Electrophysiologic control of motility in the human colon

Huizinga, Jan D.; Stern, Hartley; Chow, Edwin; Diamant, Nicholas E.; El-Sharkawy, T. Y.

doi:10.1016/0016-5085(85)90513-x

Cited by 80 publications

(65 citation statements)

References 23 publications

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“…In tissue from Hirschprung's disease patients (Kubota, Itoh & Ikeda, 1983), intracellular electrical activity was observed, which was similar to electrical activity observed in normal tissue recorded using extracellular techniques (Huizinga et al 1985). Some data on intracellular activity of longitudinal muscle cells of human colon have been obtained (Duthie & Kirk, 1978;Van Merwyk & Duthie, 1980;Huizinga et al 1985). The present study will describe the intracellular electrical activity of longitudinal muscle cells in detail and will compare it with longitudinal muscle activity from the dog colon.…”

supporting

confidence: 53%

“…Impalements were either unsuccessful (Van Merwyk & Duthie, 1980) or showed sporadic oscillatory activity (Huizinga, Stern, Chow, Diamant & El-Sharkawy, 1985). In tissue from Hirschprung's disease patients (Kubota, Itoh & Ikeda, 1983), intracellular electrical activity was observed, which was similar to electrical activity observed in normal tissue recorded using extracellular techniques (Huizinga et al 1985).…”

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confidence: 93%

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Myogenic electrical control activity in longitudinal muscle of human and dog colon.

Chow

Huizinga

1987

The Journal of Physiology

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SUMMARY1. The myogenic electrical activities of longitudinal muscle cells of the dog and human colon were investigated using intracellular microelectrodes.2. The resting membrane potentials of dog and human longitudinal muscle cells at the serosal side of the muscle layer were -49-4 + 0-9 and -44-8 + 1.3 mV respectively.3. Spontaneous electrical activity consisted of electrical oscillations of 13-7 + 1 1 mV and 8-6 + 2-1 mV amplitude, and 19-8 + 1I0 cycles/min and 2641 + 1-6 cycles/min frequency for dog and human cells respectively.4. Spiking activity only occurred superimposed on the electrical oscillations; the mean rate of rise of spikes was -150 mV/s in the dog and -260 mV/s in human cells and that of the oscillations was -18 mV/s in the dog and -16 mV in human cells.5. Spiking activity was abolished by calcium influx blockers and 0;01 mM-calcium Krebs solution. The amplitude of the electrical oscillations was reduced to 0-2-1-0 mV 30 min after calcium influx blockade or 30 min in 0-01 mM-calcium Krebs solution.6. Because of the high frequency of the oscillation-spike complexes, there was summation of associated contractile events in such a way that contraction frequency corresponded to frequency of bursts of oscillations and not to the frequency of the individual oscillations.7. The resting membrane potential of the longitudinal muscle cells at the myenteric plexus side of the layer was -44-9 + 1I0 mV, significantly lower than at the serosal side. 8. A gradient in membrane potential and slow-wave amplitude exists in circular muscle of dog colon, with the highest value at the mucosal side (-68-4 and 28-1 mV respectively) and the lowest at the myenteric side (-62-5 and 8-6 mV) of the muscle layer.

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confidence: 53%

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confidence: 93%

Myogenic electrical control activity in longitudinal muscle of human and dog colon.

Chow

Huizinga

1987

The Journal of Physiology

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“…In colonic longitudinal muscle of several species including the guinea-pig, dog, pig and human, the.application of stretch appears to promote the onset of membrane potential oscillations. The onset of oscillatory activity appears to be controlled by both myogenic and neurogenic mechanisms (Biilbring, 1955;Gillespie, 1962;El-Sharkawy, 1983;Huizinga, Diamant & El-Sharkawy, 1983;Huizinga, Stern, Chow, Diamant & El-Sharkawy, 1985;Huizinga, Chow, Diamant & El-Sharkawy, 1987;Smith et al 1987 a).…”

Section: Introductionmentioning

confidence: 99%

Neurogenic slow depolarizations and rapid oscillations in the membrane potential of circular muscle of mouse colon.

Bywater

Small

Taylor

1989

The Journal of Physiology

136

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SUMMARY1. Intracellular microelectrodes have been used to record the electrical activity of smooth muscle cells of the circular layer from full length strips of mouse colon in vitro. The membrane potential was unstable and showed slow depolarizations (mean amplitude, 10-9 mV; mean frequency, 0-008 Hz; mean duration, 56-4 s).2. A variable number (mean fifty-six) of rapid oscillations in membrane potential (mean amplitude, 10-2 mV) with a frequency of approximately 2 Hz and a duration of approximately 400 ms were superimposed on each slow depolarization. Occasionally, action potentials arose from the rapid oscillations. The action potentials, but neither the slow depolarizations nor the rapid oscillations, were abolished by 1.0 utM-nifedipine.3. The majority of the slow depolarizations and the associated rapid oscillations migrated aborally along the colon at a velocity of between 0 5 and 1.5 mm s-1; in the distal colon the slow depolarization was often preceded by a small hyperpolarization.4. During the rising and plateau phase of the slow depolarization the amplitude of electrotonic potentials was decreased. Hyperpolarization induced by passing current during the slow depolarization increased the amplitude of the rapid oscillations.5. Transmural electrical stimulation (single pulses) in the presence of nifedipine evoked (1 mm anal to the stimulating electrodes) an inhibitory junction potential which was sometimes preceded by an excitatory junction potential. The amplitude. of the evoked inhibitory junction potential was decreased during the rising and plateau phase of the slow depolarization.6. The slow depolarization and the rapid oscillations were abolished by hexamethonium (500 /SM), morphine (1-10 /lM) and tetrodotoxin (3-1 /tM). Atropine 7. Atropine (3-5 /tM) and morphine (10 ,M) abolished the evoked excitatory junction potential whilst tetrodotoxin (3-1 /iM) abolished both the excitatory and the inhibitory junction potential.

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“…The small intestine has intrinsic pacemaker activity from the duodenum to the terminal ileum, and there is also a proximal-to-distal pacemaker frequency gradient in this organ (7). However, there is no consensus regarding slow waves in the colon, such as origin, frequency, and propagation (3,9,25,16). Recently, it has been proposed that gastrointestinal slow waves are generated by interstitial cells of Cajal (10,18).…”

mentioning

confidence: 99%

Effects and mechanisms of gastrointestinal electrical stimulation on slow waves: a systematic canine study

Sun¹,

Guan²,

Yin

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Sun Y, Song GQ, Yin J, Lei Y, Chen JDZ. Effects and mechanisms of gastrointestinal electrical stimulation on slow waves: a systematic canine study. Am J Physiol Regul Integr Comp Physiol 297: R1392-R1399, 2009. First published August 26, 2009 doi:10.1152/ajpregu.00006.2009.-The aims of this study were to determine optimal pacing parameters of electrical stimulation on different gut segments and to investigate effects and possible mechanisms of gastrointestinal electrical stimulation on gut slow waves. Twelve female hound-mix dogs were used in this study. A total of six pairs of electrodes were implanted on the stomach, duodenum, and ascending colon. Bilateral truncal vagotomy was performed in six of the dogs. One experiment was designed to study the effects of the pacing frequency on the entrainment of gut slow waves. Another experiment was designed to study the modulatory effects of the vagal and sympathetic pathways on gastrointestinal pacing. The frequency of slow waves was 4.88 Ϯ 0.23 cpm (range, 4 -6 cpm) in the stomach and 19.68 Ϯ 0.31 cpm (range, 18 -22 cpm) in the duodenum. There were no consistent or dominant frequencies of the slow waves in the colon. The optimal parameters to entrain slow waves were: frequency of 1.1 intrinsic frequency (IF; 10% higher than IF) and pulse width of 150 -450 ms (mean, 320.0 Ϯ 85.4 ms) for the stomach, and 1.1 IF and 10 -20 ms for the small intestine. Electrical stimulation was not able to alter colon slow waves. The maximum entrainable frequency was 1.27 IF in the stomach and 1.21 IF in the duodenum. Gastrointestinal pacing was not blocked by vagotomy nor the application of an ␣-or ␤-adrenergic receptor antagonist; whereas the induction of gastric dysrhythmia with electrical stimulation was completely blocked by the application of the ␣-or ␤-adrenergic receptor antagonist. Gastrointestinal pacing is achievable in the stomach and small intestine but not the colon, and the maximal entrainable frequency of the gastric and small intestinal slow waves is about 20% higher than the IF. The entrainment of slow waves with gastrointestinal pacing is not modulated by the vagal or sympathetic pathways, suggesting a purely peripheral or muscle effect.

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Electrophysiologic control of motility in the human colon

Cited by 80 publications

References 23 publications

Myogenic electrical control activity in longitudinal muscle of human and dog colon.

Myogenic electrical control activity in longitudinal muscle of human and dog colon.

Neurogenic slow depolarizations and rapid oscillations in the membrane potential of circular muscle of mouse colon.

Effects and mechanisms of gastrointestinal electrical stimulation on slow waves: a systematic canine study

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