Frequency Of Spike Bursts Research Articles

Involvement of peripheral and central motor and secretory components in the action of a prostaglandin E2 analogue on colonic transit in rats

AbstractThe effects of central and peripheral administration of a prostaglandin E2 analogue (enprostil) on colonic transit time, faecal dry matter and colonic myoelectrical activity, were examined in rats chronically fitted with a cannula in a lateral ventricle of the brain and a catheter inserted in the lumen of the proximal colon, or nichrome electrodes implanted on the proximal colon. In control studies, the mean retention time (MRT) of a marker ([51Cr] sodium chromate) administered into the proximal colon and determined in the faeces collected at hourly intervals was 7.3 ± 1.7 h, the frequency of colonic long spike bursts was 59.1 ± 9.1/h and faecal dry matter (DM) 65.4 ± 3.4%. Enprostil administered orally (350 μg/kg) decreased colonic MRT (4.9 ± 0.6 h) and faecal DM (50.1 ± 3.2%) and increased by 68% the colonic myoelectric index. Administered intracerebroventricularly enprostil (12 μg/kg) also accelerated colonic transit (MRT = 5.1 ± 1.6 h) and decreased faecal DM (48.7 ± 3.4%) but did not modify colonic spiking activity. Intraperitonal administration of the PG receptor antagonist SC‐19220 (1 mg/kg) did not affect the effects of enprostil administered centrally on MRT and DM but blocked the action of oral enprostil on colonic transit time, DM and colonic spiking activity. Centrally administered, SC‐19220 (100 μg/kg) antagonized the effects of oral enprostil on colonic transit and faecal DM but not on colonic spiking activity. It is concluded that in rats the enprostil‐induced acceleration of colonic transit involves a peripheral action on colonic motility and a secretory component which is centrally mediated. Moreover these results show that colonic hypersecretion, but not hypermotility, can alone accelerate colonic transit.

Oral administration of Tyr-MIF-1 stimulates gastric emptying and gastrointestinal motility in rodents

The effects of orally administered Tyr-MIF-1, an agonist of an endogenous antiopiate system, were examined on gastric emptying in mice and gastrointestinal myoelectric activity in rats. Tyr-MIF-1 (5 mg/kg in mice, 20 mg/kg in rats) accelerated gastric emptying of a methylcellulose test meal, increased the frequency of antral spike bursts, and disrupted intestinal migrating myoelectric complexes. These effects were reproduced by a subcutaneous administration of Tyr-MIF-1 at the same dosage. They were blocked by naloxone (1 mg/kg) but not by the kappa receptor subtype antagonist MR 2266 (1 mg/kg). The GABA A antagonist bicuculline (0.5 mg/kg), but not the GABA B antagonist 2-hydroxysaclofen (4 mg/kg), also antagonized the effects of Tyr-MIF-1. These data demonstrate that oral Tyr-MIF-1 stimulates gastric emptying and gastrointestinal motility through a systemic or central action that involves opioid and GABA systems.

Studies of method of conserving grass herbage and frequency of feeding in cattle. 2. Eating behaviour, rumen motility and rumen fill.

The influence of the method of conserving grass herbage and the frequency of feeding on eating behaviour, rumen motility and rumen fill was studied in growing steers. Silage and hay were offered to twelve rumen-cannulated Friesian steers (average initial live weight (LW) 128 kg) at a restricted level of intake (20 g dry matter (DM)/kg LW) either once or eight times daily. With once daily feeding, the daily intake of hay was consumed in a single large meal which lasted about 2 h, while silage was eaten in many small meals throughout the day. The proportion of the day spent ruminating was higher (0.39) for steers offered hay once daily than for those offered silage (0.28) or hay eight times per day (0.29). There was little effect of conservation method on frequency of rumen contraction, but contractile intensity (integration of frequency and amplitude) increased during the second half of the 24 h feeding cycle in steers offered hay either once daily or eight times daily, while the same effect was only observed when silage was offered once daily. Total daily contractile activity (the integration of the frequency and duration of myoelectric spike bursts) was significantly (P less than 0.05) higher in steers offered hay, compared with silage, once daily. The mean weight of organic matter in the reticulo-rumen of steers offered hay was significantly higher than for silage both with once (1593 v. 1326 g organic matter (OM)/100 kg LW, P less than 0.01) and eight (1367 v. 1160 g OM/100 kg LW, P less than 0.05) times daily feeding. The proportion of the particulate pool which was present as small (less than 1.2 mm) particles was always greater than 0.60.

CNS vasopressin mediates emotional stress and CRH-induced colonic motor alterations in rats.

The effects of emotional stress (ES) corresponding to conditioned fear on colonic motility and its antagonism by [deamino-Pen1, Val4, D-Arg8]vasopressin, a vasopressin antagonist, were investigated by electromyography in conscious fasted rats fitted with chronically implanted electrodes. A 117% increase (19.6 +/- 2.1 vs. 9.0 +/- 0.9 cycles/10 min during the control period) in the frequency of colonic spike bursts was observed when rats were placed for 30 min in a box in which they had previously received electric foot shocks. Intracerebroventricular (icv) administration of corticotropin-releasing hormone (CRH; 0.5 micrograms/kg) mimicked the effects of ES and increased the spike burst frequency of the colon by 88.6% from 5 to 15 min after its administration. At doses between 5 and 20 micrograms/kg the antagonist [deamino-Pen1, Val4, D-Arg8]vasopressin significantly reduced or abolished the effects of ES and CRH administration on colonic motility. Injected icv at doses of 2.5 and 5 ng/kg [Arg8]vasopressin dose dependently increased the frequency of colonic spike bursts. These effects were not reproduced by similar or higher (50 ng/kg) doses given intraperitoneally, and the effects were abolished after previous administration of vasopressin at a dose of 20 micrograms/kg. It is concluded that the effects of ES on colonic motility in rats previously shown to be linked to the central nervous system (CNS) release of CRH are in turn mediated through the central release of vasopressin.

Colonic and Cardiovascular Actions of the Atypical β‐Adrenergic Agonist SR 58611A in Rats

Inhibition of colonic myoelectric activity by the new atypical β‐adrenergic agonist SR 58611A and its cardiovascular effects were investigated in orally dosed unanesthetized rats. SR 58611A and the reference compound ritodrine caused dose‐related reduction of the long spike burst frequency of the proximal colon (respective ED50 values of 0.47 and 3.1 mg/kg); this was prevented by alprenolol but not by the β1‐ or β2‐selective adrenergic antagonists CGP 20712A and ICI 118,551. The minimal effective doses of SR 58611A and ritodrine raising heart rate were about 20 and 3 times their respective ED50 values for inhibition of colonie motility. Ritodrine, unlike SR 58611A, caused a dose‐dependent increase in heart rate. Blood pressure was not affected by either drug. There was partial tolerance to the intestinal effects of SR 58611A and ritodrine, which fell by about half after 4 days' treatment but no further after 8 days. In the animal model investigated, SR 58611A was less liable than ritodrine to induce cardiovascular side effects. It should thus be of prospective therapeutic interest for intestinal hypermotility disorders.

Action of endogenous prostaglandins on postprandial pyloric motility: A possible modulation by fats

The involvement of endogenous prostaglandins (PGs) and the effect of exogenous PGs on the myoelectrical activity of the pylorus were examined for 6 hours after a meal in dogs chronically fitted with intraparietal electrodes on the gastroduodenal junction. The animals received either a standard meal or a fat meal which consisted of canned food added or not (standard meal) with arachis oil. The cyclooxygenase inhibitors, indomethacin (1 mg/kg) and piroxicam (0.2 mg/kg) given prior a fat meal singificantly increased the frequency of pyloric spike bursts did not modify the pyloric motility associated with a standard meal. Synthetic derivatives of PGE1 (misoprostol, 5–10 μg/kg) or PGE2 (enprostil 0.5–1 μg/kg) reduced the frequency of pyloric contractions after a fat but not a standard meal. It is suggested that both endogenous and exogenous prostaglandins may modulate postprandial pyloric motility when fats are present in sufficient amount into the meal.

Neuropeptide Y and sigma ligand (JO 1784) act through a Gi protein to block the psychological stress and corticotropin-releasing factor-induced colonic motor activation in rats

The effects of neuropeptide Y and sigma ligands (d-NANM and JO 1784) on corticotropin-releasing factor (CRF) and psychological stress-stimulated caecal and colonic motility were evaluated by electromyography in rats equipped with chronically implanted electrodes on the caecum and proximal colon and a small catheter into the right lateral ventricle of the brain. Exposure to a psychological stress for 30 min increased significantly ( P < 0.05) the frequency of caecal and colonic spike bursts, an effect which was mimicked by intracerebroventricular administration of CRF (300 ng/kg). Injected intracerebroventricularly, 30 min prior to the psychological stress or intracerebroven-tricular administration of CRF, neuropeptide Y (150 ng/kg) abolished the excitatory effect on caecocolonic motility. Similarly, prior administration of d-NANM (100 ng/kg) and JO 1784 (50 ng/kg) abolished the caeco-colonic hypermotility induced by psychological stress and intracerebroventricular injection of CRF. Four days after intracerebroventricular administration of pertussis toxin (150 ng/kg), both neuropeptide Y and JO 1784, when administered centrally, were unable to antagonize the stress-induced hyperkinesia. It is concluded that central administration of neuropeptide Y and σ ligands abolish the stimulatory effects of psychological stress on caeco-colonic motility by blocking the pathways by which CRF activates the motility, through a common mechanism involving a pertussis toxin-sensitive Gi protein.

Buspirone inhibits corticotropin-releasing factor and stress-induced cecal motor response in rats by acung through 5-HT 1A receptors

The effect of buspirone on corticotropin-rclcasing factor (CRF) and stress-stimulated cecal motility and its antagonism by 5-HT 1A (spiroxatrine) and σ (BMY 14802) antagonists were evaluated by electromyography in rats equipped with chronically implanted electrodes on the cecum and a small catheter into the right lateral ventricle of the brain. Exposure to mental stress. consisting of a fear-conditioned response, increased during 30 min the frequency of cecal spike bursts significantly (P < 0.01). The frequency of cecal spike bursts was also increased following intracerebroventricular injection of CRF (500 ng/kg). Buspirone (l mg/kg s.c.) abolished the stimulatory effects of mental stress and CRF on cecal motility. Whereas spiroxatrine (0.5 mg/kg s.c.) blocked the effect of buspirone on the colonie hypermotility induced by i.c.v. injection of CRF, BMY 14802 at a similar dose (0.5 mg/kg s.c.) was unable to block the action of buspirone. It is concluded that s.c. administration of buspirone suppresses the stress-induced cecal motor response through 5-HT 1A receptors, probably by inhibiting the central or peripheral pathways involved in CRF mediation of these effects.

Inhibitory effect of ileal oleate on postprandial motility of the upper gut

To determine the effect of ileal oleate on postprandial gastrointestinal motility, duodenal and paired perfusion-aspiration ileal catheters and bipolar duodenal and jejunal electrodes were surgically implanted in five dogs. The ileum was perfused with either saline or an isotonic oleic acid emulsion at 2 ml/min. A 205-kcal mixed meal containing 120 ml liquid nutrient labeled with 111In-diethylenetriamine pentaacetic acid (DTPA) and solid food labeled with 99mTc was then administered orally. Gastric emptying was assessed by a gamma camera, myoelectric activity was continuously monitored, and duodenal-ileal transit of phenol red was determined over the ensuing 240 min. Ileal oleate reduced duodenal spikeburst frequency by 50% (P less than 0.05) and delayed gastric emptying of liquids and solids. Four hours after ingesting the meal, 62% of solids and 34% of liquids were retained in the stomach during oleic acid perfusion compared with 25 and 4%, respectively, when saline was perfused (P less than 0.05). Duodenal-ileal transit was markedly slowed by ileal perfusion with the oleic acid emulsion (P less than 0.001). Ileal oleate therefore exerted a profound inhibitory effect on proximal gut motility in the early period after ingestion of a mixed-nutrient meal in dogs.

Conditioned emotional response in rats enhances colonic motility through the central release of corticotropin-releasing factor

The effect of a mental stress model corresponding to conditioned fear on cecocolonic motility was evaluated electromyographically in intact and hypophy-sectomized rats equipped with electrodes implanted in the cecum and proximal colon over a long period and a small polyethylene catheter inserted into the right lateral ventricle of the brain. Intact fasted and fed rats showed an increase of 82.3% and 67.2%, respectively, in colonic spike-burst frequency when placed for 30 minutes in a box in which they had previously received electrical shocks in their feet. Intracerebroventricular administration of corticotropin-releasing factor (0.5 μg/kg) mimicked the effects of mental stress and increased cecocolonic spikeburst frequency by 75.8%. The specific corticotropin-releasing factor receptor antagonist α-helical CRF9–41 given intracerebroventricularly (5 μ/kg) prevented both the effects of mental stress and corticotropin-releasing factor (0.5 μg/kg intracerebroventricularly) on colonic spike-burst frequency. In contrast, diazepam (0.5 mg/kg IM) suppressed colonic hypermotility induced by mental stress but not that resulting from intracerebroventricular injection of corticotropin-releasing factor (0.5 (μg/kg). Increased colonic spike-burst frequency induced either by stress or by central administration of corticotropin-releasing factor was not prevented by hypophysectomy. It was concluded that mental stress increases the frequency of cecocolonic spike-burst activity and that these effects are related to the central release of corticotropin-releasing factor because they are blocked by a corticotropin-releasing factor antagonist and reproduced by intracerebroventricular administration of corticotropin-releasing factor. Moreover, mental stress-induced colonic motor alterations are mediated by the autonomic nervous system rather than by the hypothalamopituitary axis because they are not abolished by hypophysectomy.

Role of hypothalamic cholecystokinin octapeptide in the colonic motor response to a meal in rats

The effects of hypothalamic microinfusions of cholecystokinin octapeptide and its antagonist L364,718 on cecocolonic myoelectrical activity were evaluated by electromyography in fasted and fed rats. The rats were chronically fitted with electrodes implanted on the cecum and proximal colon and cannulas placed bilaterally in either the ventromedial or lateral hypothalamus. In fasted rats, microinfusion of cholecystokinin octapeptide (10 ng/kg) into the ventromedial hypothalamus increased the spikeburst frequency of the cecum and the colon by 45.6% and 43.7%, respectively, during the 30-minute period after treatment. The injection of cholecystokinin octapeptide (10 ng/kg) into the lateral hypothalamus had no effect on either cecal or colonic motility. Feeding increased the frequency of cecal and colonic spike bursts by 52.1% and 50.1% for 30 minutes postprandially. When infused bilaterally into the ventromedial hypothalamus 10 minutes before feeding, L364,718 (1 or 5 μg/kg) abolished the increase of the frequency of cecal and colonic contractions induced by the meal. Infused into the lateral hypothalamus at similar dosages, L364,718 had no effect on the postprandial enhancement of cecocolonic motility. Increase of cecocolonic spikeburst frequency induced by feeding or by cholecystokinin octapeptide injected into the ventromedial hypothalamus was abolished by previous intracerebroventricular but not intraperitoneal administration of atropine (1 (μg) and 4-diphenylacetoxy-N-methylpiperidine (1 μg), a selective muscarinic M2-receptor antagonist. In contrast, pirenzepine (1 (μg, intracerebroventricularly) did not significantly reduce the meal- or cholecystokin octapeptideinduced increase in cecal and colonic motility. These results suggest that, in rats, (a) cholecystokinin octapeptide is involved in the generation of the cecocolonic motor response to a meal and these effects are mediated through cholecystokinin octapeptide receptors located in the ventromedial hypothalamic nuclei, and (b) these postprandial colonic motor changes involve central cholinergic activation through muscarinic M2 receptors.

Choledochoduodenal flow: Effect of the sphincter of Oddi in opossums and cats

The aim of this study was to test in vivo (a) whether the sphincter of Oddi acts as a resistor or also as a pump, (b) the effect of an IV infusion of cholecystokinin (CCK) on choledochoduodenal flow, and (c) the ability of the choledochoduodenal junction to prevent duodenobiliary reflux in two animal species, opossums (n = 11) and cats (n = 8). Opossums were implanted with bipolar electrodes on the sphincter of Oddi and the adjacent duodenum. Cats were not. Experiments were performed in vivo using a propulsion evaluation system to test whether the Sphincter of Oddi was able to pump fluid from the bile duct to the duodenum against pressure gradients. In 5 opossums and 4 cats, choledochoduodenal flow was evaluated during the IV infusion of CCK (20 ng · kg−1 · min−1). The opossum sphincter of Oddi moved fluid against duodenal pressure gradients of 6–45 cm H2O. The spike-burst frequency (6.4 ± 1.7 min−1) was maximal at peak bile duct pressures and decreased as bile duct pressure decreased (4.9 ± 1.6 min−1; P < 0.001). Pressure pulses in the bile duct were observed at a frequency that correlated with sphincter of Oddi spike-burst frequency (r = 0.84; P < 0.001). In cats, choledochoduodenal flow occurred only along a hydrostatic gradient; the sphincter of Oddi never acted as a pump but only as a resistor. Infusion of CCK significantly increased the frequency of sphincter of Oddi contractions in opossums, but the transfer of fluid from bile duct to duodenum was significantly reduced. In cats, the rate of fluid flow from the bile duct to the duodenum during CCK infusion did not differ from control values. Reflux of duodenal fluid into the biliary tree was never observed, even at duodenal pressures as high as 100 cm H2O. In conclusion, in vivo, the sphincter of Oddi is able to pump fluid from the bile duct to the duodenum against a pressure gradient in opossums, but, in cats, choledochoduodenal flow requires a bilioduodenal pressure gradient. The increase in sphincter of Oddi contraction frequency induced by CCK in opossums resulted in a decrease in active transsphincteric flow. Duodenobiliary reflux could not be elicited in opossums and cats under the conditions of these experiments.

Time-series analysis of myoelectric cycling of sphincter of Oddi: evidence of cycling during fed state

The sphincter of Oddi (SO) in the fasted opossum exhibits spontaneous cyclic spikeburst activity that is temporally related to the interdigestive migrating myoelectric complex (MMC) of the small intestine. After feeding, the cyclic activity is apparently disrupted. Our aim was to use time-series analysis to mathematically describe the periodic behavior of the fasted state and to determine whether this periodicity is present after feeding. Five opossums were chronically prepared with bipolar electrodes secured to the SO. With the animals fasted and conscious, myoelectric activity was recorded for at least two MMC cycles after which they were fed 170 kcal of cream. Spikeburst frequency data were analyzed by fast Fourier transform (FFT) and by digital band-pass filtering. Results from FFT analysis showed an intense low-frequency peak during the fasted state which persisted but was markedly depressed during the fed state. Analysis of the data after filtering also showed persistent sinusoidal activity at the MMC frequency after feeding, although the waveform was significantly depressed by both peak-to-peak amplitude and root mean square amplitude analysis. Recovery to normal fasting cyclic behavior with recovery of both FFT and filtered data was observed. We conclude that in the opossum the cyclic nature of the SO myoelectric activity observed during the fasted state persists after feeding, but is inhibited and masked by an increase in overall spikeburst activity.

Inhibitory effects of neuropeptide Y (NPY) on CRF and stress-induced cecal motor response in rats

The effects of NPY on CRF and stress-stimulated cecal motility were investigated by electromyography in rats. Intracerebroventricular (ICV) injection of NPY at 300 ng/kg significantly reduced the frequency of spike burst during the first 15 minutes after its administration while no effects was observed at a lower dose (150 ng/kg). Exposure to mental stress (MS) increased significantly (p<0.01) during 45 minutes, the frequency of cecal spike bursts. NPY (300 ng/kg) injected ICV, 30 minutes prior to MS periods abolished the excitatory effects induced by stress. The frequency of cecal spike bursts was also increased during the first 15-minutes following ICV injection of CRF (300 ng/kg). Prior (5 min) ICV administration of NPY (150 ng/kg) abolished the stimulatory effect of CRF on cecal motility. It is concluded that central administration of NPY suppresses the stress-induced cecal motor response probably by inhibiting the pathways involved in CRF mediation of these effects.

Action of Guar Gums on the Viscosity of Digestive Contents and on the Gastrointestinal Motor Function in Pigs

The apparent viscosity of three test meals containing 6% of different guar gums was measured in the gastric, duodenal and jejunal contents and related with the gastrointestinal myoelectric activity and transit time in pigs. The motility index (mV/min) and the spike burst frequency (number of spike bursts/min) were closely related to the digesta viscosity: they were significantly increased by most viscous contents in stomach and small intestine. This effect was associated with an increase in the orocecal transit time of liquids and solids.

The effect of Strongylus vulgaris larvae on equine intestinal myoelectrical activity

The myoelectrical activity of the ileum, caecum and large colon was monitored from Ag-AgCl bipolar recording electrodes in four conscious 'parasite-naive' weanling foals. All foals were inoculated with 1000 infective 3rd-stage Strongylus vulgaris larvae and alterations to the myoelectrical activity observed. The frequencies of caecal and colonic spike bursts increased significantly in all post infection periods coinciding with assumed larval penetration into the intestinal mucosa and migration through the vasculature. Peaks in caecal and colonic activity occurred at Days 1 to 5 post infection. In the caecum, peaks occurred again at Days 15 and 31 post infection, preceding similar rises in colonic spike burst frequency at Days 19 and 35. Longer term changes indicated a return towards pre-infection levels of activity suggesting smooth muscle adaptation to decreased blood flow. The analysis of caecal and colonic spike burst propagation indicated that the increases in burst frequency were not attributable to an increase in the propagation of spike bursts in any particular direction, but rather to proportional increases in all directions of activity. There was a slight decrease in the simple ileal spike burst frequency immediately post-infection. None of the experimental animals exhibited signs of abdominal pain during the trial, and there was no evidence of bowel infarction at post mortem examination despite the presence of severe parasite-induced arterial lesions. The results suggest that increased caecal and colonic motility is an important host response in susceptible foals exposed to S. vulgaris larvae.

Characterization of substance P effects on sphincter of Oddi myoelectric activity

We examined the effects of substance P (SP) on the myoelectric activity of the opossum sphincter of Oddi (SO). Myoelectric data from the SO in five adult opossums were recorded using thin stainless steel electrodes and computer-assisted analog-to-digital conversion. In fully awake and conscious animals, baseline spikeburst activity during phase I of the MMC occurred at a frequency of 28.6 ± 3.1 spikebursts (SB) per 20-min period. Intravenous infusion of graded doses of substance P (from 0.5 to 8.0 μg/kg) stimulated SO myoelectric activity in a dose-related manner (from 80 ± 8 to 235 ± 11 SB/20 min, respectively, P < 0.05 when compared to baseline). The effect of substance P on SO myoelectric activity was antagonized by administration of the H 2-blocker, cimetidine (92.0 ± 6.1 vs 48.2 ± 7.0, n = 5, P < 0.05). Administration of the antimuscarinic drug atropine only slightly affected the SO spikeburst frequency when infused prior to SP (73.0 ± 10.4 vs 70.8 ± 8.2, P > 0.05). We conclude that SP stimulated the SO spikeburst frequency in a dose-dependent fashion. Cimetidine markedly inhibited the response of the SO to SP but atropine did not. The excitatory effect of substance P on the opossum SO is mediated at least in part by a histaminergic, noncholinergic pathway.

Excitatory effects of opiates on the spontaneous EMG activity in pigeon oesophagus

The effects and the mechanism of action of morphine, methionine-enkephalin and leucine-enkephalin were examined in transverse muscular strips from pigeon oesophagus. All the opiates produced a concentration-dependent excitatory effect on the spontaneous EMG activity, characterized mainly by an increase in the spike burst frequency. The maximal excitatory response to morphine and opioid peptides was fully antagonized by naloxone and tetrodotoxin, significantly reduced by atropine and it was not affected by guanethidine pretreatment. Treatment of pigeons with reserpine abolished the excitatory effects induced by opiates. The above results suggest the existence of specific opioid receptors in pigeon oesophagus. Opiates have no direct action on smooth muscle cells, increasing the EMG activity via excitatory both cholinergic and non-adrenergic non-cholinergic neurons. The hypothesis of a possible involvement of serotonergic interneurons might be advanced.

Effects and mechanisms of action of motilin on the cat sphincter of Oddi

The effects of motilin on gallbladder and sphincter of Oddi motor activity and transphincteric flow were studied in the cat in vivo. Motilin at doses of up to 1 μg/kg had no effect on gallbladder motility. Increasing doses of intraarterial motilin (32–256 ng/kg) caused an increase in tonic pressures and in the force of phasic contractions of the sphincter of Oddi (p < 0.001). Simultaneous measurements of myoelectric activity and transphincteric flow showed that motilin caused an increase in the frequency of spike bursts with a concomitant dose-dependent decrease in flow (p < 0.001). The action of motilin was unaffected by extrinsic denervation (cervical vagotomy or splanchnicectomy), hexamethonium, and propranolol. Atropine, methysergide, or phentolamine partially blocked the excitatory effect of motilin (p < 0.05), whereas tetrodotoxin, a combination of atropine and methysergide, or naloxone completely blocked its effects (p < 0.001). It is concluded that (a) motilin decreases sphincter of Oddi flow by increasing its motor activity and (b) motilin activates an intramural excitatory pathway that appears to consist of opiate, serotonergic, and cholinergic neurons.

Changes in jejunal myoelectrical activity during exercise in fed untrained dogs.

Seven female dogs (15-20 kg) were instrumented with seven bipolar electrodes sutured at 3-cm intervals to the serosal surface of the proximal jejunum and were exercised at different intensities and durations on a motor-driven treadmill. Slow-wave frequency increased (P less than 0.05) from preexercise control during prolonged (90 min) exercise and during recovery after short-term exercise (30 min) at 70% heart rate reserve (HRR). These changes were associated with an increase in core temperature. Spike-burst frequency (SBF) increased (P less than 0.05) with moderate exercise (50% HRR), but the magnitude was small. When exercise was extended beyond 30 min and during all recovery periods, SBF decreased significantly. Exercise produced migrating myoelectrical complexes in three experiments and less dramatic pattern changes characterized as "clustered contractions" (regular spike bursts preceded and followed by the absence of spike bursts) in at least nine other experiments. We conclude that exercise does alter jejunal myoelectrical activity, but myoelectrical patterns may be more important in explaining exercise-induced gastrointestinal symptoms than changes in spike-burst frequency or duration.