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Effect of rabbit antimotilin serum on myoelectric activity and plasma motilin concentration in fasting dog.

It is known that a cyclic increase in plasma motilin concentration occurs during the interdigestive state of dog and the increase coincides with migrating myoelectric complexes (MMCs) of the antrum as well as proximal duodenum. The purpose of the present study is to determine the role of endogenous motilin in the occurrence of MMCs in 10 dogs prepared with a gastric cannula and platinum monopolar electrodes in the gastric antrum, duodenum, jejunum, and ileum. After recording at least two consecutive cycles of MMCs from the proximal duodenum, each dog received an intravenous infusion of highly specific rabbit antimotilin sera in varying doses ranging from 3.5 to 15 ml for a period of 60 or 90 min. During the motility recording period ranging from 6 to 30 h following the administration of the antimotilin serum, several changes in the motility were observed. 1) The occurrence of MMCs in the antrum, duodenum, jejunum, and ileum was temporarily interrupted for varying periods depending on the individual dog studied and the amount of antiserum administered. When the higher dose of antimotilin was administered, a more profound and prolonged inhibition occurred. 2) Phase I activity rarely occurred. Instead, a phase II-like activity continued throughout the recording period. 3) MMCs in the jejunum or ileum occurred at irregular intervals without aboral propagation of MMCs from the duodenum or jejunum. 4) The plasma motilin concentration decreased to levels lower than that observed during phase I of the duodenum and exhibited no cyclic increase until the MMCs reappeared in the proximal duodenum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Relation between intestinal motility and mesenteric blood flow in the conscious dog.

Blood flow in a mesenteric artery and electrical activity of the corresponding segment of jejunum or ileum were simultaneously measured in eight conscious dogs. Each was fitted chronically with an electromagnetic flow probe and transparietal electrodes. In some dogs an intestinal cannula was placed cephalad to the segment investigated. Continuous 24-h records were obtained in each dog receiving a daily meal. Jejunal blood flow increased after the meal, decreased progressively during the postprandial period (7-12 h), and then exhibited cyclic variations associated with the occurrence of migrating myoelectric complexes (MMCs) during the next 6-10 h. The ileal blood flow increased, then remained high and nearly constant during the postprandial disorganization of the MMC pattern, and exhibited cyclic variations associated with all MMCs even when the dog was fasted for 48 h. Cyclic variations in blood flow were abolished when the intestinal content was drained through the cannula. It is concluded that in the conscious dog the blood flow profile in a mesenteric artery is associated with the motor profile of the segment. This association is due to the presence of digestive matter, probably nutrients in the jejunum and bile in the ileum.

Animals↗

Role of prostaglandins in control of intestinal motility.

Intestinal myoelectric activity was measured in four conscious dogs with implanted monopolar electrodes after administration of prostaglandins (PG) and indomethacin (Indo), a potent inhibitor of PG biosynthesis. PGE2 and PGI2 given intravenously caused a dose-dependent decrease in the frequency of the migrating myoelectric complex (MMC) in fasted dogs and in postprandial spike activity in fed animals. In contrast, PGF2 alpha interrupted the MMC and caused a fedlike pattern in fasted dogs and did not affect the postprandial spike activity. Similar effects were observed after intra-arterial infusion of PGs. PGE2 and PGI2 infused into the superior mesenteric artery caused a dose-dependent inhibition of the fasted and postprandial pattern of myoelectric activity of the small bowel, whereas PGF2 alpha blocked the MMC and increased spike activity. Indo injected in a single intravenous dose caused a significant reduction in the MMC interval, and Indo infused intravenously in a constant dose induced fedlike motility pattern in fasted dogs but had little effect on the postprandial activity in these animals. This study demonstrates that exogenous PGs of E and I series administered intravenously or intra-arterially inhibit intestinal motility, whereas PGF2 alpha has opposite effects. The finding that Indo increases intestinal motility indicates that endogenous PGs are important in the physiological control of intestinal motility.

Animals↗

Variability of lower esophageal sphincter pressure in the fasted unanesthetized opossum.

The opossum has served as a useful animal model for in vivo studies of lower esophageal sphincter (LES) function. Previous investigations, however, have been confined to studies on anesthetized animals. In 10 opossums we investigated LES pressure during fasting cycles of the gastrointestinal migrating myoelectric complex (MMC) and examined the influences of anesthesia and feeding on LES pressure. Intraluminal pressure from the esophageal body, LES, and gastric antrum was recorded by a manometric assembly that incorporated a sleeve device. Myoelectric activity was recorded from the gastric antrum and duodenum via implanted electrodes. MMCs were readily recorded from all animals. MMC cycle length was 86 +/- 2.9 (SE) min. The LES exhibited cyclic changes in intraluminal pressure that occurred in synchrony with the gastric MMC cycle. During phase I of the gastric MMC cycle, LES pressure was essentially stable, although intermittent spontaneous oscillations at 3-4/min were sometimes noted. Forceful phasic LES contraction started during phase II of the gastric MMC, became maximal during phase III, and disappeared during phase I. The MMC-related phasic LES contraction occurred at a maximal rate of 1.4 +/- 0.05/min with amplitudes of 60-150 mmHg and were temporally associated with spike bursts and contractions in the gastric antrum. Pentobarbital sodium-induced anesthesia abolished MMC-related phasic LES activity and caused a transient rise in basal sphincter pressure. Phasic LES activity was also inhibited by atropine and feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗

Gastrointestinal myoelectric activity in conscious guinea pigs.

Myoelectric activity was recorded from the gastric antrum and small intestine of conscious, unrestrained guinea pigs using bipolar Ag-Ag chloride electrodes that had been previously implanted under pentobarbital sodium/Innovar anesthesia. In fasted guinea pigs, the migrating myoelectric complex (MMC) was recorded from the small intestine and was observed to propagate aborally at a speed that declined with distance from the pylorus (range of speeds of the front of phase 3: 17.5 cm/min in the duodenum to 4.1 cm/min in the ileum). The complex was not disrupted by feeding but occurred less frequently in the freely fed state (82-min cycle period in the fasted state versus 139 min in the fed state). The complex started in the duodenum and was accompanied by a brief (6.3 +/- 0.9 min) period of inhibition of antral myoelectric activity. Slow waves were also recorded from the gastric antrum (10.3 +/- 1.3/min) and the small intestine. The frequency of intestinal slow waves was uniform along the length of the bowel (26.2 +/- 1.3/min in the duodenum to 24.7 +/- 1.3/min in the ileum). It is concluded that the guinea pig is similar to other mammalian species, so far examined, in its pattern of gastrointestinal myoelectric activity.

Action Potentials↗

Regulation of fasting canine duodenal bile acid delivery by sphincter of Oddi and gallbladder.

Bile delivery into the duodenum during fasting is rhythmic and coordinated with the migrating myoelectric complex (MMC). To determine the role of the sphincter of Oddi (SO) and gallbladder (GB) in regulating duodenal bile acid delivery, three dogs were surgically prepared with a duodenal cannula and eight bipolar electrodes implanted from the duodenum to the terminal ileum. Fasting intestinal myoelectric activity was recorded during continuous intravenous infusion of [14C]taurocholic acid (TCA). Duodenal delivery of TCA was quantitated under four conditions: indirectly with the SO intact monitoring output with duodenal marker perfusion and directly with the SO cannulated and draining at three levels to vary outflow resistance (5 cm above, level with, or 20 cm below the SO). GB filling or emptying represented the algebraic difference between hepatic secretion (equal to the intravenous infusion rate) and rate of TCA delivery into the duodenum. With the sphincter intact the rate of bile acid delivery averaged one-half the intravenous infusion rate at 0-40% of the MMC cycle period, rose to exceed the intravenous infusion rate at 60-70% of the cycle period, and then fell to lower levels before the next MMC began. The pattern of delivery was identical with the SO cannulated, but the rate and percent infused TCA delivered into the duodenum depended significantly (P less than 0.01) on outflow resistance. They were least with the reservoir elevated 5 cm, intermediate when level, and greatest when 20 cm lower. Thus, duodenal bile acid delivery and GB filling or emptying during fasting were cyclically coordinated with the MMC. Peak rates of duodenal bile acid delivery and active GB emptying occur at 70% of the duodenal cycle period. Elimination of the SO does not eliminate the pulsatile pattern of fasting duodenal bile acid delivery, but outflow resistance determines the quantities delivered into the duodenum or stored in the GB. Thus, during the interdigestive period the net effect of SO function does not differ from a constant output resistance favoring the partition of hepatic biliary secretion into the GB and away from the duodenum, while the pulsatile pattern of duodenal bile acid delivery associated with the MMC results from cyclic active contraction of the GB.

Ampulla of Vater↗

Contraction pattern of opossum gallbladder during fasting and after feeding.

Our major aims in this study were to determine in unanesthetized opossums the gallbladder volume, pressure, and tone during fasting as well as after feeding, model the kinetics of changes in gallbladder volume, and correlate gallbladder contractility with concurrent spike burst activity in the upper gastrointestinal tract and sphincter of Oddi (SO). In 10 animals, we implanted electrodes on the gastric antrum, duodenum, SO, and jejunum. An indwelling catheter monitored gallbladder pressure and volume. In two animals, a force transducer sutured to the gallbladder wall monitored gallbladder tone. In each animal, fasting migrating myoelectric complexes (MMCs) were recorded in the stomach and small bowel. Cyclic changes in SO spike bursts occurred in synchrony with the MMCs. During fasting, gallbladder pressure, tone, and volume showed cyclic variations. During the second half of the duodenal MMC cycle, the gallbladder exhibited phasic as well as tonic contractions associated with net gallbladder emptying, whereas during the first half of the cycle the gallbladder relaxed and refilled. Minimal gallbladder volume during the MMC cycle averaged 4.8 +/- 0.7 (SE) ml compared with a maximal volume of 7.0 +/- 0.9 ml. Decreases in gallbladder volume occurred as an exponential function, whereas increases in gallbladder were linear. After feeding, the gallbladder underwent a sustained tonic contraction, without superimposed phasic contractions. Decreases in gallbladder volume occurred exponentially to a residual volume of 2.0 +/- 0.5 ml. Net postprandial gallbladder emptying was maximal by 40 min; then the volume remained unchanged for 2-3 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of duodenal bile acid delivery on fasting intestinal motor activity.

Fasting duodenal bile acid delivery is pulsatile and is cyclically coordinated with the duodenal migrating myoelectric complex (MMC). To determine whether duodenal bile acid delivery influences the duodenal cycle period (CP) of the MMC or the intensity of duodenal motor activity, three dogs were prepared with a duodenal cannula, permitting cannulation of the common bile duct, duodenal infusion, and manometry. CP was measured with the enterohepatic circulation intact and after the common bile duct was cannulated to divert endogenous bile from the duodenum during continuous duodenal infusion (1.6 ml/min) of 0, 2.5, 12.5, or 25 mM sodium taurocholic acid in 154 mM NaCl. During a second protocol with the enterohepatic circulation intact, a control and subsequent CP were measure, and a pulse (1 ml/min for 10 min) of pooled dog bile (112 mM total bile acids) or 0, 20, 80, or 140 mM sodium taurocholic acid in 154 mM NaCl was infused into the duodenum at 40% of the second CP (as estimated from control CP). A motility index was calculated for an interval commencing at 40% of the control CP and at the start of pulse infusion in the succeeding CP. There was no significant difference in CP with the enterohepatic circulation intact compared with that during continuous duodenal infusion of sodium taurocholic acid. There was no significant change in CP or motility index after premature pulse infusion of sodium taurocholic acid or pooled dog bile. Variation in duodenal bile acid delivery did not modulate intensity of duodenal motor activity or cycling of the MMC.

Animals↗

Physiological characteristics of ovine pyloric sphincter.

A special probe was validated to record in situ pyloric sphincter activity by changes in fiber-optic light transmission and sleeve pressure associated with the propagation of antroduodenal contractions, the onset of the phase of regular spiking activity (RSA) of the migrating myoelectric complex, the RSA-like events elicited by duodenal acidification, and the pharmacological stimulation of the gastroduodenal junction. Rapid changes in light transmission associated with antroduodenal contractions were super-imposed on slow variations, suggesting the existence of both phasic and tonic components in pyloric sphincter activity. The phasic activity coincided with isolated closures of the pyloric orifice, closures associated with antral or duodenal bulb contractions, and with long-lasting rhythmic closures during the development of the RSA phase. The resting tone increased during antral and/or duodenal stimulation and by feeding "appetizers" but decreased during antroduodenal quiescence and at the onset of general anesthesia. It is concluded that the ovine pylorus predominantly exists in a state of low resting tone but can act as a true sphincter with both inherent tonic and phasic activity.

Animals↗

Role of GIP and insulin in glucose-induced changes in intestinal motility patterns.

This study was designed to correlate the intestinal motility patterns with duodenal glucose loads and the increments in plasma gastric inhibitory peptide (GIP) and insulin levels after these loads or after the administration of exogenous hormones in conscious dogs. Isotonic glucose instilled intraduodenally at lower loads (5.2-42.4 mmol/h) only caused a moderate increase in spike activity, but at higher loads (84.8 mmol/h) it disrupted migrating myoelectric complexes (MMC), being accompanied by marked increases in plasma GIP and insulin levels. Duodenal loads of isotonic mannitol resulted in similar motility changes but without alteration in plasma GIP or insulin. Hypertonic glucose (20%) in the duodenum also caused an increase in spike activity, and at higher loads (72 mmol/h or higher) it disrupted MMCs and resulted in significant increments in plasma GIP and insulin levels. Physiological doses of exogenous GIP (25-400 pmol X kg-1 X h-1) or insulin (12-24 mU X kg-1 X h-1) did not affect the motility pattern, but at higher doses, raising plasma hormone over the levels occurring after a mixed meal, GIP (400 pmol X kg-1 X h-1) increased significantly the MMC interval, whereas insulin (48-96 pmol X kg-1 X h-1) induced a fed-like motility pattern. Intravenous 20% glucose (72 mmol/h) caused a marked rise in plasma insulin (but not GIP) levels but failed to affect the intestinal motility as did 20% mannitol infused intravenously in the same dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Electrical control activity of the lower esophageal sphincter in unanesthetized opossums.

We recorded lower esophageal sphincter (LES) pressure and myoelectrical activity concurrently from the esophagus, LES, stomach, and proximal small intestine in unanesthetized opossums. LES electrical activity was characterized by almost continuous, spikelike oscillations at 15-40/min, which were accompanied by minicontractions 5-15 mmHg in amplitude. Basal LES pressure, however, did not depend on electrical oscillations. The LES exhibited cyclic changes in pressure and electrical activity synchronous with gastric contractions associated with the migrating myoelectric complex (MMC). During phase I, the LES pressure was stable and its electrical activity showed continuous low-amplitude (less than 0.3 mV) oscillations at a rate of 20 +/- 2 per min. During phases II and III of MMC-related gastric activity, the LES developed strong phasic contractions, while the electrical oscillations grouped into clusters with an increased rate (32 +/- 1 per min) and amplitude (0.4-0.8 mV), each cluster corresponding to a phasic contraction. Feeding, pentobarbital, and cholinergic blockade abolished MMC-related LES activity and resulted in a steady rate of LES electrical oscillations. LES relaxation induced by swallows or esophageal balloon distention abolished the LES electrical oscillations. Increases in LES pressure induced by pharmacological and hormonal stimulation correlated with concurrent increases in the rate of electrical oscillations. We conclude that the opossum LES has a unique pattern of electrical activity that differs from the electrical activity recorded from smooth muscle elsewhere in the gastrointestinal tract. This electrical activity is a form of control wave associated with a minicontraction. Phasic LES contractions during the intestinal MMC cycle may result from an increase in the rate and amplitude of the LES electrical control waves and fusion of minicontractions.

Anesthesia↗

Myoelectric activity of the small intestine during morphine dependence and withdrawal in rats.

We investigated the effect of morphine dependence on the migrating myoelectric complex (MMC) of the small intestine, whether bacterial overgrowth developed in morphine-dependent rats, and the effect of naloxone, 0.5 mg/kg sc, and methylbromide naltrexone, 1.0 mg/kg sc, a peripheral opioid antagonist, on the MMC in morphine-naive and morphine-dependent rats. We also evaluated intestinal motility during naloxone-induced withdrawal in animals pretreated with clonidine, 100 micrograms/kg sc. Intestinal myoelectric activity was monitored by four indwelling electrodes in unanesthetized, fasted rats. D-[14C]xylose breath tests were performed before and after morphine-pellet implantation to evaluate the presence of bacterial overgrowth of the small intestine. Naloxone had no effect on myoelectric activity of the small intestine in morphine-naive rats. Cycling activity fronts were present in morphine-dependent animals, but there was a significant prolongation of activity front periodicity and slowing of the propagation velocity. No significant increase in 14CO2 excretion was noted in the morphine-dependent rats. After injection of naloxone, the morphine-dependent rats had a marked increase in spike activity with no identifiable activity fronts for 89 +/- 8 min. Similarly, methylbromide naltrexone disrupted activity fronts, but for a significantly shorter period. Clonidine prevented the marked increase in spike activity that occurred during naloxone-induced withdrawal. We conclude from our studies that myoelectric activity of the small intestine develops incomplete tolerance to morphine; bacterial overgrowth is not a feature of morphine dependence in the rat; alterations of intestinal myoelectric activity are a component of the opiate withdrawal syndrome, and they appear at least partially mediated by a peripheral mechanism that can be suppressed by an alpha 2-adrenergic agonist.

Animals↗

Influence of motilin and cholecystokinin on sphincter of Oddi and duodenal mobility.

The sphincter of Oddi and the duodenum exhibit cyclical activity in phase with the migrating myoelectric complex. Both motilin and cholecystokinin have been shown to modulate gastrointestinal and sphincter of Oddi motility. However, previous studies have not monitored the effects of these hormones on simultaneously recorded sphincter of Oddi and duodenum pressures. The present investigation was undertaken, therefore, to determine the influence of both motilin and cholecystokinin on simultaneously recorded sphincter of Oddi and duodenal motility. In seven anesthetized prairie dogs, a triple-lumen, side-hole, pressure-monitored perfusion catheter was positioned with the proximal port in the sphincter of Oddi and the distal port in the duodenal lumen. Sphincter of Oddi and duodenal motility was recorded before and during 20-min infusions of motilin and cholecystokinin octapeptide (CCK-8) at 1, 10, and 100 ng.kg-1.min-1. Both hormones produced dose-related increases in sphincter of Oddi and duodenal motility. No response was observed with either hormone at 1 ng.kg-1.min-1. At 10 ng.kg-1.min-1, the duodenum was slightly more sensitive to motilin than to CCK-8, while the sphincter of Oddi was equally affected by both hormones. At 100 ng.kg-1.min-1, both hormones stimulated the sphincter of Oddi and the duodenum equally. These data indicate that in the prairie dog, both motilin and cholecystokinin stimulate sphincter of Oddi and duodenal motility.

Ampulla of Vater↗

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.

Animals↗

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.

Ampulla of Vater↗

Prostaglandins and modulation of small bowel myoelectric activity.

We explored the effects of prostaglandins (PG) F2 alpha and E2 on the motor and myoelectric activity of the small intestine using closed intra-arterial injections in conscious chronically instrumented dogs. PGF2 alpha (0.125-5 micrograms) and PGE2 (1-10 micrograms) were injected via a T tube into a branch of the superior mesenteric artery perfusing a 15-cm segment of jejunum. Experiments were performed on four dogs in which the recording devices had been implanted above, below, and within the perfused segment. PGF2 alpha given during phase I of the migrating myoelectric complex cycle induced phasic contractions in the perfused segment of intestine in a dose-dependent manner. Atropine (50-100 micrograms), hexamethonium (15 mg), or TTX (10-15 micrograms) administered before the injection of PGF2 alpha failed to inhibit the effects of PGF2 alpha. In contrast pretreatment of the perfused segment with verapamil (2.5 mg) or PGE2 (1-5 micrograms) abolished the effects of PGF2 alpha. Moreover, PGE2 injected 5 min after the administration of PGF2 alpha inhibited the PGF2 alpha-induced contractions. Administration of PGE2 alone (3-10 micrograms) before the arrival of phase III activity in the perfused segment abolished phase III from this segment of intestine. Our studies indicate opposing effects of PGF2 alpha and PGE2 on small intestinal myoelectric and contractile activities. PGF2 alpha has a direct excitatory effect on the intestinal smooth muscle, which is calcium channel dependent but independent of intrinsic nerves. PGE2 has an inhibitory effect both on the spontaneous and PGF2 alpha-induced small intestinal myoelectric and contractile activity.

Animals↗

Neural modulation of canine duodenal bile acid delivery in the interdigestive and postprandial periods.

The neural modulation of gallbladder filling-emptying and duodenal delivery of canine hepatic biliary output was studied in conscious dogs using transient cold blockade or transection of the cervical vagosympathetic nerves previously isolated in skin loops on either side of the neck. Gallbladder filling-emptying was defined as the algebraic difference between a steady-state rate of hepatic secretion [established by a continuous intravenous infusion of [14C]taurocholic acid (TCA)] and the duodenal rate of delivery of [14C]TCA (measured by duodenal marker perfusion). Duodenal motility was recorded manometrically. Experiments in the fasted and fed state were performed under control conditions, during cold blockade, and after transection of the cervical vagosympathetic nerves. Under control conditions: 1) during fasting, the majority of hepatic [14C]TCA output was stored in the gallbladder during the first half of the migrating myoelectric complex (MMC). An increased rate of duodenal delivery and partial gallbladder emptying occurred before phase III of the MMC. 2) Feeding induced an immediate increase in duodenal bile acid delivery and gallbladder emptying. After cold blockade or transection: 1) partial gallbladder emptying before phase III of the MMC was abolished. 2) The immediate postprandial increase in duodenal bile acid delivery and gallbladder emptying was abolished even when the animal received a continuous duodenal infusion of the duodenal aspirate of another fed animal (to control for the effect of impaired gastric emptying after cold blockade). In addition, cold blockade significantly reduced the effect of an exogenous infusion of cholecystokinin octapeptide on gallbladder emptying. These results suggest that neurons in the canine cervical vagosympathetic nerves play a major role in the regulation of rhythmic partial emptying of the gallbladder in the interdigestive period, coordinate a cephalic phase of postprandial gallbladder emptying, and are important in mediating the effects of cholecystokinin on the gallbladder during the gastric and enteric phases of postprandial gallbladder emptying.

Animals↗

Effect of splanchnectomy on jejunal motility and fos expression in brain stem after intestinal anaphylaxis in rat.

This study was to determine whether alterations in jejunal motility observed after antigen challenge of sensitized rats occurred after extirpation of the celiac-superior mesenteric ganglia. Hooded-Lister rats were prepared with an intact or extirpated celiac-superior mesenteric ganglion, an isolated Thiry-Vella loop of ileum for instillation of antigen, and jejunal electrodes for myoelectric recording. Animals were sensitized by injection of 10 microg egg albumin (EA, ip), and specific anti-EA IgE titers were determined to be >1:64. In both control and splanchnectomized rats, normal fasting migrating myoelectric complexes (MMC) were observed before challenge with EA. MMCs were disrupted, and diarrhea was observed immediately after EA challenge of control but not splanchnectomized animals. Brain stems were removed and processed for Fos immunoreactivity. The absence of perivascular neuropeptide Y immunoreactivity in the submucosa was used to confirm the success of splanchnectomy. The number of Fos-immunoreactive neuronal nuclei was significantly reduced in the brain stem after splanchnectomy. Thus the mesenteric sympathetic ganglia are an integral part of the extramural neuronal pathways required for altered motility in this model of intestinal anaphylaxis.

Anaphylaxis↗