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Neural control of the intestinal migrating myoelectric complex. A pharmacological analysis

Taher Y. El-Sharkawy, H. Markus, Nicholas E. Diamant

Open publisher page 40 citations

Abstract

A pharmacological analysis of the participation of autonomic nerves in the control of the intestinal migrating myoelectric complex (MMC) was conducted on six conscious fasting dogs with implanted bipolar electrodes. All dogs exhibited regularly recurring MMC's. Hexamethonium (2-10 mg/kg i.v.) or atropine (25-100 micrograms/kg i.v.) immediately suppressed all spiking activity, stopped the progression of the ongoing complexes, and prevented the initiation of new complexes for 2.5 to 5 h. Phentolamine (2-4 mg/kg i.v.) and propranolol (2 mg/kg i.v.) given separately or in combination had no observable effect on any of the different phases of the complex, its progression, or its frequency. Phenylephrine (0.5-1 mg/kg) inhibited the spiking phases of the complex. Isopropylnoradrenaline had no effect on the complex at doses (up to 30 micrograms/kg) which produced maximal cardiac chronotropic effect. The effects of these agonists were totally blocked by the doses of respective adrenergic antagonists used. Phenoxybenzamine given in a dose of 10-15 mg/kg i.v. produced effects similar to atropine apparently owing to blockade of cholinergic muscarinic receptors. It is concluded that (a) the regular spiking phases of the migrating complex result from cyclical and sequential activation of preganglionic fibers forming nicotinic synapses on postganglionic cholinergic excitatory neurones; and (b) the function of adrenergic nerves is not normally required for the MMC.

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What this paper is about

A pharmacological analysis of the participation of autonomic nerves in the control of the intestinal migrating myoelectric complex (MMC) was conducted on six conscious fasting dogs with implanted bipolar electrodes. All dogs exhibited regularly recurring MMC's. Hexamethonium (2-10 mg/kg i.v.) or atropine (25-100 micrograms/kg i.v.) immediately suppressed all spiking activity, stopped the progression of the ongoing complexes, and prevented the initiation of new complexes for 2.5 to 5 h. Phentolamine (2-4 mg/kg i.v.) and propranolol (2 mg/kg i.v.) given separately or in combination had no observable effect on any of the different phases of the complex, its progression, or its frequency. Phenylephrine (0.5-1 mg/kg) inhibited the spiking phases of the complex. Isopropylnoradrenaline had no effect on the complex at doses (up to 30 micrograms/kg) which produced maximal cardiac chronotropic effect. The effects of these agonists were totally blocked by the doses of respective adrenergic antagonists used. Phenoxybenzamine given in a dose of 10-15 mg/kg i.v. produced effects similar to atropine apparently owing to blockade of cholinergic muscarinic receptors. It is concluded that (a) the regular spiking phases of the migrating complex result from cyclical and sequential activation of preganglionic fibers forming nicotinic synapses on postganglionic cholinergic excitatory neurones; and (b) the function of adrenergic nerves is not normally required for the MMC.

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Available abstract

A pharmacological analysis of the participation of autonomic nerves in the control of the intestinal migrating myoelectric complex (MMC) was conducted on six conscious fasting dogs with implanted bipolar electrodes. All dogs exhibited regularly recurring MMC's. Hexamethonium (2-10 mg/kg i.v.) or atropine (25-100 micrograms/kg i.v.) immediately suppressed all spiking activity, stopped the progression of the ongoing complexes, and prevented the initiation of new complexes for 2.5 to 5 h. Phentolamine (2-4 mg/kg i.v.) and propranolol (2 mg/kg i.v.) given separately or in combination had no observable effect on any of the different phases of the complex, its progression, or its frequency. Phenylephrine (0.5-1 mg/kg) inhibited the spiking phases of the complex. Isopropylnoradrenaline had no effect on the complex at doses (up to 30 micrograms/kg) which produced maximal cardiac chronotropic effect. The effects of these agonists were totally blocked by the doses of respective adrenergic antagonists used. Phenoxybenzamine given in a dose of 10-15 mg/kg i.v. produced effects similar to atropine apparently owing to blockade of cholinergic muscarinic receptors. It is concluded that (a) the regular spiking phases of the migrating complex result from cyclical and sequential activation of preganglionic fibers forming nicotinic synapses on postganglionic cholinergic excitatory neurones; and (b) the function of adrenergic nerves is not normally required for the MMC.

Key concepts: Hexamethonium, Atropine, Phentolamine, Phenoxybenzamine, Propranolol, Chronotropic, Cholinergic, Endocrinology

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