Vagal control of gastric electrical control activity and motility.
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The nerves of Latarjet and those going directly to the fundus and the body of the stomach were stimulated to determine their effect on gastric electrical control activity (ECA) and contractions. The lower limits of effective stimulation parameters were: pulse frequency 2 pulses per sec, pulse width 2 msec, pulse amplitude 0.3 ma or 5 v. Stimulation at or near the lower limits of stimulation parameters caused contractions with little effect on gastric ECA. At higher pulse repetition rates and amplitudes, vagal stimulation caused premature control potentials (PCP's), delayed control potentials (dcp's), and contractions throughout the electrically active region. The PCP's and DCP's in the antrum became phase-unlocked from those in the corpus. After 2 to 5 min of such vagal stimulation, PCP's and DCP's disappeared; gastric control waves became phase-locked at normal frequency and aboarad phase lag. Contractions continued to occur. Atropine and hexamethonium blocked all effects of vagal stimulation. After gastric ECA became insensitive to vagal stimulation, PCP's could still be produced by intraarterial acetylcholine or dimethylphenylpiperazinium, or by an electrical stimulus applied to gastric muscle, and physostigmine could temporarily restore ECA sensitivity to vagal stimulation. The ECA-insensitive state to vagal stimulation represents depletion of acetycholine at preganglionic sites.
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