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ACUTE EFFECTS OF VOMITING ON ESOPHAGEAL MOTILITY IN CATS
MJ Beyak, S Xue, PI Collman, NE Diamant
Departments of Medicine and Physiology, University of Toronto, Toronto, Ontario
Vomiting involves activation of contractions of the small intestine, stomach and abdominal wall musculature, at the same time the esophagus must be inhibited. These motor events are coordinated by a brainstem vomiting centre. Superior laryngeal nerve (SLN) stimulation can induce vomiting in the cat (Beyak et al. Neurogastro. Mot. ’97). We characterized the changes in esophageal motility subsequent to an episode of vomiting in the cat, and examined a role for peripherally released nitric oxide (NO) in mediating the inhibitory changes.
METHODS: Studies were performed in urethane anesthetised cats. Vomiting was induced using long train SLN stimulation (30 Hz, 10-15s). Motility was recorded before and after an episode of vomiting.
RESULTS: Spontaneous swallows induced peristaltic contractions with a mean amplitude of 27.2 ± 5.9mmHg in the striated muscle (ST) esophagus and 73.2 ± 15.3 mmHg in the smooth muscle (SM) esophagus. If vomiting was induced, ST amplitude increased to 40.2 ± 13.0 mmHg (p>0.05) while SM amplitude was reduced markedly to 15.6 ± 3.7 mmHg. This inhibition lasted for 2-3 hours. Basal lower esophageal sphincter pressure (LESP) was also markedly reduced from 25.6 ± 6.5 to 8.9 ± 6.5 mmHg. The NO synthase inhibitor, L-NNA 10-4 mol/kg i.v. was given to 3 animals and there was no significant effect on the changes of contraction amplitude or LESP with vomiting.
CONCLUSIONS: Vomiting results in a prompt, profound inhibition of smooth muscle esophageal motility which persists. Our results suggest that this inhibition is not due to the peripheral release of NO, but likely results from turning off excitatory cholinergic output to the smooth muscle esophagus from the dorsal motor nucleus of the vagus. Such inhibition in the face of protracted vomiting (eg bulimia nervosa, post op or chemotherapy-induced vomiting), may predispose the patients to further gastroesophageal reflux and its consequences.