链脲佐菌素诱导豚鼠回肠神经刺激毒蕈碱和神经激肽收缩增强

J. Cellini, R. Pommier, R. Porter, K. J. LePard
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引用次数: 3

摘要

糖尿病可引起肠神经元的神经病变,导致肠道运动异常。这些研究研究了乙酰胆碱激活毒毒碱M3受体和神经激肽激活神经激肽NK1受体对STZ豚鼠(胰岛素缺乏但轻度高血糖的1型糖尿病模型)神经刺激的回肠纵向条收缩的电压依赖性作用。与对照组相比,糖尿病患者回肠对乙二酚、P -甲酯物质和神经刺激的收缩更大。与对照动物相比,较低电压下的毒蕈碱M3受体拮抗剂4-DAMP和较高电压下的神经激肽NK1受体拮抗剂SR140333,而非神经激肽NK1受体拮抗剂cp - 96345,在抑制神经刺激的糖尿病回肠立即峰值收缩和总收缩面积方面更有效。对于糖尿病回肠,在4-DAMP和CP-96,345存在时,观察到神经刺激收缩区域的电压依赖性增加,但SR140333不存在。仅在低电压下,与对照组相比,糖尿病患者的神经刺激的乙酰胆碱释放量更大。与对照动物相比,糖尿病患者回肠肌肠神经节中快激肽样免疫反应性荧光强度增加。在糖尿病豚鼠中,更强的回肠神经刺激收缩反映了低电压下乙酰胆碱和高电压下速激肽的释放增加,以及平滑肌M3和NK1受体对乙酰胆碱和速激肽的敏感性增加。低胰岛素血症可能是1型糖尿病患者肠道运动功能障碍的主要原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Enhanced nerve-stimulated muscarinic and neurokinin contractions of ileum from streptozotocin guinea-pigs

  1. Diabetes mellitus can lead to neuropathy of enteric neurons, resulting in abnormal gut motility. These studies investigated voltage-dependent contributions of muscarinic M3 receptor activation by acetylcholine and neurokinin NK1 receptor activation by neurokinins to nerve-stimulated contractions of longitudinal ileal strips from STZ guinea-pigs, a type 1 diabetic model with insulin deficiency, but mild hyperglycaemia.
  2. Contractions to bethanechol, substance P methyl ester, and nerve stimulation were greater in diabetic as compared to control ileum.
  3. The muscarinic M3 receptor antagonist 4-DAMP at lower voltages and the neurokinin NK1 receptor antagonist SR140333 at higher voltages, but not the neurokinin NK1 receptor antagonist CP-96,345, were more effective at inhibiting nerve-stimulated immediate peak contractions and total areas of contraction of ileum from diabetic as compared to control animals. For diabetic ileum, voltage-dependent increases in the areas of nerve-stimulated contraction were observed in the presence of 4-DAMP and CP-96,345 but not SR140333.
  4. At low voltages only, nerve-stimulated release of acetylcholine was greater from diabetic as compared to control ileum.
  5. Fluorescence intensity of tachykinin-like immunoreactivity was increased in ileal myenteric ganglia from diabetic as compared to control animals.
  6. In diabetic guinea-pigs, stronger ileal nerve-stimulated contractions reflected increased release of acetylcholine at lower voltages and tachykinins at higher voltages, as well as increased sensitivity of smooth muscle M3 and NK1 receptors to acetylcholine and tachykinins. Hypoinsulinaemia may be a primary contributor to intestinal motility dysfunction in type 1 diabetes mellitus.
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