磁处理党参药液对小肠平滑肌收缩活动影响的研究

目的 :探讨磁处理党参药液对离体兔小肠平滑肌收缩活动的影响。方法 :通过正常台氏液对照组与磁处理党参药液实验组 ,以及磁处理党参药液组与非磁处理党参药液组进行比较 ,观察对离体兔小肠平滑肌的作用 ,同时观察药液对氯化钡引起离体兔小肠平滑肌收缩活动的影响。结果 :低浓度 ( 5 %、1 0 %、2 0 % )磁处理党参药液对离体兔小肠有轻度抑制作用 ;浓度加大 ( 4 0 %、60 % ) ,有明显促进作用 (P <0 .0 1 ) ;当浓度为 1 0 0 % ,药液有强烈的抑制作用 ,波形几乎呈直线。磁处理药液能解除Bacl2 引起的痉挛性收缩。磁处理与非磁处理党参药液组比较 ,只有浓度 5 %的波幅明显下降 (P <0 .0 1 ) ,其余浓度均无差异显著 (P>0 .0 5 ) ;结论 :磁处理党参药液对小肠平滑肌的收缩活动有明显影响     

哌替啶对肠道平滑肌运动的抑制作用及其机制

目的：研究哌替啶对肠道平滑肌运动的影响及其作用机制。方法：制备家兔离体小肠,记录小肠平滑肌张力,观察哌替啶对肠肌运动的影响。并进一步测定哌替啶灌胃前后小鼠小肠推进运动的变化。结果：在不同浓度的哌替啶作用下家兔离体肠肌收缩活动减弱：哌替啶灌胃后小鼠小肠推进减慢。哌替啶对离体肠肌的抑制作用不能被纳洛酮所阻断。结论：哌替啶对肠肌运动有抑制作用,其肠道作用可能与阿片受体无关。     

化学药物对家兔离体小肠平滑肌电生理特性的影响

观察各种化学药物对家兔离体小肠各段平滑肌的作用,采用常规离体灌流的十二指肠、空肠及回肠平滑肌标本作舒缩运动实验,记录用药前后各段小肠平滑肌的收缩活动特征及变化规律.结果显示：不同浓度的乙酰胆碱和磷酸组织胺能增强小肠各段平滑肌的收缩频率与幅度,其幅值变化与用药前有显著性差异（P＜0.01） ,并呈剂量依赖性;而不同浓度的肾上腺素和阿托品则抑制小肠各段平滑肌（P＜0.01） .不同肠段对各种化学药物的作用存在着差异,一般十二指肠作用最强,空肠次之,回肠最差.     

氢溴酸高乌甲素对小肠平滑肌运动的作用

目的：研究氢溴酸高乌甲素对小肠平滑肌运动的影响并探讨其可能的作用机制。方法：记录氢溴酸高乌甲素对家兔离体小肠平滑肌运动的影响,并测定氢溴酸高乌甲素处理后小鼠小肠推进运动的变化。结果：氢溴酸高乌甲素抑制家兔离体小肠平滑肌收缩的发展张力。纳洛酮对氢溴酸高乌甲素的肠肌抑制作用无明显影响（P〉0.05）。乙酰胆碱（0.1 mg/L）可使家兔小肠舒张末张力明显增加。氢溴酸高乌甲素处理后,乙酰胆碱对肠肌舒张末张力的增加百分比降低（P〈0.05）。氢溴酸高乌甲素对小鼠小肠推进运动有显著抑制作用（P〈0.05）。结论：氢溴酸高乌甲素对小肠平滑肌收缩有抑制作用,并可以部分阻断乙酰胆碱的肠肌收缩作用,阿片受体可能不参与该抑制作用。     

磁处理白术药液对消化功能影响的药效研究

目的 :研究磁处理白术药液对消化功能影响的药效作用。方法 :用碳末法比较生理盐水、磁处理白术药液与非磁处理白术药液对小鼠肠推进运动的影响 ;用对比法 ,比较磁处理白术药液与正常台氏液及与非磁处理白术药液对离体兔小肠平滑肌收缩运动的影响。结果 :小鼠肠碳末推进率 :与生理盐水组比较 ,磁处理白术药液有促进作用 (p <0 .0 1 ) ,磁处理白术药液与非磁处理白术药液相比差异不显著 ;离体兔小肠平滑肌收缩运动 :与正常台氏液相比 ,磁处理白术药液有促进作用 (p <0 .0 1 ) ,磁处理白术药液与非磁处理白术药液相比 ,有抑制作用。结论 :磁处理白术药液对小鼠肠推进运动功能及对离体兔小肠平滑肌收缩运动有明显作用。     

小檗碱对平滑肌肌球蛋白功能及胃肠平滑肌收缩性的影响

目的:探讨小檗碱对平滑肌肌球蛋白功能及胃肠平滑肌收缩性的影响.方法:以平滑肌肌球蛋白Mg2+-ATPase活性、肌球蛋白磷酸化以及胃与肠道平滑肌的收缩振幅为指标,考察小檗碱对平滑肌肌球蛋白Mg2+-ATPase活性和肌球蛋白磷酸化程度的影响,及其对离体小肠与胃平滑肌条收缩性的影响.结果:(1)在肌球蛋白轻链的Ca2+依赖性磷酸化反应中.小檗碱能抑制磷酸化肌球蛋白Mg2+-ATPase活性;(2)在肌球蛋白轻链的Ca2+依赖性磷酸化反应中,小檗碱可显著抑制磷酸化肌球蛋白轻链磷酸化程度;(3)小檗碱对大鼠离体小肠及胃平滑肌条收缩性均具有抑制作用.且均呈剂量依赖性.结论:小檗碱可通过抑制平滑肌肌球蛋白的功能,抑制胃肠道平滑肌的收缩性.     

不同浓度的磁处理山药药液对小肠平滑肌收缩活动的影响

目的 :探讨磁处理山药药液对离体兔小肠平滑肌收缩活动的影响。方法 :用正常台氏液对照组与不同浓度的磁处理山药药液试验组 ,以及用不同浓度的磁处理山药药液组与非磁处理山药药液组的波幅和波频进行比较 ,观察对离体兔小肠平滑肌的作用。结果 :低浓度 ( 5 %、1 0 %、2 0 % )磁处理山药药液对收缩活动有轻度抑制作用 ,波幅值下降 ,均达差异显著性 ;浓度加大 ( 4 0 %、60 % )收缩力增强 ,波幅值上升 (P<0 .0 1 ) ;当浓度增至 1 0 0 %时 ,则有明显的抑制作用 ,波幅值下降 (P <0 .0 1 )。而波频变化除 5 %、1 0 %以外 ,均达差异极显著。磁处理与非磁处理山药药液组比较 ,波幅 ( 2 0 %、60 % )、波频 ( 5 %、1 0 %、60 % )均有差异显著性。结论 :磁处理山药药液对小肠平滑肌收缩活动有明显效应。     

磁处理冬虫夏草精粉药液对消化功能影响的药效研究

目的：研究磁处理冬虫夏草精粉药液对消化功能影响的药效作用。方法：用对比法,比较磁处理冬虫夏草精粉药液与正常台氏液对离体兔小肠平滑肌收缩运动的影响;用碳末法比较生理盐水与磁处理冬虫夏草精粉药液对小鼠肠推进运动的影响。结果：离体兔小肠平滑肌收缩运动：与正常台氏液相比,磁处理冬虫夏草精粉药液（20％、60％）有促进作用（p〈0．01、p〈0．05）;小鼠肠碳末推进率：与生理盐水组比较,磁处理冬虫夏草精粉药液未见明显的作用（p〉0．05）。结论：磁处理冬虫夏草精粉药液对离体免小肠平滑肌收缩运动有明显作用,对小鼠肠推进运动功能未见明显的作用。     

NaOH、HCl、BaCl_2对家兔小肠段平滑肌收缩的影响

平滑肌对一些酸碱等化学物质较为敏感,其可能会影响小肠的肌电活动,进而影响小肠的运动。本研究试图探讨氢氧化钠(Na OH)、盐酸(HCl)、氯化钡(Ba Cl_2)对离体家兔小肠段平滑肌收缩功能的影响,以期了解不同化学药物对小肠肌电活动的影响,为肠道疾病的诊断和治疗提供参考。本研究选取健康家兔,处死后取家兔的十二指肠、空肠、回肠离体后进行恒温灌流,分别给予1 mol/L的Na OH溶液、1 mol/LHCl溶液、1 mol/L Ba Cl_2溶液,并选择相对应肠段作为对照组,仅给予等量生理盐水恒温灌流,对比各组小肠平滑肌电活动变化。研究表明,Ba Cl_2干预下,十二指肠、空肠、回肠的收缩频率均高于对照组、Na OH组、HCl组,差异均具有统计学意义(p0.05);Ba Cl_2组、Na OH组、HCl组离体家兔小肠平滑肌的最大振幅均显著的高于对照组(p0.05),Ba Cl_2组离体家兔小肠平滑肌的最大振幅均显著的高于Na OH组、HCl组(p0.05);Ba Cl_2组、Na OH组离体家兔小肠平滑肌的负波最大振幅均显著的高于对照组、HCl组(p0.05),Ba Cl_2组离体家兔小肠平滑肌的负波最大振幅均显著的高于Na OH组(p0.05)。我们的研究初步表明:Ba Cl_2能显著的增强离体家兔小肠段平滑肌收缩功能,Na OH和HCl溶液会增强体家兔小肠平滑肌的最大振幅。研究显示Ba Cl_2的作用机制可能是促使平滑肌强直性收缩,而Na OH和HCl酸碱类物质的刺激可使肠壁内神经元兴奋,促进小肠平滑肌的运动。     

三七总皂苷对家兔离体小肠平滑肌自发收缩活动的影响

目的：观察三七总皂苷对家兔离体小肠平滑肌收缩活动的影响,并探讨其作用机制。方法：取健康家兔,雌雄不拘,将小肠离体后恒温灌流,观察三七总皂苷对家兔小肠自发收缩活动的影响;在灌流液中分别加入BayK8644、左旋硝基精氨酸甲酯（L-NAME）后再加入三七总皂苷,研究其作用机制;在无钙台式液中加入rynodine后再加入三七总皂苷,研究其作用机制。结果：三七总皂苷剂量依赖性的抑制家兔离体小肠平滑肌收缩的幅度。BayK8644和L-NAME均可完全阻断三七总皂苷对家兔小肠平滑肌收缩活动的抑制作用。在无钙台式液中,三七总皂苷显著抑制rynodine引起的细胞内钙收缩活动。结论：三七总皂苷显著抑制家兔小肠平滑肌的收缩活动,其抑制收缩活动机制可能是：增加小肠平滑肌NO浓度,从而抑制细胞外钙内流和内钙释放。     

Effect of lignocaine on intestinal smooth muscle of rat ileum

The effect of lignocaine on tone and contractility of intestinal smooth muscle, and on contractures produced by ACh or TEA, was studied in isolated ileum of the rat. Lignocaine (0.1-100 microM) produced concentration-dependent contractures in the rat ileum. In low concentrations, lignocaine increased the amplitude of spontaneous contractions and contractions produced by transmural stimulation. High concentrations of lignocaine abolished all contractile responses and produced a marked contracture in rat ileum. Lignocaine (10 microM) also reduced the contractures produced by ACh (0.01-10 microM). In contrast, the contractures produced by TEA (0.1-10 mM) were markedly increased by lignocaine. Furthermore, the contracture produced by lignocaine was reduced by lowering the external calcium from 2.5 mM to 1.5 mM. It was concluded that lignocaine in moderate and high concentrations produces a contracture in rat intestinal smooth muscle. Whereas lignocaine reduces the ACh-induced contracture, it increases that produced by TEA in the same preparation. The results further suggest that lignocaine modifies cholinergic responses and affects excitation-contraction coupling in rat intestinal smooth muscle.     

Effects of Ginkgo biloba extract on the proliferation of vascular smooth muscle cells in vitro and on intimal thickening and interleukin-1beta expression after balloon injury in cholesterol-fed rabbits in vivo

Restenosis may develop in response to cytokine activation and smooth muscle cell proliferation. Ginkgo biloba extract (EGb) has been used to treat cardiovascular and cerebrovascular diseases. In the present study, the effects of EGb on the growth of cultured vascular smooth muscle cells (VSMC), as well as on the expression of interleukin-1beta (IL-1beta) and the intimal response in balloon-injured arteries of cholesterol-fed rabbits, were investigated. Using bromodeoxyuridine incorporation as an index of cell proliferation, EGb was found to inhibit serum-induced mitogenesis of cultured rat aorta VSMC in a dose-dependent manner. In vivo, EGb and probucol ( positive control) reduced the atheroma area in thoracic aortas of male New Zealand white rabbits fed a 2% cholesterol diet for 6 weeks with balloon denudation of the abdominal aorta being performed at the end of the third week. Intimal hyperplasia, expressed as the intimal/medial area ratio, in the abdominal aortas was significantly inhibited in the both the EGb group (0.61 +/- 0.06) and the probucol group (0.55 +/- 0.03) compared to the C group (0.87 +/- 0.02). In the balloon-injured abdominal aorta, both EGb and probucol significantly reduced IL-1beta mRNA and protein expression and the percentage of proliferating cells. The inhibitory effects of EGb on the intimal response might be attributed to its antioxidant capacity. EGb may have therapeutic potential for the prevention of restenosis after angioplasty.     

Intestinal inflammation downregulates smooth muscle CPI-17 through induction of TNF-alpha and causes motility disorders

Motility disorders are frequently observed in intestinal inflammation. We previously reported that in vitro treatment of intestinal smooth muscle tissue with IL-1beta decreases the expression of CPI-17, an endogenous inhibitory protein of smooth muscle serine/threonine protein phosphatase, thereby inhibiting contraction. The present study was performed to examine the pathophysiological importance of CPI-17 expression in the motility disorders by using an in vivo model of intestinal inflammation and to define the regulatory mechanism of CPI-17 expression by proinflammatory cytokines. After the induction of acute ileitis with 2,4,6,-trinitrobenzensulfonic acid, CPI-17 expression declined in a time-dependent manner. This decrease in CPI-17 expression was parallel with the reduction of cholinergic agonist-induced contraction of smooth muscle strips and sensitivity of permeabilized smooth muscle fibers to Ca(2+). Among the various proinflammatory cytokines tested, TNF-alpha and IL-1beta were observed to directly inhibit CPI-17 expression and contraction in cultured rat intestinal tissue. Moreover, both TNF-alpha and IL-1beta inhibited CPI-17 expression and contraction of smooth muscle tissue isolated from wild-type and IL-1alpha/beta double-knockout mice. However, IL-1beta treatment failed to inhibit CPI-17 expression and contraction in TNF-alpha knockout mice. In beta-escin-permeabilized ileal tissues, pretreatment with anti-phosphorylated CPI-17 antibody inhibited the carbachol-induced Ca(2+) sensitization in the presence of GTP. These findings suggest that CPI-17 was downregulated during intestinal inflammation and that TNF-alpha plays a central role in this process. Downregulation of CPI-17 may play a role in motility impairments in inflammation.     

Heterogeneity of desmin, the muscle-type intermediate filament protein, in blood vessels and astrocytes

Monoclonal antibodies were isolated from mice immunized with chicken gizzard desmin. Antibodies reacting with desmin on immunoblots and selectively decorating chicken and rat intestinal smooth muscle as well as the Z-line in striated muscle, were selected for this study. Based on their staining pattern on cryostat sections of chicken and rat cerebellum, spleen, kidney, aorta and femoral artery, monoclonal supernatants could be divided in three groups: (i) antibodies decorating astrocytes and vascular smooth muscle; (ii) antibodies decorating only vascular smooth muscle; (iii) antibodies decorating only astrocytes. Antibodies in group (i) and (iii) also stained GFA-negative Bergmann glia in chicken cerebellum. It is proposed that desmin may vary depending on the histological localization.     

SWI/SNF complexes containing Brahma or Brahma-related gene 1 play distinct roles in smooth muscle development

SWI/SNF ATP-dependent chromatin-remodeling complexes containing either Brahma-related gene 1 (Brg1) or Brahma (Brm) play important roles in mammalian development. In this study we examined the roles of Brg1 and Brm in smooth muscle development, in vivo, through generation and analysis of mice harboring a smooth muscle-specific knockout of Brg1 on wild-type and Brm null backgrounds. Knockout of Brg1 from smooth muscle in Brg1(flox/flox) mice expressing Cre recombinase under the control of the smooth muscle myosin heavy-chain promoter resulted in cardiopulmonary defects, including patent ductus arteriosus, in 30 to 40% of the mice. Surviving knockout mice exhibited decreased expression of smooth muscle-specific contractile proteins in the gastrointestinal tract, impaired contractility, shortened intestines, disorganized smooth muscle cells, and an increase in apoptosis of intestinal smooth muscle cells. Although Brm knockout mice had normal intestinal structure and function, knockout of Brg1 on a Brm null background exacerbated the effects of knockout of Brg1 alone, resulting in an increase in neonatal lethality. These data show that Brg1 and Brm play critical roles in regulating development of smooth muscle and that Brg1 has specific functions within vascular and gastrointestinal smooth muscle that cannot be performed by Brm.     

Smooth muscle overexpression of IGF-I induces a novel adaptive response to small bowel resection

Prior studies of intestinal adaptation after massive small bowel resection (SBR) have focused on growth factors and their effects on amplification of the gut mucosa. Because adaptive changes have also been described in intestinal smooth muscle, we sought to determine the effect of targeted smooth muscle growth factor overexpression on resection-induced intestinal adaptation. Male transgenic mice with smooth muscle cell overexpression of insulin-like growth factor I (IGF-I) by virtue of an alpha-smooth muscle actin promoter were obtained. SMP8 IGF-I transgenic (IGF-I TG) and nontransgenic (NT) littermates underwent 50% proximal SBR or sham operation and were then killed after 3 or 28 days. NT mice showed the expected alterations in mucosal adaptive parameters after SBR, such as increased wet weight and villus height. The IGF-I TG mice had inherently taller villi, which did not increase significantly after SBR. In addition, IGF-I TG mice had a 50% postresection persistent increase in remnant intestinal length, which was associated with an early decline and later increase in relative mucosal surface area. These results indicate that growth factor overexpression within the muscularis layer of the bowel wall induces significant postresection adaptive intestinal lengthening and a unique mucosal response. IGF-I signaling within the muscle wall may play an important role in the pathogenesis of resection-induced adaptation.     

Smooth muscle NOS, colocalized with caveolin-1, modulates contraction in mouse small intestine

Neuronal nitric oxide synthase (nNOS) in myenteric neurons is activated during peristalsis to produce nitric oxide which relaxes intestinal smooth muscle. A putative nNOS is also found in the membrane of intestinal smooth muscle cells in mouse and dog. In this study we studied the possible functions of this nNOS expressed in mouse small intestinal smooth muscle colocalized with caveolin-1(Cav-1). Cav-1 knockout mice lacked nNOS in smooth muscle and provided control tissues. 60 mM KCl was used to increase intracellular [Ca(2+)] through L-type Ca(2+) channel opening and stimulate smooth muscle NOS activity in intestinal tissue segments. An additional contractile response to LNNA (100 muM, NOS inhibitor) was observed in KCl-contracted tissues from control mice and was almost absent in tissues from Cav-1 knockout mice. Disruption of caveolae with 40 mM methyl-beta cyclodextrin in tissues from control mice led to the loss of Cav-1 and nNOS immunoreactivity from smooth muscle as shown by immunohistochemistry and a reduction in the response of these tissues to N-omega-nitro-L-arginine (LNNA). Reconstitution of membrane cholesterol using water soluble cholesterol in the depleted segments restored the immunoreactivity and the response to LNNA added after KCl. Nicardipine (1 muM) blocked the responses to KCl and LNNA confirming the role of L-type Ca(2+) channels. ODQ (1 muM, soluble guanylate cyclase inhibitor) had the same effect as inhibition of NOS following KCl. We conclude that the activation of nNOS, localized in smooth muscle caveolae, by calcium entering through L-type calcium channels triggers nitric oxide production which modulates muscle contraction by a cGMP-dependent mechanism.     

纳豆枯草杆菌培养滤液对家兔离体肠平滑肌的作用

目的观察纳豆枯草杆菌培养滤液（culture filtrate,CF）对家兔离体肠平滑肌的作用,并初步探讨其作用机制。方法制备兔离体回肠标本,分别记录肠平滑肌的正常收缩张力和收缩频率作为给药前对照,然后按累积剂量分别加入CF小剂量（每次0．2mL）、CF大剂量（每次0．5mL）、肉汤（每次0．5mL）,给药间隔3min,共给药8次,并描记收缩曲线。观察不同剂量cF对肠平滑肌的作用。另取肠段按毛果芸香碱、CF或阿托品、再毛果芸香碱的顺序给药,观察CF对M胆碱受体的作用。结果CF小剂量组在累积给药达1．6mL时,CF大剂量组在累积给药达3．5mL和4．0mL时,兔离体肠平滑肌收缩张力下降,与给药前比较差异有统计学意义（P〈0．05）,其余各点差异均无统计学意义（P〉0．05）。CF小剂量组在累积给药达1．2、1．4、1．6mL时,CF大剂量组在累积给药达4．0mL时,兔离体肠平滑肌收缩频率明显降低,与给药前比较差异有统计学意义（P〈0．05或P〈0．01）,其余各点差异均无统计学意义（P〉0．05）。CF或阿托品可明显对抗毛果芸香碱引起的兔离体肠平滑肌收缩张力的增加（P〈0．05或P〈0．01）,同时CF还能使其收缩频率明显减少（P〈0．01）。结论纳豆枯草杆菌CF能明显抑制兔离体肠平滑肌蠕动,其作用机制可能与阻断M胆碱受体有关。     

Dependence of IL-4, IL-13, and nematode-induced alterations in murine small intestinal smooth muscle contractility on Stat6 and enteric nerves

IL-4 and IL-13 promote gastrointestinal worm expulsion in part through effects on nonlymphoid cells, such as intestinal smooth muscle cells. The roles of Stat6 in IL-4-, IL-13-, and parasitic nematode-induced effects on small intestinal smooth muscle contractility were investigated in BALB/c wild-type and Stat6-deficient mice treated with a long-lasting formulation of recombinant mouse IL-4 (IL-4C) or IL-13 for 7 days. Separate groups of BALB/c mice were infected with Nippostrongylus brasiliensis or were drug-cured of an initial Heligmosomoides polygyrus infection and later reinfected. Infected mice were studied 9 and 12 days after inoculation, respectively. Segments of jejunum were suspended in an organ bath, and responses to nerve stimulation and to acetylcholine and substance P in the presence and absence of tetradotoxin, a neurotoxin, were determined. Both IL-4 and IL-13 increased smooth muscle responses to nerve stimulation in wild-type mice, but the effects were greater in IL-13-treated mice and were absent in IL-13-treated Stat6-deficient mice. Similarly, hypercontractile responses to nerve stimulation in H. polygyrus- and N. brasiliensis-infected mice were dependent in part on Stat6. IL-13, H. polygyrus, and N. brasiliensis, but not IL-4, also increased contractility to acetylcholine by mechanisms that involved Stat6 and enteric nerves. These studies demonstrate that both IL-4 and IL-13 promote intestinal smooth muscle contractility, but by different mechanisms. Differences in these effects correlate with differences in the relative importance of these cytokines in the expulsion of enteric nematode parasites.     

葛根素对小鼠的通便作用及其机制研究

目的:研究葛根素对便秘小鼠的通便作用,探讨其通便机制。方法:采用复方地芬诺酯制造小鼠便秘模型,观察葛根素对便秘模型小鼠的首次排便时间,12h内排便粒数,粪便性状及重量的影响;采用肠段称重法,观察葛根素对大肠水分吸收的影响;采用PowerLab信号处理系统,观察葛根素对大肠平滑肌活动的影响。结果:①三个剂量组与便秘模型组相比,小鼠首次排便时间明显缩短(P<0.05),12h内粪便粒数、重量明显增加(P<0.05),并呈剂量效应。②低、中剂量组与便秘模型组相比,大肠含水量明显增加(P<0.05),高剂量组以上指标不但明显高于便秘模型组(P<0.05),而且明显高于空白对照组(P<0.05)。③与单纯给予复方地芬诺酯相比,葛根素进一步降低了小鼠大肠平滑肌收缩幅度、频率和曲线下面积,具有显著差异性(P<0.05)。结论:葛根素具有通便作用,其机制可能是葛根素增加肠道水分促肠运动的作用大于它对肠道运动的直接抑制作用。