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首页> 外文期刊>Cardiovascular Diabetology >Remodelling of the intracardiac ganglia in diabetic Goto-Kakizaki rats: an anatomical study
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Remodelling of the intracardiac ganglia in diabetic Goto-Kakizaki rats: an anatomical study

机译:糖尿病五岛崎崎大鼠心内神经节的重塑:一项解剖学研究

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Background Although cardiac autonomic neuropathy is one of major complications of diabetes mellitus (DM), anatomical data on cardiac innervation of diabetic animal models is scant and controversial. We performed this study to check whether long-term diabetic state impacts the anatomy of intracardiac ganglia in Goto-Kakizaki (GK) rats, a genetic model of type 2 DM. Methods Twelve GK rats (276?±?17?days of age; mean?±?standard error) and 13 metabolically healthy Wistar rats (262?±?5?days of age) as controls were used for this study. Blood glucose was determined using test strips, plasma insulin by radioimmunoassay. Intrinsic ganglia and nerves were visualized by acetylcholinesterase histochemistry on whole hearts. Ganglion area was measured, and the neuronal number was assessed according to ganglion area. Results The GK rats had significantly elevated blood glucose level compared to controls (11.0?±?0.6 vs. 5.9?±?0.1?mmol/l, p?p?=?0.17). The GK rats contained significantly fewer intracardiac ganglia, decreased total area of intracardiac ganglia (1.4?±?0.1 vs. 2.2?±?0.1?mm2, p?p? Conclusions Results of our study demonstrate the decreased number of intracardiac neurons in GK rats compared to metabolically healthy Wistar rats of similar age. It is likely that the observed structural remodelling of intracardiac ganglia in GK rats is caused by a long-term diabetic state.
机译:背景技术尽管心脏自主神经病变是糖尿病(DM)的主要并发症之一,但有关糖尿病动物模型的心脏神经支配的解剖学数据却很少且有争议。我们进行了这项研究,以检查长期糖尿病状态是否会影响Goto-Kakizaki(GK)大鼠(一种2型DM的遗传模型)的心内神经节的解剖结构。方法采用12只GK大鼠(276±±17日龄;平均±标准差)和13只代谢健康的Wistar大鼠(262±±5日龄)作为对照组。使用试纸和血浆胰岛素通过放射免疫测定法测定血糖。通过乙酰胆碱酯酶组织化学对整个心脏可见内在神经节和神经。测量神经节面积,并根据神经节面积评估神经元数目。结果与对照组相比,GK大鼠的血糖水平显着升高(11.0±±0.6±5.9 vs.5.9±0.1±mmol / l,p <p = 0.17)。 GK大鼠心脏内神经节明显减少,心脏内神经节总面积减少(1.4?±?0.1 vs. 2.2?±?0.1?mm 2 ,p?p?)结论我们的研究结果表明,与代谢健康的Wistar大鼠相比,GK大鼠的心内神经元数量减少了,很可能是由于长期的糖尿病状态引起的。

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