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首页> 外文期刊>Fundamental & clinical pharmacology. >Cooling-induced gastrointestinal smooth muscle contractions in the rat.
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Cooling-induced gastrointestinal smooth muscle contractions in the rat.

机译:冷却引起的大鼠胃肠道平滑肌收缩。

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The aim of this study was to assess the effect of cooling on smooth muscle contraction in various parts of the gastrointestinal tract (esophagus, stomach, duodenum, jejunum and colon) and to investigate the basic mechanism underlying cooling-induced (CIC) tonic and rhythmic contractions. Recordings of isometric tension from smooth muscle strips of different parts of the rat gastrointestinal tract were performed using organ-bath techniques, and stepwise cooling was applied. Cooling was tested before and after the addition of various standard agents interfering with known neurogenic (autonomic blockers, tetrodotoxin, capsaicin) and myogenic mechanims of contraction (calcium channel blockers, Sarcoplasmatic and Ca2+-ATPase pump inhibitors). Step-wise cooling (37 degrees C to 5 degrees C) of all gastrointestinal smooth muscle preparations induced reproducible graded tonic contractions, inversely proportional to temperature. CIC was most pronounced in the jejunum. Cooling abolished rhythmic smooth muscle activity. CIC was not dependent on a neural mechanism nor the release of neurotransmitters, but linked to translocation of calcium. It was reduced by incubation in Ca2+-free solution. Blockage of the Ca2+-ATPase pump, which inhibits the extrusion of calcium, plays a significant role in the process and enhances CIC. Cooling of gastrointestinal smooth muscle preparations induces graded myogenic contractions inversely proportional to the temperature. The mechanism is not dependent on local nervous control but related to a temperature-sensitive process of calcium translocation.
机译:这项研究的目的是评估冷却对胃肠道各个部位(食道,胃,十二指肠,空肠和结肠)平滑肌收缩的影响,并研究冷却诱发(CIC)滋补和节律的基本机制收缩。使用器官浴技术记录大鼠胃肠道不同部位平滑肌条的等轴测张力,并逐步冷却。在添加各种干扰已知神经源性(自主神经阻滞剂,河豚毒素,辣椒素)和肌原性收缩机制(钙通道阻滞剂,肌浆蛋白和Ca2 + -ATPase泵抑制剂)的标准剂之前和之后测试冷却。所有胃肠道平滑肌制剂的逐步冷却(从37摄氏度到5摄氏度)会引起可再现的渐变性强直收缩,与温度成反比。 CIC在空肠中最明显。冷却消除了节律性平滑肌活动。 CIC既不依赖神经机制也不依赖神经递质的释放,而与钙的转运有关。通过在不含Ca2 +的溶液中孵育来减少它。 Ca2 + -ATPase泵的堵塞可抑制钙的挤出,在该过程中起重要作用并增强CIC。胃肠道平滑肌制剂的冷却引起与温度成反比的分级肌原性收缩。该机制不依赖于局部神经控制,而是与钙转运的温度敏感过程有关。

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