首页> 外文期刊>American Journal of Physiology >Ameliorating effects and mechanisms of electroacupuncture on gastric dysrhythmia, delayed emptying, and impaired accommodation in diabetic rats.
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Ameliorating effects and mechanisms of electroacupuncture on gastric dysrhythmia, delayed emptying, and impaired accommodation in diabetic rats.

机译:电针对胃畸形,延迟排空和糖尿病大鼠障碍障碍的改善效应及机制。

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摘要

The aim of this study was to investigate the effects and mechanisms of electroacupuncture (EA) on gastric accommodation, gastric dysrhythmia, and gastric emptying (GE) in streptozotocin (STZ)-induced diabetic rats. Five experiments were performed in five groups of STZ-induced diabetic rats to study the effects of EA at ST-36 (Zusanli) on gastric slow-wave dysrhythmia, delayed GE and intestinal transit, impaired gastric accommodation, and the mechanisms of EA involving the autonomic and opioidergic pathways. We found the following: 1) EA improved gastric dysrhythmia in the diabetic rats. The normal percentage of slow waves was 55.4 +/- 2.9% at baseline and significantly increased to 69.2 +/- 2.2% with EA (P = 0.01); this effect was blocked by naloxone. 2) EA resulted in a 21.4% increase in GE and 18.2% increase in small intestinal transit in the diabetic rats. 3) EA restored diabetes-induced impairment in gastric accommodation. Gastric accommodation was 0.98 +/- 0.13 ml with sham EA and significantly increased to 1.21 +/- 0.15 ml with EA (P = 0.01), and this effect was blocked by naloxone. 4) EA increased vagal activity assessed by the spectral analysis of the heart rate variability. We concluded that EA at ST-36 improves gastric dysrhythmia, delayed GE and intestinal transit, and impaired accommodation in STZ-induced diabetic rats, and the improvement seems to be mainly mediated via the vagal pathway. EA may have a promising therapeutic potential for diabetic gastroparesis.
机译:本研究的目的是探讨电针(EA)对胃间隙,胃发育性和胃排空(GE)在链脲佐菌素(STZ)诱导的糖尿病大鼠中的影响和机制。在五组STZ诱导的糖尿病大鼠中进行五个实验,研究EA在ST-36(Zusanli)对胃慢波缺血性,延迟GE和肠道过境,胃置换受损的影响,以及涉及的机制自主和opioidergic途径。我们发现以下内容:1)EA改善糖尿病大鼠的胃畸形。基线的慢波的正常百分比为55.4 +/- 2.9%,ea(p = 0.01)显着增加至69.2 +/- 2.2%;纳洛酮阻断这种效果。 2)EA导致GE增加21.4%,在糖尿病大鼠中的小肠过渡的增加18.2%。 3)EA恢复糖尿病造成胃地间损伤。胃部ea胃容纳为0.98 +/- 0.13毫升,ea(p = 0.01)显着增加至1.21 +/- 0.15 ml,并通过纳洛酮阻断这种效果。 4)EA增加缩小活动通过心率变异性的光谱分析评估。我们得出结论,ST-36的EA改善了胃缺血,延迟GE和肠道过境,并在STZ诱导的糖尿病大鼠中受损,并且改善似乎主要通过迷走途径介导。 EA可能对糖尿病性胃病产生有前途的治疗潜力。

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