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一氧化氮合酶与血管活性肠肽在特发性慢性便秘患者肠神经系统中的分布

Nitric oxide synthase and VIP distribution in enteric nervous system in idiopathic chronic constipation.

作者信息

Cortesini C, Cianchi F, Infantino A, Lise M

机构信息

Clinica Chirurgíca Generale, Università di Firenze, Florence, Italy.

出版信息

Dig Dis Sci. 1995 Nov;40(11):2450-5. doi: 10.1007/BF02063253.

Abstract

Idiopathic chronic constipation has been correlated to neural abnormalities that consist of a reduced number of myenteric plexus neurons and a decreased concentration of VIP-positive nerve fibers within the circular muscle. Recent studies hypothesized the involvement of nitric oxide in motility disorders of the human gut. To date, no information is available on nitric oxide involvement in idiopathic chronic constipation. The density of VIP- and nitric oxide-producing neurons was evaluated by immunocytochemistry using anti-VIP and anti-nitric oxide synthase antibodies in five patients with idiopathic chronic constipation. A low total neuron density was found at the myenteric plexus. The density of VIP-positive neurons was low while that of nitric oxide synthase-positive neurons was high at both plexuses. Our data confirm that idiopathic slow-transit chronic constipation is due to abnormal neurogenic factors. The presence of numerous nitric oxide synthase-positive neurons, all along the colon and at both plexuses, supports the hypothesis that an excessive production of nitric oxide may cause the persistent inhibition of contractions.

摘要

特发性慢性便秘与神经异常有关,这些神经异常包括肌间神经丛神经元数量减少以及环行肌内血管活性肠肽(VIP)阳性神经纤维浓度降低。最近的研究推测一氧化氮与人肠道运动障碍有关。迄今为止,尚无关于一氧化氮参与特发性慢性便秘的信息。使用抗VIP和抗一氧化氮合酶抗体,通过免疫细胞化学方法对5例特发性慢性便秘患者中产生VIP和一氧化氮的神经元密度进行了评估。在肌间神经丛发现总神经元密度较低。两个神经丛中VIP阳性神经元的密度较低,而一氧化氮合酶阳性神经元的密度较高。我们的数据证实特发性慢传输型慢性便秘是由异常神经源性因素引起的。在整个结肠和两个神经丛中都存在大量一氧化氮合酶阳性神经元,这支持了一氧化氮产生过多可能导致收缩持续受抑制的假说。

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