strips of rats treated with Ach or 5-HT and isolated ileum guinea pigs treated with Ach or CaCI2, and both of them behaved as non-competitive muscarinic antagonists. Magnolol and honokiol inhibited the contraction induced by Ach in Ca2+-free medium and extracellular Ca2+-dependent contraction induced by Ach. Each group of magnolol and honokiol experiments significantly decreased the residual rate of nuclein in the stomach and increased the intestinal propulsive ratio in mice. CONCLUSION: The inhibitory effect of magnolol and honokiol on contractility of the smooth muscles of isolated gastric fundus strips of rats and isolated ileum of guinea pigs is associated with a calcium-antagonistic effect. Magnolol and honokiol can improve the gastric emptying of a semi-solid meal and intestinal propulsive activity in mice. 相似文献
14.
K Taniyama I Sano S Nakayama S Matsuyama K Takeda C Yoshihara C Tanaka 《Gastroenterology》1991,101(6):1579-1587
Preparations of longitudinal muscle attached to myenteric plexus from guinea pig ileum were used to observe the effect of trimebutine on intestinal motility. Electrical stimulation at 0.2 Hz and 5 Hz produced contraction mediated by the release of acetylcholine in the preparations. The response to low-frequency stimulation (0.2 Hz) was inhibited by trimebutine (10(-8)-10(-5) mol/L), and the response to high-frequency stimulation (5 Hz) was enhanced by the drug at low concentrations (10(-8)-10(-7) mol/L) and inhibited by high concentrations (10(-6)-10(-5) mol/L). This enhancement was mimicked by [D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin, and was antagonized by naloxone but not by MR2266. Enhancement by trimebutine was inhibited by yohimbine. Trimebutine (greater than or equal to 10(-8) mol/L) inhibited stimulation (5 Hz)-evoked release of norepinephrine, and the trimebutine effect was antagonized by naloxone but not by MR2266. Low concentrations of trimebutine inhibit norepinephrine release via the mu-opioid receptor and enhance intestinal motility by preventing the adrenergic inhibition of acetylcholine release. Inhibition by trimebutine was antagonized either by naloxone or MR2266. High concentrations of trimebutine may inhibit acetylcholine release via the mu- and kappa-opioid receptors, after which the intestinal motility is inhibited. Trimebutine at further high concentrations (greater than 10(-5) mol/L) contracted single smooth muscle cells from the circular muscle layers but not from the longitudinal muscle layers. The usual dose of trimebutine may exert dual effect on the intestinal motility indirectly through cholinergic and adrenergic neurons without direct effect on the smooth muscle. 相似文献
15.
目的 观察血管钠肽(VNP)对大鼠腹主动脉的舒张作用及对ATP敏感性钾通道(ATP-sensitive potassium channel,KATP)的作用。方法 采用离体血管灌流方法,测定VNP对血管环张力的影响。采用膜片钳方法观察VNP对KATP通道的影响。结果 VNP对大鼠的腹主动脉具有浓度依赖性舒张作用,该作用无内皮依赖性:VNP对内皮完整的腹主动脉最大舒张率(Emax)为(81±8)%,对内皮缺失腹主动脉Emax为(74±6)%。在浴槽内预先孵育优降糖(1×10-6 mol/L)可降低血管对VNP的舒张效应。VNP可增强腹主动脉血管平滑肌细胞KATP通道电流: VNP(1×10-6 M)增强KATP通道Emax为(112±24)%,优降糖(1×10-6 mol/L)可消除这一作用。结论 VNP有舒张血管作用,这一作用与增强KATP通道电流有关。 相似文献
16.
四磨汤对大鼠胃窦平滑肌影响及其机制的研究 总被引:1,自引:0,他引:1
临床证实四磨汤可改善胃肠动力障碍疾病的症状。但机制不明。目的:研究四磨汤对大鼠离体胃窦平滑肌收缩活动的影响及其机制。方法:处死Sprague-Dawlev大鼠后收集胃窦纵行和环行平滑肌条,检测不同剂量四磨汤(1μl、5μl、25μl、50μl、100μl、150μl和200μl)对胃窦平滑肌收缩的影响,同时观察M受体阻断剂阿托品(100mol/L)、M受体激动剂乙酰胆碱(10-6mol/L)对四磨汤诱导的胃窦平滑肌收缩的影响。结果:低一中剂量(1~100μl)四磨汤剂量依赖性地诱导大鼠胃窦纵行肌和环行肌收缩增强,但两者之间的作用无明显差异。阿托品可完全阻断四磨汤对胃窦环行肌、纵行肌的促收缩作用,且对环行肌的阻断效应更明显。以乙酰胆碱预处理后,四磨汤对胃窦纵行肌和环行肌的促收缩作用进一步增强.且对环行肌的作用更明显。结论:四磨汤对大鼠胃窦纵行肌和环行肌具有明显的促收缩作用.该作用主要通过M受体介导。 相似文献
17.
Effect of pinaverium bromide on stress-induced colonic smooth muscle contractility disorder in rats 总被引:7,自引:0,他引:7
AIM: To investigate the effect of pinaverium bromide, a L-type calcium channel blocker with selectivity for the gastrointestinal tract on contractile activity of colonic circular smooth muscle in normal or cold-restraint stressed rats and its possible mechanism. METHODS: Cold-restraint stress was conducted on rats to increase fecal pellets output. Each isolated colonic circular muscle strip was suspended in a tissue chamber containing warm oxygenated Tyrode-Ringer solution. The contractile response to ACh or KCl was measured isometrically on ink-writing recorder. Incubated muscle in different concentrations of pinaverium and the effects of pinaverium were investigated on ACh or KCl-induced contraction. Colon smooth muscle cells were cultured from rats and (Ca(2+))(i) was measured in cell suspension using the Ca(2+) fluorescent dye fura-2/AM. RESULTS: During stress, rats fecal pellet output increased 61 % (P<0.01). Stimulated with ACh or KCl, the muscle contractility was higher in stress than that in control. Pinaverium inhibited the increment of (Ca(2+))(i) and the muscle contraction in response to ACh or KCl in a dose dependent manner. A significant inhibition of pinaverium to ACh or KCl induced (Ca(2+))(i) increment was observed at 10(-6) mol/L. The IC(50) values for inhibition of ACh induced contraction for the stress and control group were 1.66X10(-6) mol/L and 0.91X10(-6) mol/L, respectively. The IC(50) values for inhibition of KCl induced contraction for the stress and control group were 8.13X10(-7) mol/L and 3.80X10(-7) mol/L, respectively. CONCLUSION: Increase in (Ca(2+))(i) of smooth muscle cells is directly related to the generation of contraction force in colon. L-type Ca(2+) channels represent the main route of Ca(2+) entry. Pinaverium inhibits the calcium influx through L-type channels; decreases the contractile response to many kinds of agonists and regulates the stress-induced colon hypermotility. 相似文献
18.
We investigated the relaxant effects of forskolin, a diterpene derivative isolated from the roots of Coleus forskohlii, on guinea pig airway smooth muscle by measuring the isometric tension of tracheal smooth muscle in vitro and transcutaneous Po2 during the histamine inhalation test (HIT) in vivo. Forskolin (10(-9)-10(-5) M) caused dose-dependent relaxant effects on resting tone and on leukotriene C4 (10(-7) M)-, leukotriene D4 (10(-7) M)-, and carbachol (3 X 10(-6) M)-induced contraction of tracheal smooth muscle. Moreover, with propranolol pretreatment the relaxant effect of forskolin on tracheal smooth muscle did not change, whereas with the same pretreatment the relaxant effect of isoproterenol diminished. Forskolin (10(-8)-10(-6) M) raised tissue cyclic AMP levels dose-dependently in tracheal smooth muscle (6.7-359.9 pmol/mg protein). Forskolin (1 mg/kg) administered subcutaneously raised the respiratory threshold of (RT-histamine in the HIT. The determination of the RT-histamine by measuring tcPo2 was possible without anesthesia. These results suggest that forskolin relaxes airway smooth muscle in guinea pigs in vitro and in vivo by raising tissue cyclic AMP levels and that its actions are independent of beta-adrenoceptors. 相似文献
19.
一氧化氮在四磨汤诱导大鼠胃窦平滑肌收缩中的作用 总被引:1,自引:0,他引:1
背景:临床实践显示四磨汤具有全胃肠促动力效应。鉴于一氧化氮(NO)在胃肠神经介导胃肠平滑肌松弛中起重要中介作用,推测其可能参与了四磨汤对胃窦平滑肌收缩的调节。目的:研究NO在四磨汤诱导大鼠胃窦平滑肌收缩中的作用。方法:分别以梯度剂量(1~200μL)四磨汤和10-4mol/L NO供体左旋精氨酸(L-Arg)+梯度剂量(1~200μL)四磨汤作用于大鼠离体胃窦纵肌条和环肌条,记录肌条基础状态和给药后收缩活动。结果:四磨汤能剂量依赖性地促进胃窦纵肌条和环肌条收缩(P=0.000)。经L-Arg预处理的胃窦纵、环肌条加入梯度剂量四磨汤后,肌条收缩活性量效曲线较单用四磨汤显著下移(L-Arg+5~200μL四磨汤对单用5~200μL四磨汤,P均〈0.05),表明NO可部分阻断四磨汤对胃窦平滑肌的兴奋效应。经L-Arg+低中剂量(1~50μL)四磨汤作用的环肌条,收缩活性增幅显著低于纵肌条(P均〈0.05)。结论:四磨汤对大鼠胃窦平滑肌具有明显促收缩作用,该作用部分是通过抑制NO释放实现的。四磨汤对胃窦环肌的兴奋效应较纵肌更多依赖于抑制NO释放。 相似文献