Sung Tae-Sik, La Jun-Ho, Kim Tae-Wan, Yang Il-Suk
Department of Physiology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea.
J Vet Sci. 2006 Jun;7(2):143-50. doi: 10.4142/jvs.2006.7.2.143.
Nitric oxide (NO) is a non-adrenergic, non-cholinergic neurotransmitter found in the enteric nervous system that plays a role in a variety of enteropathies, including inflammatory bowel disease. Alteration of nitrergic neurons has been reported to be dependent on the manner by which inflammation is caused. However, this observed alteration has not been reported with acetic acid-induced colitis. Therefore, the purpose of the current study was to investigate changes in nitrergic neuromuscular transmission in experimental colitis in a rat model. Distal colitis was induced by intracolonic administration of 4 % acetic acid in the rat. Animals were sacrificed at 4 h and 48 h postacetic acid treatment. Myeloperoxidase activity was significantly increased in the acetic acid-treated groups. However, the response to 60 mM KCl was not significantly different in the three groups studied. The amplitude of phasic contractions was increased by Nomega-nitro-L-arginine methyl ester (L-NAME) in the normal control group, but not in the acetic acid-treated groups. Spontaneous contractions disappeared during electrical field stimulation (EFS) in normal group. However, for the colitis groups, these contractions initially disappeared, and then reappeared during EFS. Moreover, the observed disappearance was diminished by L-NAME; this suggests that these responses were NO-mediated. In addition, the number of NADPH-diaphorase positive nerve cell bodies, in the myenteric plexus, was not altered in the distal colon; whereas the area of NADPH-diaphorase positive fibers, in the circular muscle layer, was decreased in the acetic acidtreated groups. These results suggest that NO-mediated inhibitory neural input, to the circular muscle, was decreased in the acetic acid-treated groups.
一氧化氮（NO）是一种存在于肠神经系统中的非肾上腺素能、非胆碱能神经递质，在包括炎症性肠病在内的多种肠道疾病中发挥作用。据报道，氮能神经元的改变取决于炎症引发的方式。然而，在乙酸诱导的结肠炎中尚未报道过这种观察到的改变。因此，本研究的目的是调查大鼠实验性结肠炎中氮能神经肌肉传递的变化。通过向大鼠结肠内注射4%的乙酸诱导远端结肠炎。在乙酸处理后4小时和48小时处死动物。乙酸处理组的髓过氧化物酶活性显著增加。然而，在所研究的三组中，对60 mM氯化钾的反应没有显著差异。在正常对照组中，Nω-硝基-L-精氨酸甲酯（L-NAME）增加了相性收缩的幅度，但在乙酸处理组中没有。在正常组中，电场刺激（EFS）期间自发收缩消失。然而，对于结肠炎组，这些收缩最初消失，然后在EFS期间重新出现。此外，L-NAME减少了观察到的收缩消失；这表明这些反应是由NO介导的。此外，肌间神经丛中NADPH-黄递酶阳性神经细胞体的数量在远端结肠中没有改变；而在乙酸处理组中，环肌层中NADPH-黄递酶阳性纤维的面积减少。这些结果表明，乙酸处理组中向环肌的NO介导的抑制性神经输入减少。
