Characterization of peristaltic motility in the striated muscle portion of the esophagus using a novel in vivo method in rats
Autor: | Takahiko Shiina, Kazuhiro Horii, Kiyotada Naitou, Yuuki Horii, Hiroki Shimaoka, Yasutake Shimizu, Hiroyuki Nakamori |
---|---|
Rok vydání: | 2018 |
Předmět: |
Male
0301 basic medicine Physiology medicine.medical_treatment Motility Vagotomy Catheterization Nitric oxide Tonic (physiology) Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound Esophagus 0302 clinical medicine medicine Animals Peristalsis biology Endocrine and Autonomic Systems Gastroenterology Vagus Nerve Muscle Striated Deglutition Rats Cell biology Nitric oxide synthase 030104 developmental biology medicine.anatomical_structure chemistry biology.protein Reflex 030217 neurology & neurosurgery |
Zdroj: | Neurogastroenterology & Motility. 31:e13518 |
ISSN: | 1365-2982 1350-1925 |
Popis: | Background Esophageal peristalsis is controlled by the brainstem via vago-vagal reflex. However, the precise regulatory mechanisms in the striated muscle portion are largely unknown. The aim of this study was to characterize peristaltic motility in the portion of the esophagus using a novel in vivo method in rats. Methods A balloon-tipped catheter was placed in the esophagus of a rat anesthetized with urethane. To induce esophageal peristalsis, the balloon was inflated by water injection. Key results When the balloon was inflated near the bronchial bifurcation, the balloon was transported in the aboral direction. Vagotomy abolished the peristaltic response. The threshold volume for inducing esophageal peristalsis varied according to the velocity of balloon distention; the volume being effective to induce peristalsis at a low inflation speed was smaller than the threshold volume at a rapid inflation speed. Even in the absence of inflation, keeping the balloon inside the esophagus during an interval period prevented subsequent induction of peristaltic motility. In addition, a nitric oxide synthase inhibitor abolished the induction of esophageal peristalsis. Conclusions and inferences Our findings suggest that (a) in addition to the intensity, the velocity of distention is important for activating the mechanosensory mechanism to induce esophageal peristalsis, (b) tonic inputs from afferent fibers located at the mucosa may reduce the excitability of mechanosensors which is necessary for inducing peristalsis, and (c) nitric oxide plays essential roles in the induction of esophageal peristalsis. These results provide novel insights into the regulatory mechanisms of esophageal motility. |
Databáze: | OpenAIRE |
Externí odkaz: |