Study on effects of electrical stimulation on rabbit esophageal body motility in vivo
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
29303604
DOI
10.33549/physiolres.933652
PII: 933652
Knihovny.cz E-resources
- MeSH
- Adrenergic alpha-Antagonists pharmacology MeSH
- Muscarinic Antagonists pharmacology MeSH
- Atropine pharmacology MeSH
- Electric Stimulation * MeSH
- Esophagus drug effects physiology MeSH
- Phentolamine pharmacology MeSH
- Gastrointestinal Motility drug effects physiology MeSH
- Rabbits MeSH
- Manometry MeSH
- NG-Nitroarginine Methyl Ester pharmacology MeSH
- Esophageal Motility Disorders physiopathology MeSH
- Muscle Contraction MeSH
- Animals MeSH
- Check Tag
- Rabbits MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Adrenergic alpha-Antagonists MeSH
- Muscarinic Antagonists MeSH
- Atropine MeSH
- Phentolamine MeSH
- NG-Nitroarginine Methyl Ester MeSH
Electric stimulation (ES) could induce contraction of intestinal smooth muscle. The aim of this study was to analyze the effects of ES on esophageal motility and the underlying mechanism in vivo. Twenty-eight rabbits were equipped with a pair of subserosa electrodes (connected to an electrical stimulator) in the lower segment of the esophagus. The ES signal consisted of bipolar rectangular pulse trains, lasting for 3 s, with different amplitudes (1 mA, 3 mA, 5 mA and 10 mA), and frequencies (10 Hz, 20 Hz and 50 Hz). The amplitude of the contraction was recognized by high-resolution manometry. The effect of ES was tested under anesthesia and following administration of atropine, phentolamine or L-NAME. ES induced esophageal contraction at the stimulated site. A statistically significant increase in esophageal pressure was observed when the stimulation amplitude was above 3 mA. The increase in esophageal pressure was associated with the amplitude of stimulus as well as the frequency. During stimulation, atropine, phentolamine and L-NAME had no effect on the increase of esophageal pressure induced by ES. These findings implied that ES induced esophageal contraction were not mediated via the NANC, adrenergic or cholinergic pathway. The amplitude of esophageal contraction was current and frequency dependent.
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