牛磺酸对前列腺素E2兴奋大鼠胃底平滑肌作用的影响

目的：观察了牛磺酸对大鼠胃底平滑肌收缩性的影响。方法：采用离体平滑肌实验技术观察胃底条收缩作用。结果：牛磺酸使前列腺素Ｅ２（ＰＧＥ２）累加量效曲线明显降低。结论：牛磺酸能对抗;ＰＧＥ２兴奋大鼠胃底平滑肌作用。     

大鼠胃底平滑肌细胞5-HT受体的信号转导通路的研究

目的　以 5 HT引起胞内Ca2 + 变化为指标 ,研究大鼠胃底平滑肌细胞 5 HT受体的信号转导机制。方法　采用Ca2 + 指示剂Fluo - 3/AM负载培养的胃底平滑肌细胞 (SF SMC) ,共聚焦显微术检测细胞内钙荧光强度的变化。结果　基础状态下SFSMC[Ca2 + ]i 荧光强度 (fluorescenceintensi ty ,FI)为 2 6 4± 1 5 ,5 HT 10 μmol·L-1使荧光强度缓慢升高 ;这一作用与细胞外钙内流和内钙释放有关 ;10 μmol·L-1米安舍林 (mianserin)可部分拮抗 5 HT升高 [Ca2 + ]i 的作用 ,钙拮抗剂拉西地平 (lacidipine)、G蛋白拮抗剂NEM均能完全抑制 5 HT升高 [Ca2 + ]i 的作用 ;5 HT引起 [Ca2 + ]i的升高被PLC抑制剂部分地取消 ;PKC激动剂拮抗了 5 HT引起的钙动员 ,而PKC特异性抑制剂D 鞘氨醇取消了这一抑制作用。结论　 5 HT部分通过激动了胃底平滑肌细胞的G 蛋白偶联的 5 HT2B受体引起细胞去极化 ,从而激发L型钙通道使外Ca2 + 内流 ,并促进SR上的ryanodine受体的开放 ,引起 [Ca2 + ]i 升高。而这一升高 [Ca2 + ]i 的作用又受到PLC和PKC的调控     

二氢吡啶类钙拮抗剂对抗5-HT引起的胃底平滑肌细胞的增殖及其机制

目的　通过对大鼠胃底平滑肌细胞 (SFSMCs)的研究 ,揭示二氢吡啶类钙拮抗剂对抗 5 HT促增殖作用的机制。方法　采用MTT法、免疫组化法及PKC活性测定观察在二氢吡啶类钙拮抗剂Mn92 0 2及lacidipine作用下 ,培养的大鼠胃底平滑肌细胞对 5 HT引起的增殖活性的变化及增殖信号的变化。结果　 5 HT(1 μmol·L- 1 )具有明显的促大鼠SFSMCs增殖作用 ,并促进MAPK和PKC活性的增加 ,高剂量 (1 μmol·L- 1 )的钙拮抗剂Mn92 0 2和lacidipine能够有效地抑制大鼠胃底平滑肌细胞的生长 ,同时也抑制MAPK的表达以及PKC由胞质向胞膜的转移。结论　二氢吡啶类钙拮抗剂的这一抗增殖作用 ,除与其阻断 5 HT引起的Ca2 + 内流有关 ,还可能干预 5 HT与细胞膜上的 5 HT2B受体结合 ,从而阻断了增殖信号的传递。     

大鼠胃平滑肌细胞收缩模型及其药物研究

目的 建立胃平滑肌收缩的实验模型并且对相应治疗药物的作用进行评价。方法 采用分离大鼠胃底平滑肌,用胶原酶和胰蛋白酶进行消化培养,得到离体平滑肌细胞悬液。用Trypan blue稀释法检查,通过带刻度显微镜观察和标测细胞的形态和长度,并观察在不同的时间范围内细胞形态和长度的变化情况,计算细胞存活率和存活时间。于细胞悬液加入各种神经介质乙酰胆碱(ACh)、5-羟色胺(5-HT、组织胺(His)引起刺激反应,同时加入其相应的拮抗剂阿托品(atropine)、多潘立酮(Domp)、苯海拉明(Diph)时,观察细胞形态和长度的前后变化,从而对模型和药物的作用进行评价。结果 每只大鼠胃底均能收获1×10~6以上个细胞,细胞存活率在95％以上,细胞至少可存活2.5 h。ACh能引起胃平滑肌细胞的收缩,具有明显的量效关系,1×10~(-8)mol·L~(-1)即可产生最大收缩反应(38.0％)。atropine对乙酰胆碱的拮抗作用有明显的量效关系。5-HT对大鼠胃底平滑肌细胞具有明显的收缩作用,井有明显的量效关系。Domp能够拮抗5-HT的细胞收缩作用,并具有一定的量效关系。5-HT的量效曲线比较平坦,可能至少有2种受体参与细胞的收缩作用,它们引起细胞收缩的最大效应分别为20.7％和10.5％。His引起的平滑肌细胞收缩,在1×10~(-13)～1×10~(-10) mol·L~(-1)内有?     

肉毒中毒34例临床观察

肉毒中毒在新疆发病率较高 ,新疆自治区急救中心 1994～ 2 0 0 0年共接诊 34例患者 ,现报告如下。1　临床资料与治疗方法1 1　一般资料　 34例均为汉族 ,男 15例 ,女 19例 ;年龄 2～ 78岁。潜伏期 6ｈ～ 3周 ,发病至就诊 1ｈ～ 2 0ｄ。发病原因均为食用家制臭豆腐、豆瓣酱所致。 34例中 ,轻度中毒 13例 ,临床表现为头晕、头痛、睁眼困难、视物模糊、复视、抬头困难 ;中度中毒 4例 ,除前述症状外 ,有咽部阻塞感、张口与伸舌困难 ,语言不清、声嘶等症状。重度中毒 14例 ,除前述症状外 ,有吞咽困难、饮水呛咳。极重度中毒 3例 ,并发呼吸肌麻痹…     

组织粘合剂注射治疗胃底静脉曲张的有效护理

目的探讨内镜下组织粘合剂注射治疗肝硬化胃底静脉曲张破裂出血患者的护理。方法对35例手术患者术前进行有针对性的指导,讲解术中的配合要点,重点加强术后护理及并发症的观察。结果35例胃底静脉消失成直线,半年内无复发。结论合理有效的护理是组织粘合剂注射治疗胃底静脉曲张成功的关键。     

胃平滑肌瘤一例

胃平滑肌瘤起源于胃的平滑肌组织,主要起自胃壁肌层,极少起自粘膜肌层或血管壁肌层,约占胃肿瘤的1%。无特征性临床症状,我科曾收治一例,经术后病理检查证实为胃平滑肌瘤,现报告如下。患者男,57岁。上腹部隐痛不适8年,腹痛20天,伴恶心呕吐,于1990—03—23入     

牛磺酸对前列腺素E_2兴奋大鼠胃底平滑肌作用的影响

目的 :观察了牛磺酸对大鼠胃底平滑肌收缩性的影响。方法 :采用离体平滑肌实验技术观察胃底条收缩作用。结果 :牛磺酸能使前列腺素E2 (PGE2 )累加量效曲线明显降低。结论 :牛磺酸能对抗PGE2 兴奋大鼠胃底平滑肌作用     

胃巨大平滑肌肉瘤2例报道

<正>1病例资料例1:患者男性,78岁,因左上腹部肿块近1年入院。上腹部可触及直径约18cm的圆形肿块,表面凹凸不平,可推动。钡餐检查:胃体小弯侧有一半圆型巨大压迹,边缘不整齐,局部黏膜不规则,胃壁柔软,可触及肿物。     

胃平滑肌肿瘤的外科治疗

目的探讨胃平滑肌肿瘤诊断与外科治疗方法。方法对1995年8月~2005年6月本院收治的胃平滑肌肿瘤68例临床资料进行回顾性总结分析。结果胃平滑肌肿瘤肿块较大,大多位于胃底体区,胃平滑肌肉瘤多以出血、上腹痛、上腹包块为临床表现。胃镜、X线钡餐、CT检查有助于诊断。结论对考虑胃平滑肌肿瘤患者应积极手术治疗,术中积极进行快速冰冻切片,确定肿瘤性质,合理选择手术方式。     

中药莪术对大鼠十二指肠平滑肌收缩的影响

目的探讨中药莪术(Curcumna Rhizoma)水提液对大鼠离体十二指肠平滑肌收缩运动的影响,并初步探索其作用机制。方法制作大鼠离体十二指肠标本,用恒温灌流的方法,使用BL-420生物机能实验系统观察不同浓度莪术对大鼠离体十二指肠平滑肌的收缩效应。选适当终浓度莪术分别与阿托品、去甲肾上腺素、异丙肾上腺素、维拉帕米共同孵育,观察莪术对它们引起平滑肌收缩作用的影响;制作不同浓度新斯的明肠管收缩作用的量效曲线,与莪术组进行对比,初步探讨其可能的作用机制,并作胆碱酯酶活性测定辅助证明是否与新斯的明作用机制相似。结果莪术可以对大鼠离体十二指肠的收缩有兴奋作用,呈剂量依赖性;莪术可以部分被M受体阻断药阿托品阻断、β受体激动药异丙肾上腺素和钙通道阻滞剂维拉帕米对肠管收缩的抑制作用;对α受体激动药去甲肾上腺素无影响;与乙酰胆碱酯酶抑制剂新斯的明的作用相似。结论莪术明显促进大鼠离体十二指肠平滑肌收缩作用,呈剂量依赖性。其作用机制可能是通过抑制胆碱酯酶,与M受体介导有关,同时还可能与抑制α和β受体有关。     

Cellular Ca2+ Dynamics in Urinary Bladder Smooth Muscle From Transgenic Mice Overexpressing Na+-Ca2+ Exchanger

The rise of Ca²⁺ concentration ([Ca²⁺] _i ) by reducing external Na⁺ in urinary bladder smooth muscle cells (UBSMCs) from transgenic mice overexpressing Na⁺/Ca²⁺ exchanger type-1.3 (NCX1.3^tg/tg) was about 4 times as large as that in the wild-type (WT). NCX1 protein expression in UB increased about 4-fold in NCX1.3^tg/tg. The Ca²⁺ release by caffeine in UBSMCs was comparable between NCX1.3^tg/tg and WT, but [Ca²⁺]_i decay was faster in NCX1.3^tg/tg. Contractions induced by acetylcholine, 60 mM K⁺, or electrical stimulation were significantly smaller in UB segments of NCX1.3^tg/tg. NCX worked in Ca²⁺-extrusion mode during these contractions in UBSMCs of both WT and NCX1.3^tg/tg.     

食管胃前壁吻合加胃底重建预防反流性食管炎临床研究

目的探讨食管胃前壁吻合及胃底重建在胃底贲门癌切除术后预防反流性食管炎的价值。方法对310例胃底贲门癌患者常规经上腹正中切口行近端胃根治术后,170例行食管胃前壁吻合加胃底重建重新形成His角(A组),140例单纯行食管胃后壁吻合(B组)。术后观察临床症状和通过上消化道造影及胃镜检查来评定其抗反流效果。结果食管胃前壁吻合抗反流优良率达78%。食管胃后壁吻合抗反流优良率35%,经统计学处理二者抗反流差别有显著性意义(<0.01)。结论食管胃前壁吻合加胃底重建能有效预防反流性食管炎,是一种简便、较理想的消化道重建术式。     

水蛭素对高磷诱导的大鼠血管平滑肌细胞钙化的影响

目的 探讨水蛭素对高磷诱导的血管平滑肌细胞（vascular smooth muscle cells,VSMCs）钙化的影响及机制。方法 采用β-甘油磷酸诱导体外培养的大鼠VSMCs,建立钙化模型,加入不同浓度水蛭素进行干预,实验设置5个组：对照组、钙化组、低浓度水蛭素组、中浓度水蛭素组、高浓度水蛭素组。通过茜素红S染色及细胞内钙含量检测各组细胞钙化情况;用qRT-PCR及Western blotting检测各组细胞α-SMA、RUNX2、BMP2的mRNA和蛋白表达量及细胞内碱性磷酸酶（alkaline phosphatase,ALP）活性以测定各组细胞转分化情况。结果 与对照组比较,高磷诱导的钙化组中茜素红S染色可见明显橘红色钙化结节,钙含量检测显示细胞内钙含量明显增加（P<0.01）,细胞内ALP活性升高（P<0.01）,α-SMA的mRNA及蛋白表达量降低（P<0.01）,RUNX2、BMP2的mRNA及蛋白表达量升高（P<0.01）。与钙化组比较,水蛭素组茜素红S染色结果显示的橘红色钙化结节呈浓度依赖性减少,细胞内钙含量及ALP活性呈浓度依赖性降低（P<0.05或P<0.01）,α-SMA的mRNA及蛋白表达量呈浓度依赖性升高（P<0.05或P<0.01）,RUNX2、BMP2的mRNA及蛋白表达量呈浓度依赖性降低（P<0.05或P<0.01）。结论 水蛭素通过抑制高磷诱导大鼠VSMCs转分化来减轻VSMCs的钙化,其机制可能与上调α-SMA的表达,下调ALP活性、RUNX2及BMP2的表达有关。     

Alteration of Ryanodine-receptors in Cultured Rat Aortic Smooth Muscle Cells

Vascular smooth muscle cells can obtain a proliferative function in environments such as atherosclerosis in vivo or primary culture in vitro. Proliferation of vascular smooth muscle cells is accompanied by changes in ryanodine receptors (RyRs). In several studies, the cytosolic Ca(2+) response to caffeine is decreased during smooth muscle cell culture. Although caffeine is commonly used to investigate RyR function because it is difficult to measure Ca(2+) release from the sarcoplasmic reticulum (SR) directly, caffeine has additional off-target effects, including blocking inositol trisphosphate receptors and store-operated Ca(2+) entry. Using freshly dissociated rat aortic smooth muscle cells (RASMCs) and cultured RASMCs, we sought to provide direct evidence for the operation of RyRs through the Ca(2+)- induced Ca(2+)-release pathway by directly measuring Ca(2+) release from SR in permeabilized cells. An additional goal was to elucidate alterations of RyRs that occurred during culture. Perfusion of permeabilized, freshly dissociated RASMCs with Ca(2+) stimulated Ca(2+) release from the SR. Caffeine and ryanodine also induced Ca(2+) release from the SR in dissociated RASMCs. In contrast, ryanodine, caffeine and Ca(2+) failed to trigger Ca(2+) release in cultured RASMCs. These results are consistent with results obtained by immunocytochemistry, which showed that RyRs were expressed in dissociated RASMCs, but not in cultured RASMCs. This study is the first to demonstrate Ca(2+) release from the SR by cytosolic Ca(2+) elevation in vascular smooth muscle cells, and also supports previous studies on the alterations of RyRs in vascular smooth muscle cells associated with culture.     

Nitric Oxide-mediated Relaxation by High K in Human Gastric Longitudinal Smooth Muscle

This study was designed to elucidate high-K(+)induced response of circular and longitudinal smooth muscle from human gastric corpus using isometric contraction. Contraction from circular and longitudinal muscle stripes of gastric corpus greater curvature and lesser curvature were compared. Circular smooth muscle from corpus greater curvature showed high K(+) (50 mM)-induced tonic contraction. On the contrary, however, longitudinal smooth muscle strips showed high K(+) (50 mM)-induced sustained relaxation. To find out the reason for the discrepancy we tested several relaxation mechanisms. Protein kinase blockers like KT5720, PKA inhibitor, and KT5823, PKG inhibitor, did not affect high K(+)-induced relaxation. K(+) channel blockers like tetraethylammonium (TEA), apamin (APA), glibenclamide (Glib) and barium (Ba(2+)) also had no effect. However, N(G)-nitro-L-arginine (L-NNA) and 1H-(1,2,4) oxadiazolo (4,3-A) quinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase (sGC) and 4-AP (4-aminopyridine), voltage-dependent K(+) channel (K(V)) blocker, inhibited high K(+)-induced relaxation, hence reversing to tonic contraction. High K(+)-induced relaxation was observed in gastric corpus of human stomach, but only in the longitudinal muscles from greater curvature not lesser curvature. L-NNA, ODQ and K(V) channel blocker sensitive high K(+)-induced relaxation in longitudinal muscle of higher portion of corpus was also observed. These results suggest that longitudinal smooth muscle from greater curvature of gastric corpus produced high K(+)-induced relaxation which was activated by NO/sGC pathway and by K(V) channel dependent mechanism.     

吡格列酮和罗格列酮对脂多糖诱导大鼠血管平滑肌细胞增殖的影响

目的:观察胰岛素增敏剂——噻唑烷二酮类(TZD)药物吡格列酮和罗格列酮对脂多糖(LPS)诱导的血管平滑肌细胞(VSMCs)异常增殖的影响。方法:组织块贴壁法培养大鼠胸主动脉血管平滑肌细胞;LPS(0.1,1,10mg·L-1)干预血管平滑肌细胞不同时间(0,12,24,48,72h)后,分别用吡格列酮和罗格列酮与10mg·L-1LPS共同孵育72h,四甲基偶氮咗盐微量酶比色(MTT)法检测血管平滑肌细胞增殖。结果:10mg·L-1LPS孵育72h导致血管平滑肌细胞增殖程度最明显(P<0.01);吡格列酮和罗格列酮可明显抑制LPS诱导的血管平滑肌细胞增殖。结论:噻唑烷二酮类代表药吡格列酮和罗格列酮均对LPS诱导的血管平滑肌细胞异常增殖具有抑制作用,该类药物可能在治疗心血管疾病方面有较好的应用前景。     

罗氟司特和齐留通对哮喘大鼠气道平滑肌收缩功能的影响

目的 通过观察磷酸二酯酶4抑制剂罗氟司特和5-脂氧酶抑制剂齐留通对哮喘气道平滑肌收缩功能的影响,探讨罗氟司特和齐留通对气道平滑肌的药理作用。方法 取正常及哮喘大鼠的气道平滑肌条,采用乙酰胆碱（acetylcholine,Ach）梯度累积给药进行肌条收缩功能研究,并进行罗氟司特或齐留通梯度累积给药的肌条舒张功能研究,同时设置药物预孵处理,利用张力换能器和计算机生物信号采集系统观察和记录各种方式处理下其收缩功能的变化。结果 采用累积剂量给药法加入收缩剂Ach（10^-8~10^-3 mol·L^-1）后,正常大鼠和哮喘模型大鼠气道平滑肌收缩无显著性差异。由Ach诱发平滑肌条收缩达到最大程度,采用累积剂量给药法加入罗氟司特或齐留通（10^-8~10^-3 mol·L^-1）后,哮喘大鼠气道平滑肌对罗氟司特的敏感性高于正常大鼠,而对齐留通的敏感性低于正常大鼠。使用罗氟司特预孵,并采用累积给药法加入收缩剂Ach（10^-8~10^-3 mol·L^-1）,哮喘大鼠气道平滑肌和正常大鼠对Ach的反应性无明显差异,而齐留通预孵后,累积给药法加入Ach（10^-8~10^-3 mol·L^-1）,哮喘大鼠平滑肌对Ach的反应性明显高于正常健康大鼠。结论 罗氟司特能抑制哮喘气道平滑肌的收缩功能,同时不诱导气道的高反应性,而齐留通对哮喘气道平滑肌的收缩抑制作用不明显,且可能诱导气道高反应性。     

Isolation and Inhibitory Effects of Eupatilin,a Flavone Isolated from Artemisia monosperma Del., on Rat Isolated Smooth Muscle

The isolation for the first time from Artemisia monosperma (Compositae) of the known flavone eupatilin and its effects on rat isolated smooth muscle preparations are described. In concentrations from 10 -7 M to 3×10 -4 M, eupatilin (5, 7-dihydroxy-6, 3', 4'-trimethoxyflavone) inhibited in a reversible manner the phasic contractions and the tone of rat isolated ileum, uterus, and urinary bladder. It relaxed the tonic contractions of the phenylephrine-precontracted pulmonary artery and acetylcholine-precontracted trachea. Eupatilin also shifted the concentration-effect curves of acetylcholine and calcium chloride on rat isolated ileum, oxytocin concentration-effect curve on uterine smooth muscle and phenylephrine concentration-effect curve on pulmonary artery smooth muscle. These observations indicate that eupatilin possesses a nonspecific antispasmodic effect on rat isolated smooth muscle. They also suggest that the inhibitory effect of eupatilin may be mediated by changes in Ca 2+ metabolism in these preparations.