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Effects of electroacupuncture on gastric migrating myoelectrical complex in dogs.

The aim-of this study was to investigate the characteristics of the gastric slow wave during different phases of the migrating myoelectrical complex (MMC) and the effect of electroacupuncture on the MMC. The experiment was performed in eight hound dogs implanted with one pair of bipolar serosal electrodes 2 cm proximal to the pylorus. Gastric myoelectrical activity was recorded for three complete cycles of the MMC in two sessions, one with electroacupuncture at points ST36 and PC6 and the other at sham points. The acupuncture was performed for 30 min in phase I of the second cycle of the MMC. Spectral analysis was performed to compute the frequency and power (amplitude) of the gastric slow wave, whereas blind visual analysis was applied to compute the appearance of spike potentials and the length of each phase of the MMC. It was found that there was a significant difference in the frequency and power of the gastric slow wave during different phases of the MMC (P < 0.05). Phase I was characterized with the highest frequency and lowest power of the gastric slow wave, whereas phase III exhibited the highest power in the slow wave. It was also found that in comparison with the sham points, electroacupuncture at the acupoints increased the number of spike bursts. This increase was not significant during the MMC cycle with electroacupuncture (34.4+/-4.1 vs 27.5+/-2.5%, P > 0.05) but became significant during the cycle after electroacupuncture (39.8+/-3.3% vs 27.5+/-2.5%, P < 0.0005). Similarly, during the MMC cycle after electroacupuncture at the acupoints, there was a significant decrease in the length of phase I (14.8+/-2.2 vs 46.9+/-6.1 min, P < 0.003) and a significant increase in the length of phase II (75.6+/-9.9 vs 30.6+/-4.1 min, P < 0.003) and phase III (25.8+/-0.6 vs 22.1+/-0.7 min, P < 0.003). A similar increase was observed during the MMC cycle with electroacupuncture but was not statistically significant. In conclusion, the gastric slow wave has the highest power during phase III of the MMC, indicating that the antral contraction is characterized not only by the appearance of spikes, but also by the increased power of the slow wave. Electroacupuncture at acupoints of ST36 and PC6 enhances the gastric MMC by reducing the length of phase I and increasing the length of phases II and III.

Acupuncture Points↗

Vasoactive intestinal peptide suppresses migrating myoelectric complex of rat small intestine independent of nitric oxide.

The involvement of nitric oxide (NO) in the biological response to vasoactive intestinal peptide (VIP) on the migrating myoelectric complex (MMC) of small bowel and systemic arterial blood pressure was investigated in the rat. Animals were supplied with bipolar electrodes for electromyography of the small intestine and blood pressure was assessed by a pressure transducer connected to a carotid artery. In the first session, Nomega-nitro-L-arginine (L-NNA) was administered intravenously at 1, 2, 4 and 20 mg kg(-1). Effects of L-NNA at 1 and 20 mg kg(-1) were also studied after L-arginine 300 mg kg(-1). In the second session, intravenous infusion of VIP 500 pmol kg(-1) min(-1) was administered before and after L-NNA at 1 and 20 mg kg(-1). L-NNA at increasing doses stimulated myoelectric spiking of the small bowel until at 4 mg kg(-1) the MMC was disrupted and irregular spiking induced. Neither at 1 nor 20 mg kg(-1) did L-NNA affect the inhibitory motility response or decrease of blood pressure induced by VIP at a dose of 500 pmol kg(-1) min(-1). Our results show that effects of VIP on motility of the small intestine and systemic arterial blood pressure are direct and not dependent on NO as a common final link.

Animals↗

Migrating myoelectric complex and jejunal slow-wave propagation after Roux gastrectomy in dogs.

Roux-en-Y gastrectomy is associated with a high incidence of symptoms of gastric stasis. Retrograde propagation of jejunal electrical slow waves and spike bursts has been implicated in the Roux Y stasis syndrome. Since the fasted state may persist after feeding, this study examined the extent of retrograde slow-wave propagation in the fasted state, particularly during aboral migration of phase III. Six dogs underwent Roux gastrectomy and placement of bipolar electrodes along the Roux limb. Four normal dogs with electrodes acted as controls. Thirty-five migrating myoelectric complexes were recorded in Roux dogs and 13 in controls. In Roux dogs, the incidences of retrograde propagation of slow waves during the migrating myoelectric complex were phase I 56 +/- 13%, phase II 60 +/- 12% and phase III 58 +/- 14% (not significant). For controls, the incidences were 0%, 0%, and 1%, respectively (P < 0.006 versus Roux dogs). In the Roux limb, retrograde propagation of slow waves, and hence spike bursts, occurs even during aboral migration of phase III. This abnormality may contribute to the Roux Y stasis syndrome.

Anastomosis, Roux-en-Y↗

Effects of neurotensin and neurotensin analogues on the migrating myoelectrical complexes in the small intestine of rats.

The purpose of the present experiments was to study the effect of neurotensin and neurotensin analogues on the migrating myoelectrical complexes in the small intestine of rats. Four bipolar electrodes were implanted into the muscular wall of the small intestine. The electrodes were placed 5, 15, 25 and 35 cm distal to the pylorus. 7-10 days after the operation the animals were fasted for 48 h with free access to water. Some experiments were performed on conscious rats and in others the rats were anesthetized with pentobarbital, 30 mg/kg. I.v. infusion of either neurotensin (NT) or (Gln4)-neurotensin at doses of 1.8, 3.6 and 7.1 pmol X kg-1 X min-1 abolished the migrating myoelectric complexes, which were replaced by increased spiking activity along the whole length of the small intestine from which activity was recorded. The changes in myoelectrical activity were observed within 2-4 min after commencement of the infusion. The activity returned to control levels within 5-15 min after the end of the infusion period. The neurotensin sequences NT 9-13, NT 8-13, NT 4 -13, NT 1-9 and (Gln4)-NT 1-11 did not induce any changes in the electrical activity in the small intestine. The effects of NT and (Gln4)-neurotensin on the myoelectrical activity in the small intestine were indistinguishable. The changes induced by NT or (Gln4)-NT resemble those found after the ingestion of food. The present data indicate that the intact NT sequence, rather than smaller NT fragments, is necessary to induce changes in myoelectrical activity in the small intestine.

Action Potentials↗

Mechanism of cycling of migrating myoelectric complexes: effect of morphine.

Morphine was injected intravenously at various phases of the migrating myoelectric complex (MMC) cycle to study the oscillatory characteristics of MMCs by the premature initiation of phase IIIs. All injection timings were represented as a percentage of the normal MMC period at the most proximal duodenal electrode. During the initial 20% of the MMC cycle, the mechanism of initiation of MMCs was in an absolutely refractory state in the sense that a supramaximal dose of morphine (200-300 micrograms/kg) did not initiate a premature phase III. During the remainder of the MMC cycle, the control mechanism was in a relatively refractory state. As this state progressed, premature phase III activity was initiated with diminishing doses of morphine. This was called the relatively refractory state. The initiation of a premature phase III by morphine did not affect the phase III already in progress, except that its propagation velocity was increased. Truncal vagotomy did not affect the refractory characteristics of MMCs or the action of morphine. Only large doses of naloxone (2 mg/kg) blocked the above action of morphine. The study shows that the MMC cyclic phenomenon has the characteristics of relaxation oscillators that may result from enteric neural biological clocks. The period of these oscillators can be altered by stimulants such as morphine.

Animals↗

Selective myenteric neuronal denervation of the rat jejunum. Differential control of the propagation of migrating myoelectric complex and basic electric rhythm.

Serosal application of benzalkonium chloride (BAC), a cationic surfactant, was used to selectively ablate the myenteric neurons of the rat jejunum. The myoelectric activity of the BAC-treated area and the areas both orad and caudad to it were assessed. In the jejunal segment devoid of myenteric neurons, the basic electric rhythm (BER) pattern was erratic and the amplitude of the BER was attenuated. The BER frequency of the jejunal area caudad to the BAC-treated area was 30.7 +/- 0.73 cycles/min, which was significantly reduced from the normal BER frequency (37.7 +/- 0.64 cycles/min). Spike activity was normal in areas both orad and caudad to the treated area, existing in regular cycling bursts (migrating myoelectric complex). Spiking in the treated area did not appear until approximately 13-17 days after BAC treatment. These spikes, though of greater duration and lower frequency than the adjacent areas, always appeared after an orad burst and were followed by a caudad burst. In addition, the following motility parameters of the regions orad and caudad to the treated area were not significantly different from control animals: burst duration, period, and burst propagation velocity. In conclusion, the present investigation has demonstrated that BAC-induced ablation of the myenteric neurons in the rat jejunum disrupts the BER but not the migrating myoelectric complex propagation. This suggests that the myenteric neurons play a modulatory role in the generation and propagation of the BER, whereas humoral factors or the submucosal neurons may be more important in the control of the migrating myoelectric complex.

Action Potentials↗

Nitrergic inhibition of migrating myoelectric complex in the rat is mediated by vasoactive intestinal peptide.

The role of vasoactive intestinal peptide (VIP) for the action of nitric oxide (NO) as a nonadrenergic noncholinergic inhibitory mediator was investigated regarding effects on migrating myoelectric complex (MMC) in rat. Animals were supplied with implanted bipolar electrodes at 5, 15 and 25 cm distal to pylorus for electromyography of small intestine. First, basal recordings with saline were followed by intravenous infusions of glyceryl trinitrate or VIP at different infusion rates to achieve dose-response relationships. Second, effects of different doses of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine (L-NNA) were studied. Third, the action of L-NNA (1 mg kg-1) on the effect of VIP (500 pmol kg-1 min-1), and of the VIP receptor antagonist (4-Cl-D-Phe6, Leu17), VIP (45 nmol 20 min-1), on the action of glyceryl trinitrate (44 nmol kg-1 min-1) was investigated. Glyceryl trinitrate prolonged the MMC cycle length from 16.3 +/- 1.3 to 44.9 +/- 8.0 min (P < 0.001), while VIP completely disrupted the MMC for the whole infusion period (P < 0.05). Higher doses of either compound induced quiescence. L-NNA shortened MMC cycle length from 14.7 +/- 1.2 to 8.6 +/- 1.4 min (P < 0.05), increased its propagation velocity from 2.0 +/- 0.4 to 18.3 +/- 8.4 cm min-1 (P < 0.01) and increased calculated length from 6.3 +/- 1.0 to 55.4 +/- 18.4 cm (P < 0.01). Pretreatment with (4-Cl-D-Phe6, Leu17) VIP blocked the inhibitory action of glyceryl trinitrate and preserved MMC pattern (P < 0.05). In contrast, L-NNA had no effect on the inhibition of MMC caused by VIP. Our results indicate that inhibition of MMC is related to production of NO, which may mediate its actions through VIP.

Animals↗

Cause-and-effect relationship between motilin and migrating myoelectric complexes.

We investigated the cause-and-effect relationship between plasma motilin levels and migrating myoelectric complexes (MMCs). Each dog was implanted with a set of eight bipolar electrodes on the small intestine. Premature phase IIIs were initiated by morphine bolus injections. Plasma samples were assayed for motilin and gastrin. All spontaneous and morphine-initiated phase IIIs were associated with peaks of plasma motilin, which always occurred after phase IIIs had started in the proximal duodenum. The plasma motilin level decreased consistently during phase I and started to increase again only after phase II had started in the duodenum. Either a meal or somatostatin infusion disrupted MMC cycling, but morphine boluses overcame this disruption and initiated phase IIIs that propagated distally. The phase IIIs thus initiated were associated with peaks in plasma motilin levels. In contrast, bolus injections of motilin did not initiate phase IIIs during the fed state or during somatostatin infusion. Our findings suggest that endogenous motilin does not initiate spontaneous MMCs. Instead, MMC contractions release motilin. The physiological role of motilin, thus released, may be to act as an endocrine agent to coordinate secretory and motor events with the start of phase III activity in the upper small intestine.

Animals↗

Variation of slow-wave frequency and locking during the migrating myoelectric complex in dogs.

Slow waves determine rhythm and polarity of spike bursts. We measured the variation of slow-wave frequency (swf) and locking (swl) in the canine jejunum during the various phases of the migrating myoelectric complex (MMC) and during induced phase III (erythromycin 125 micrograms/kg iv bolus or somatostatin 2.5 micrograms.kg-1.h-1 iv infusion), blocked phase III (atropine 20 micrograms/kg iv bolus), and so-called stationary phase III activity (cisapride 150 micrograms/kg iv bolus). The EMG of 4 dogs, implanted with 10 bipolar electrodes, was recorded on a polygraph. Our results indicate that swf and swl change during the MMC from a stepwise swf gradient with slow waves locked in plateaus during phase I to a continuous swf gradient without or with significantly reduced phase locking during phase III. The length of the first swf plateau decreases significantly from 42 +/- 12 cm post Treitz during phase I to 11 +/- 4 cm during spontaneous phase III. Atropine block of phase III activity prevents phase unlocking and development of a continuous swf gradient. Our hypothesis is that phase unlocking may be one of the induction mechanisms of spike-burst activity.

Animals↗

[Effects of human chorionic gonadotrophin and progesterone on small intestinal migrating myoelectric complex in rats].

The effects of human chorionic gonadotrophin (HCG) and progesterone (P) on migrating myoelectric complex (MMC) of the small intestine in ovariectomized rats were investigated by implanted monopolar-electrode in the intestinal wall of the duodenum, jejunum and ileum. The results showed (1) after i.v. administration of HCG the periodicity of the duodenal and upper jejunal MMC was interrupted by irregularly prolonged phases II occurring intermittently; (2) after i.m. administration of P the duration of phases I and II of the duodenal MMC was significantly prolonged, but the periodicity was not affected; (3) the effect of P plus HCG on MMC was similar to that of HCG alone, but the combined effect was spread over the whole small intestine. These results suggest that HCG can induce remarkable changes of the small intestinal MMC, which are similar to those observed in pregnant rats. In the presence of P, the effect of HCG is enhanced markedly.

Animals↗

Generation of phases I and II of migrating myoelectric complex in the dog.

The mechanisms of generation of most of the phases of the migrating myoelectric complex (MMC) are unclear. Except for phase III activity, this issue has not been investigated directly. We have qualitatively examined the relations between different phases of the MMC cycle in order to provide an objective basis for the formation of theories. Eight dogs of either sex were implanted with 10 bipolar electrodes distributed along the gastrointestinal tract. Myoelectric activity was recorded during the fasted state or after feeding until the return of the MMC cycle. The relations between phase I duration, phase II duration, phase III migration time, and phase III period were examined using simple linear-regression methods. We found that only phase I duration was highly correlated (r = 0.87, P less than 0.01) with phase III migration time and that only phase II duration was highly correlated (r = 0.90, P less than 0.01) with phase III period. In either the fed or fasted state, phase III activity that began in the midjejunum was accompanied concurrently with phase I activity of the duodenum and upper jejunum, where phase III activity had not occurred. Also, the position of phase III activity in the lower small intestine when phase I activity of the upper small intestine ended was 277 +/- 24 cm (83 +/- 5% of the small intestinal length) from the pylorus, and the coefficient of variation of this position was significantly smaller (P less than 0.01) than that of the other cycle variables.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Influence of various feeding conditions, the migrating myoelectric complex and cholinergic drugs on antral slow waves in sheep.

The presented study was designed to elucidate whether the cholinergic mechanisms control ovine antral slow waves in various physiological conditions, including feeding and various phases of migrating myoelectric complex (MMC). The investigations were carried out on six adult sheep of Polish Merino breed with seven bipolar electrodes surgically implanted onto the antral and small intestinal wall. In the course of chronic experiments, the myoelectric activity was recorded from these regions using the multichannel electroencephalograph. Experiments were performed on 48 h fasted and non-fasted animals. During some of these experiments, sheep were fed with standard fodder. During control experiments 0.15 M NaCl was slowly administered i.v. through the indwelling catheter and during other experiment, hexamethonium bromide (2.0 and 5.0 mg/kg). atropine sulfate (0.02; 0.1; 0.5 and 1.5 mg/kg) and pirenzepine dihydrochloride (0.02; 0.5 and 2.0 mg/kg) were administered i.v. during phase 1-2a or 2b MMC. The drugs were also given in combinations. The recordings were analysed and the antral slow wave amplitudes and frequencies were calculated. Unlike the slow wave amplitude, either feeding or the anticholinergic drugs significantly increased slow wave frequency, especially when the given procedure was started during phase 2b MMC. The most pronounced effects were observed after hexamethonium given alone or in combinations. Thus, the cholinergic system modulates antral slow wave frequency in sheep.

Animals↗

Altered migrating myoelectrical complex in an animal model of cholesterol gallstone disease: the effect of erythromycin.

BACKGROUND: The ground squirrel on a high cholesterol diet exhibits prolonged intestinal transit, a pathogenetic factor in cholesterol gallstone formation. AIMS: To examine the effect of a high cholesterol diet on the characteristics of the migrating myoelectrical complex (MMC) and the potential benefit of erythromycin. METHODS: Twenty four animals received either a trace (controls) or a 1% (high) cholesterol diet. After four weeks, five bipolar jejunal and terminal ileal electrodes were implanted. Seven days later, myoelectric activity was measured in conscious, fasted animals before and after treatment with erythromycin. Biliary lipid composition was assessed. RESULTS: Compared with controls, animals fed the high cholesterol diet exhibited a prolonged MMC cycle period (70 (6) versus 83 (3) minutes; p<0.05), whereas MMC migration velocity and the proportions of the MMC represented by phases I, II, and III were unchanged. Oral erythromycin significantly shortened the MMC cycle period in animals on the control and high cholesterol diet by 59% and 54% respectively, and increased the proportion of the cycle period occupied by phase III of the MMC in both dietary groups. Gall bladder bile became saturated with cholesterol and crystals developed in nine of 12 animals on the high cholesterol diet; controls had none. CONCLUSION: Animals fed a high cholesterol diet had a prolonged MMC cycle period. This, along with diminished gall bladder motility, impairs the enterohepatic cycling of bile salts and reduces their hepatic secretion, contributing to the formation of abnormal bile. Erythromycin initiated more frequent cycling of the MMC. Its therapeutic value in cholesterol gallstone formation warrants further evaluation.

Animals↗

Periodic fluctuations of gut regulatory peptides in phase with the duodenal migrating myoelectric complex in preruminant calves: effect of different sources of dietary protein.

Four preruminant calves with implanted electrodes in the duodenum and a catheter in the external jugular vein were used for investigation of plasma gut regulatory peptide profiles during different phases of migrating myoelectric complex (MMC) in the small intestine. The effects of different dietary proteins on the rhythmic activity of gut peptides and gastrointestinal motility were compared. In particular, the effects of skimmed-milk protein (retaining physiological patterns of abomasal clotting, and abomaso-intestinal digesta flow) v. fish protein (devoid of clotting activity and modifying the digesta flow) were studied. In calves fed on the milk diet, plasma concentrations of pancreatic polypeptide, motilin, secretin, cholecystokinin (CCK) and somatostatin, but not vasoactive intestinal polypeptide or gastrin, fluctuated in phase with the duodenal MMC in the preprandial period. Feeding transiently affected the intestinal MMC and abolished the peptide fluctuations in a specimen-specific manner. In contrast, calves fed on the fish-protein diet showed more profound changes in intestinal MMC. In these animals the MMC-related fluctuations were significant only for plasma CCK. In conclusion, the source of dietary protein has an impact on the physiological endocrine function of the small intestine. Observed fluctuations of plasma gut regulatory peptides seem to be secondary to duodenal motility cycles.

Animals↗

Opioid receptors and the initiation of migrating myoelectric complexes in dogs.

The role of endogenous opioids and opioid receptors in the control of migrating myoelectric complexes (MMCs) was studied in conscious dogs implanted with silver-silver chloride electrodes. In normal fasted dogs, MMC cycle times were 103 +/- 7 min in the duodenum. During naloxone infusion (1-2 mg/kg iv, then 0.2-1.0 mg.kg-1.h-1 iv) cycle times increased to 219 +/- 29 min (P less than 0.01). Naloxone (2 mg/kg iv, then 1 mg.kg-1.h-1 iv) had no effect on the response of the small intestine to bethanecol (5 mg sc) or to feeding. Pretreatment with naloxone (2 mg/kg iv) 5 min before the administration of motilin (400-500 micrograms/kg iv) did not block the initiation of MMCs by motilin. In separate experiments, animals were pretreated with the positive or negative isomer of the opioid receptor antagonist WIN-44,441 (0.2 mg/kg iv) 5 min before morphine administration. The negative isomer binds to opioid receptors whereas the positive isomer does not. The negative but not the positive isomer antagonized all effects of morphine on intestinal myoelectric activity. These studies suggest that endogenous opioids and opioid receptors may play a role in control of the initiation of MMCs and that motilin and exogenous opioids act via different mechanisms to initiate MMCs.

Animals↗