Mizuguchi Sumito, Ohno Takashi, Hattori Youichiro, Kamata Kazuhisa, Arai Katsuharu, Saeki Takeo, Saigenji Katsunori, Hayashi Izumi, Kuribayashi Yoshikazu, Majima Masataka
Department of Internal Medicine, School of Medicine, Kitasato University, Sagamihara, Japan.
J Gastroenterol Hepatol. 2005 Apr;20(4):611-8. doi: 10.1111/j.1440-1746.2004.03764.x.
It is widely accepted that the inhibition of gastric motor activity as well as the maintenance of gastric mucosal blood flow and mucous secretion are important for the homeostasis of the gastric mucosa. The present study was performed to ascertain whether or not capsaicin, which can protect the stomach from noxious stimuli, affects gastric motor activity.
Male Sprague-Dawley rats were anesthetized with urethane, and the stomach was cannulated by two catheters from esophageal and duodenal sides. A biopolar electrode was fixed to the serosal surface of the antrum and myoelectrical activity was recorded during the instillation of a small volume of solutions.
The myoelectrical activity of rat gastric smooth muscle was increased at intragastric pressures of >2 cmH(2)O. Replacement of intragastric physiological saline with 1.6 mmol/L capsaicin solution significantly suppressed this myoelectrical activity by 50%. Intragastric capsaicin administration caused a significant release of substance P (SP) and calcitonin gene-related peptide (CGRP). The maximum released levels of CGRP in the gastric perfusates were 100-fold those of SP. The myoelectrical activity observed at an intragastric pressure of 2 cmH(2)O was avoided by continuous infusion of CGRP (0.1-3.0 nmol/kg per min) into the gastric artery in a dose-dependent manner, but not by that of SP (1.0 nmol/kg per min). Continuous CGRP-(8-37) infusion into the gastric artery completely blocked the reduction by intragastric capsaicin of myoelectrical activity.
These results suggest that the suppression of the myoelectrical activity of gastric smooth muscle by capsaicin is attributable to the endogenous CGRP released.
人们普遍认为,抑制胃运动活性以及维持胃黏膜血流和黏液分泌对胃黏膜的稳态很重要。本研究旨在确定能保护胃免受有害刺激的辣椒素是否会影响胃运动活性。
雄性Sprague-Dawley大鼠用乌拉坦麻醉,通过两根导管分别从食管侧和十二指肠侧对胃进行插管。将双极电极固定在胃窦的浆膜表面,并在滴注少量溶液期间记录肌电活动。
当胃内压>2 cmH₂O时,大鼠胃平滑肌的肌电活动增强。用1.6 mmol/L辣椒素溶液替代胃内生理盐水可使这种肌电活动显著抑制50%。胃内给予辣椒素导致P物质(SP)和降钙素基因相关肽(CGRP)显著释放。胃灌流液中CGRP的最大释放水平是SP的100倍。通过以剂量依赖的方式持续向胃动脉内输注CGRP(0.1 - 3.0 nmol/kg每分钟)可避免在胃内压为2 cmH₂O时观察到的肌电活动,但输注SP(1.0 nmol/kg每分钟)则不能。持续向胃动脉内输注CGRP-(8 - 37)完全阻断了胃内辣椒素对肌电活动的降低作用。
这些结果表明,辣椒素对胃平滑肌肌电活动的抑制作用归因于释放的内源性CGRP。