The role of myogenic and neural control systems in esophageal motility was studied in anesthetized opossums by applying electrical pulses at 20 to 40 v, and 100 to 400-msec pulse width directly to muscle layers, by cervical vagal stimulation (10 to 25 pulses per sec, 0.5-msec pulse width, 10 to 40 v), and by balloon distension. Direct muscle stimulation resulted in a propagated contraction in 13 of 22 opossums (proximal propagation from a distal stimulation site and vice versa). The velocity of propagation was of the same order of magnitude as that of a spontaneous swallow (<5 cm per sec). The propagated contractions were not blocked by intravenous or close intraarterial atropine and hexamethonium or by intraarterial tetrodotoxin. Smooth muscle depolarization by intraarterial KCl or tetraethylammonium brought about propagated contractions in those opossums that did not show this in the first place. Generally, these propagated contractions could also be initiated in these opossums by applying 2 to 3 stimulating pulses 1 to 1.5 sec apart. The propagated contractions in response to direct muscle stimulation were observed in all opossums 2 to 20 min after death. Cessation of vagal stimulation and balloon relaxation produced 'off-responses' which were blocked by tetrodotoxin. The propagation of off-responses was much faster than the swallow-induced peristaltic contractions. In conclusion, the myogenic control system in the esophagus is capable of producing propagated contractions independently which resemble normal esophageal peristalsis in propagation velocity, and may be the underlying system responsible for it. This system may, however, be modulated by the extrinsic and intrinsic nerves.
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