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Recurrent Crohn's disease in the duodenum and jejunum following extensive small bowel resection and jejunocolonic anastamosis: radiologic findings in twenty-five patients.

BACKGROUND: To evaluate the radiologic features of recurrent Crohn's disease after extensive enteric resection and jejunocolostomy. METHODS: We reviewed the small bowel studies of 25 patients with recurrent enteritis and less than 125 cm of jejunum following enteric resection and jejunocolostomy and the studies of 27 patients with jejunitis in an intact jejunum. RESULTS: Twenty-three patients with recurrences had neoterminal jejunitis, six under 10 cm, 10 over 10 cm and continuous, and seven with skip lesions (six jejunal, one duodenal). Two had isolated jejunitis or duodenitis. Three with continuous disease had lengthy recurrences. Enteritis showed only one or two abnormalities in 12 of 25 patients with recurrences and in two of 27 with disease in the intact jejunum. Recurrent jejunitis and jejunitis in the intact jejunum showed similar frequencies of mucosal thickening, strictures, ulceration and its complications, skip lesions, sacculation, obstructive dilatation, featureless mucosa, and polyps, and significantly different frequencies only of mesenteric masses. Recurrent jejunitis and terminal ileitis showed significantly different frequencies of mucosal thickening, strictures, ulceration and its complications, skip lesions, sacculation, obstructive dilatation, and mesenteric masses, and similar frequencies only of a featureless mucosa. CONCLUSIONS: The neoterminal jejunum is the most common site of recurrence and the only site in almost 25%. Jejunitis remote from the fecal stream is also frequent, but duodenitis is not. Recurrences are seldom extensive and often show only one or two radiographic findings. The frequencies of most lesions in recurrent jejunitis do not differ significantly from those in jejunitis in the intact jejunum but do differ from those in terminal ileitis.

Adolescent↗

Nitric oxide mediates inhibitory nerve input in human and canine jejunum.

BACKGROUND: Nitric oxide (NO) may be an inhibitory neurotransmitter in the intestinal muscle. The present study examined its role in human and canine jejunum. METHODS: Mechanical and intracellular electrical activity were recorded simultaneously from the circular muscle layer. RESULTS: In the human jejunum, nerve stimulation inhibited mechanical activity and evoked an inhibitory junction potential that consisted of an initial fast hyperpolarization followed by a late sustained hyperpolarization. NO inhibited mechanical activity and evoked a dose-dependent hyperpolarization that mimicked the late hyperpolarization. In the canine jejunum, nerve stimulation inhibited mechanical activity and evoked an inhibitory junction potential that consisted of only a fast hyperpolarization. NG-Monomethyl-L-arginine and NG-nitro-L-arginine attenuated nerve-mediated inhibition of mechanical activity in both species. However, the effect of the synthase inhibitors on inhibitory junction potentials differed in the two species. In canine jejunum, both inhibitors reduced the amplitude of the initial fast hyperpolarization. In human jejunum, both inhibitors reduced only the late sustained hyperpolarization. CONCLUSIONS: NO mediates neural inhibition in circular muscle of both human and canine jejunum through different mechanisms.

Animals↗

Combined determination with functional and morphological studies of origin of nerve fibers expressing transient receptor potential vanilloid 1 in the myenteric plexus of the rat jejunum.

The aim of this study was to determine the action of capsaicin in isolated rat intestine and the origin of nerve fibers expressing transient receptor potential vanilloid 1 (TRPV1: capsaicin receptor) in the rat jejunum by combination of functional and immunohistochemical experiments. Capsaicin (1 microM) produced a prolonged relaxation response (52. +/-15.3% of the relaxation response to papaverine, mean +/- S.D., n=27) of the isolated jejunum in the presence of atropine and guanethidine. Pretreatment with the TRPV1 antagonist, capsazepine (10 microM) and ruthenium red (3 microM) significantly reduced the relaxation response to capsaicin by 78% (P<0.01) and 38% (P<0.05), respectively. Tetrodotoxin and calcitonin gene-related peptide (CGRP)-desensitization significantly reduced the response to capsaicin by 72% (P<0.01) and 42% (P<0.01), respectively. Therefore, we investigated the distribution of TRPV1-immunoreactivity (IR) in the myenteric plexus of the rat jejunum. Using antisera raised against either the N-terminal or C-terminal domains of rat TRPV1, TRPV1-IR was present in the nerve fibers, but not in the cell bodies of myenteric neurons. These TRPV1-immunoreactive nerve fibers were running in myenteric ganglia and their interconnecting strands. Most TRPV1-immunoreactive nerve fibers showed CGRP-IR, whereas few VR1-immunoreactive nerve fibers showed substance P-IR. After chronic denervation of the extrinsic nerve supply to the jejunum, both the relaxation response to capsaicin and TRPV1-immunoreactive nerve fibers completely disappeared. These findings indicate that these TRPV1-immunoreactive nerve fibers in the rat jejunum derive from extrinsic neurons and that activation of TRPV1 produces the relaxation response in the rat jejunum, at least in part, through the release of CGRP from nerve fibers expressing TRPV1.

Action Potentials↗

Aging-related alterations in the contractile responses to acetylcholine, muscarinic cholinoceptors and cholinesterase activities in jejunum and colon of the male Fischer 344 rats.

In an attempt to examine whether the muscarinic receptor-activated intestinal function is altered by aging, we studied the changes in (1) contractile responses to acetylcholine (Ach), (2) muscarinic cholinoceptors and (3) cholinesterase (ChE) activities, in jejunum and colon of the young (2-3 months) and aged (24-28 months) Fischer 344 rats. In the physiological contraction experiments of jejunum and colon, Ach concentration-dependently increased the force of contraction, and the contractile responses to Ach were not affected by aging. In addition, the true- and pseudo-ChE activities were not significantly changed by aging. The Ach-induced contraction was competitively inhibited by muscarinic M3-selective antagonist hexahydro-sila-difenidolhydrochloride p-fluoroanalog (p-F-HHSiD), suggesting that the contractile responses in the rat jejunum and colon were mediated through M3-cholinoceptor. Age-related changes in muscarinic cholinoceptors of jejunum and colon were determined with the use of specific muscarinic radioligand [3H]-quinuclidinylbenzilate (QNB). The [3H]QNB saturation binding experiments revealed that the maximal binding (B(max)) was increased only in aged jejunum without changes in K(D) values. These results suggest that aging may not attenuate the Ach-induced intestinal contraction via muscarinic M3 receptor, although the expression of muscarinic cholinoceptor is differentially modulated in jejunum and colon.

Acetylcholine↗

Contractile activity of circular smooth muscle in rats one year after small bowel transplantation: differing adaptive response of the jejunum and ileum to denervation.

The aim of the present study was to determine the long-term effects of isogeneic small bowel transplantation (SBT) on jejunal and ileal circular smooth muscle contractile activity in the rat. Transmural strips of circular muscle were prepared from proximal jejunum and distal ileum of 1-year-old control rats and rats 1 year after SBT (SBT-1Y) to measure isometric force. Spontaneous contractile activity and the dose-responses to bethanechol and norepinephrine were studied. Electrical field stimulation (EFS) at varying frequencies (1 to 20 Hz) was evaluated under adrenergic and cholinergic blockade to investigate inhibitory nerves. Spontaneous activity both in the jejunum and ileum in SBT-1Y rats was not different compared to control rats. Sensitivity to bethanechol did not differ between control and SBT-1Y rats in the jejunum or ileum. Sensitivity to norepinephrine, however, was significantly increased after SBT in the ileum but not in the jejunum. During EFS, inhibition was seen at low frequencies, and contractions were induced at high frequencies in all groups. The degree of inhibition did not differ between control and SBT-1Y rats in the jejunum; however, it tended to be increased in the ileum after SBT. The long-term adaptive response of smooth muscle to the extrinsic denervation accompanying SBT differs between the jejunum and the ileum.

Adaptation, Physiological↗

Proteolytic and peptidase activities of the jejunum and ileum of the rat during postnatal development.

1. Proteolytic (substrate nitrocasein), tripeptidase (substrate glycylglycylgly-cine) and aminopeptidase (substrate leucyl-beta-naphthylamide) activities were studied in homogenates of jejunal and ileal mucosa of 7-, 10-, 14-, 21-, 35- and 60-day-old rats. 2. Proteolytic activity was practically the same in jejunum of 7-, 10-, 14- and 21-day-old rats, but after day 21 a significant increase was observed. The activity of the ileum changed very little during postnatal development and was always higher than that of the jejunum. 3. Tripeptidase activity was low in the jejunum of 7- and 14-day-old rats, an increase was observed between day 14 and 21, but later no substantial changes were found. There were no changes in the ileum. The activity in the jejunum of 7- and 14-day-old rats was lower than in the ileum, but later the jejunum was more active than the ileum. 4. Aminopeptidase activity had a similar developmental pattern to tripeptidase activity. A low activity was found in the jejunum of 7- and 14-day-old rats, the maximum was in 21-day-old rats and then a decrease was observed, though values for 60-day-old rats were still higher than for 7- and 10-day-old rats. The activity in the ileum was practically the same in all age groups studied except in 14- and 21-day-old rats, where a transient peak was observed.

Aminopeptidases↗

Effect of octreotide on fluid absorption and secretion by the normal human jejunum and ileum in vivo.

BACKGROUND: We hypothesized that part of the non-specific antidiarrhoeal effect of octreotide is mediated by a proabsorptive or antisecretory effect on small intestinal active electrolyte transport. METHODS: To measure the effect of octreotide on net absorption, the jejunum and ileum of normal human subjects were perfused with a balanced electrolyte solution; to measure the effect of octreotide on normal active chloride secretion, the jejunum was perfused with a bicarbonate-free solution. RESULTS: During perfusion of a balanced electrolyte solution, octreotide increased basal net fluid absorption in the jejunum and ileum by about 40 mL/h per 30 cm. In the jejunum, octreotide markedly inhibited basal and sham feeding-stimulated active chloride secretion and inhibited water secretion by 28 and 51 mL/h per 30 cm, respectively. CONCLUSIONS: Octreotide causes an increase in the net epithelial cell absorption rate of a balanced electrolyte solution in the normal jejunum and ileum. In the jejunum, this proabsorptive effect is mediated mainly by the reduction of normal active electrolyte secretion, rather than by stimulation of normal active electrolyte absorption. These results support the hypothesis that part of the antidiarrhoeal action of octreotide is due to its effects on active electrolyte transport mechanisms by normal epithelial cells of the small intestine.

Adult↗

Differential effects of metformin on bile salt absorption from the jejunum and ileum.

AIMS: The antidiabetic drug metformin is often associated with a small reduction in total circulating cholesterol, but the mechanism responsible is unknown. As bile salts contribute significantly to cholesterol homeostasis, this study has investigated the effect of metformin on the absorption of bile salts by the jejunum and ileum, and their transfer into bile. METHODS: Sodium-[1-14C]-glycocholate was administered into the jejunum or ileum of anaesthetized rats with and without metformin (250 mg/kg). Appearance of 14C-glycocholate in plasma and bile was followed for 150 min. RESULTS: Absorption of 14C-glycocholate from the ileum, which is a high-capacity active process, was 10-fold greater than absorption from the jejunum, which is mainly a passive process. Metformin increased threefold the absorption of 14C-glycocholate from the jejunum. Metformin similarly increased the appearance of jejunal 14C-glycocholate in plasma and bile. In contrast to the jejunum, absorption of 14C-glycocholate from the ileum was suppressed by more than half with metformin. This was associated with corresponding reductions of 14C-glycocholate in plasma and bile. DISCUSSION: Thus, metformin induced a large suppression of active bile salt absorption from the ileum compared with a small increase in passive absorption from the jejunum. This suggests that the ileal effect of metformin to reduce overall bile salt absorption could contribute to the modest cholesterol-lowering effect of this drug.

Animals↗

Dietary carbohydrate and fat independently modulate disaccharidase activities in rat jejunum.

The role of carbohydrate and fat in diet-induced modifications of jejunal disaccharidase activities was evaluated with an isoenergic diet containing a nonmetabolizable sugar, alpha-methylglucoside. Rats previously fed a high fat, low starch diet or a high starch low fat diet were force-fed three times over 12 h isoenergic high fat diets with or without alpha-methylglucoside, or a low fat diet containing alpha-methylglucoside. Regardless of the previous diet fed, force-feeding the high fat, alpha-methylglucoside diet produced significantly greater sucrase and lactase activities in the upper jejunum than force-feeding the high fat diet without alpha-methylglucoside; comparable or only slightly greater sucrase and lactase activities were seen in the lower jejunum. The animals fed the low fat, alpha-methylglucoside diet exhibited significantly greater sucrase and lactase activities in the lower jejunum than did the rats fed the high fat, alpha-methylglucoside diet; a less marked difference (< 30%) was observed between these two groups for disaccharidase activities in the upper jejunum. The lower sucrase and lactase activities observed in the jejunum of animals force-fed the high fat diet after consuming the high starch, low fat diet were accompanied by greater trypsin activity in the lumen of the upper and lower jejunum, suggesting that proteolytic degradation of sucrase and lactase might be stimulated in rats fed the high fat diets. These results suggest that both dietary carbohydrate and dietary fat independently and by different mechanisms modulate jejunal disaccharidase activities.

Animals↗

Effect of UK-84149 on voltage-activated calcium currents of single smooth muscle cells from guinea-pig and rabbit jejunum and rabbit coronary artery.

1. Smooth muscle cells of the longitudinal muscle of the guinea-pig and the rabbit jejunum and rabbit coronary artery were dispersed by enzyme treatment and recordings of membrane current were made in the standard whole cell voltage-clamp mode and by perforated patch technique. The effect of UK-84149 on the voltage-dependent calcium inward current of single isolated smooth muscle was studied at room temperature. 2. When inward and outward currents were evoked by stepping to 0 mV or + 10 mV from -80 mV every 20 s, UK-84149 reduced the voltage-dependent inward current in guinea-pig jejunum smooth muscle cells with a ID50 of 2.3 microM, and also reduced voltage-dependent outward current with a ID50 of 7.2 microM. The effect of UK-84149 was difficult to wash out. 3. The inactivation of the inward current was studied by holding at various potentials for 10 s before evoking inward current at a test potential of 0 mV. The voltage-inactivation curve was shifted to the left by 3 microM UK-84149. The voltage at which current was 50% available (Vh) was changed from -37 +/- 2 mV to -50 mV +/- 2.2 (n = 6, means +/- s.e. mean). 4. When inward current was evoked by stepping to 0 mV from -80 mV for 50 ms, every 20 s, nicardipine immediately, and verapamil and UK-84149 slowly, reduced the peak amplitude. Inhibition by the latter two drugs depended on the number of stimulations applied. So, like verapamil, UK-84149 had a use-dependent action. 5. The effect of UK-84149 on inward current from rabbit jejunum and coronary artery smooth muscle cells was compared with the effect of nicardipine and D600. When inward current was evoked by stepping to 0 mV from - 80 mV every 20 s, UK-84149 inhibited inward currents from both types of smooth cell with an ID50 of 1.7 microM for jejunum and an ID50 of 3.2 microM for coronary artery. ID50 values of D600 were 8.1 microM for jejunum and 3.9 microM for coronary artery. ID50 values of nicardipine were 24 nM for jejunum and 12 nM for coronary artery.6. The results of the present studies indicate that UK-84149 has a calcium-antagonist action that can explain its inhibitory action on bowel motility. Its bowel selectivity may arise due to its use-dependent,and persistent, action.

Animals↗

Somatostatin sst(2) receptors inhibit peristalsis in the rat and mouse jejunum.

Somatostatin [somatotropin release-inhibitory factor (SRIF)] has widespread actions throughout the gastrointestinal tract, but the receptor mechanisms involved are not fully characterized. We have examined the effect of selective SRIF-receptor ligands on intestinal peristalsis by studying migrating motor complexes (MMCs) in isolated segments of jejunum from rats, mice, and sst(2)-receptor knockout mice. MMCs were recorded in 4- to 5-cm segments of jejunum mounted horizontally in vitro. MMCs occurred in rat and mouse jejunum with intervals of 104.4 +/- 10 and 131.2 +/- 8 s, respectively. SRIF, octreotide, and BIM-23027 increased the interval between MMCs, an effect fully or partially antagonized by the sst(2)-receptor antagonist Cyanamid154806. A non-sst(2) receptor-mediated component was evident in mouse as confirmed by the observation of an inhibitory action of SRIF in sst(2) knockout tissue. Blocking nitric oxide generation abolished the response to SRIF in rat but not mouse jejunum. sst(2) Receptors mediate inhibition of peristalsis in both rat and mouse jejunum, but a non-sst(2) component also exists in the mouse. Nitrergic mechanisms are differentially involved in rat and mouse jejunum.

Animals↗

Hepatic cytochrome P-450 reductase-null mice show reduced transcriptional response to quercetin and reveal physiological homeostasis between jejunum and liver.

Using mice deficient in hepatic cytochrome P-450 oxidoreductase (POR), which disables the liver cytochrome P-450 system, we examined the metabolism and biological response of the anticarcinogenic flavonoid, quercetin. Profiling circulating metabolites revealed similar profiles over 72 h in wild-type (WT) and POR-null (KO) mice, showing that hepatic P450 and reduced biliary secretion do not affect quercetin metabolism. Transcriptional profiling at 24 h revealed that two- to threefold more genes responded significantly to quercetin in WT compared with KO in the jejunum, ileum, colon, and liver, suggesting that hepatic P450s mediate many of the biological effects of quercetin, such as immune function, estrogen receptor signaling, and lipid, glutathione, purine, and amino acid metabolism, even though quercetin metabolism is not modified. The functional interpretation of expression data in response to quercetin (single dose of 7 mg/animal) revealed a molecular relationship between the liver and jejunum. In WT animals, amino acid and sterol metabolism was predominantly modulated in the liver, fatty acid metabolism response was shared between the liver and jejunum, and glutathione metabolism was modulated in the small intestine. In contrast, KO animals do not regulate amino acid metabolism in the liver or small intestine, they share the control of fatty acid metabolism between the liver and jejunum, and regulation of sterol metabolism is shifted from the liver to the jejunum and that of glutathione metabolism from the jejunum to the liver. This demonstrates that the quercetin-mediated regulation of these biological functions in extrahepatic tissues is dependent on the functionality of the liver POR. In conclusion, using a systems biology approach to explore the contribution of hepatic phase 1 detoxification on quercetin metabolism demonstrated the resiliency and adaptive capacity of a biological organism in dealing with a bioactive nutrient when faced with a tissue-specific molecular dysfunction.

Animals↗

Ion transport by rabbit jejunum in vivo.

Net ion and H2O transport by jejunum adjacent to the ligament of Treitz (proximal jejunum) and midjejunum were measured in vivo by continuous perfusion with HCO3-Ringer solution containing a volume marker. Proximal jejunum secreted Na and H2O, whereas midjejunum absorbed Na and H2O. Both segments secreted CO2 and absorbed K and Cl. D-glucose stimulated absorption of Na and H2O and the transmural electrical potential difference (PD) in both segments, but these changes were not accompanied by alterations in Cl, CO2, or K fluxes. However, the increse in Na absorption caused by 3-O-methylglucose was matched by an increase in Cl absorption. This, in addition to increased tissue lactate concentration after addition of D-glucose, suggests that organic anion maintains electroneutrality for Na transport enhanced by D-glucose. Cholera toxin had no effect on ion transport or PD in proximal jejunum, but cholera toxin stimulated secretion and increased the PD in more distal jejunum. Although proximal jejunum shows spontaneous secretory activity, its capacity for secretion is not as great as more distal small intestine.

Animals↗

Functional and structural changes in the jejunum of the rat following cysteamine and stress-induced duodenal ulcer.

The effects of cysteamine and stress-induced duodenal ulcer on the functional and structural properties of the rat jejunum were investigated. The absorptive capacity of the jejunum was determined using alanine as the permeant solute and the single-pass perfusion technique. A statistically significant decrease (p < 0.01) in alanine absorption was observed after 8 h and 3 days of duodenal ulcer induction by stress and cysteamine respectively. However, alanine transport measured 7 days after cysteamine or stress ulcer induction showed no significant change from control values. Cysteamine and stress-induced duodenal ulcer did not show any significant change in water absorption across the jejunum when measured after 8 h, 3 and 7 days of ulcer induction. Microscopically, the jejunum of rats with 3-day cysteamine-induced ulcer exhibited diffuse type of apical derangements with excessive swelling of the villi and progressive degenerative changes. No such changes were noticed on the 7th day nor in the jejunum of the rats with stress-induced duodenal ulcer. The results suggest that cysteamine-induced duodenal ulcer produces an inhibition in the absorptive capacity of the jejunum which is time-dependent and reversible.

Alanine↗

Intestinal adaptation after extensive small bowel resection: differential changes in growth and insulin-like growth factor system messenger ribonucleic acids in jejunum and ileum.

The distal small bowel exhibits greater adaptive growth than proximal segments after partial small intestine resection. To explore this process, we evaluated adaptive cellularity, intestinal insulin-like growth factor (IGF) system messenger RNA (mRNA) transcripts, and effects of recombinant IGF-I treatment in jejunum and ileum of adult rats. Gastrostomy-fed animals underwent 80% jejuno-ileal resection or intestinal transection and reanastomosis without resection, followed by infusion of human recombinant IGF-I (2.4 mg/kgXday) or vehicle. After 7 days, resected rats demonstrated modest adaptive growth in jejunum and marked cell proliferation in ileum. Resection increased IGF-I mRNA in both jejunum (183%) and ileum (249%) and up-regulated IGFBP-4 mRNA levels in both tissues. IGFBP-3 mRNA fell significantly in ileum after resection. IGF-I infusion modestly increased ileal cellularity after resection, but had no effect in jejunum. IGF-I markedly increased IGFBP-3 mRNA levels in jejunum after both transection and resection. These data confirm that bowel resection induces greater adaptive growth in ileum than jejunum. IGF-I administration modestly increases ileal, but not jejunal, growth after resection. Increased levels of intestinal IGF-I and IGFBP-4 mRNA suggest roles for IGF-I and IGFBP-4 in mediating small bowel adaptation. Higher levels of jejunal IGFBP-3 mRNA may be related to limited jejunal vs. ileal growth after extensive jejuno-ileal resection.

Adaptation, Physiological↗

Effects of fasting, refeeding, and intraluminal triglyceride on proglucagon expression in jejunum and ileum.

Intestinal proglucagon is thought to be synthesized primarily by the distal gut, although the role of proglucagon-derived glucagon-like peptide I (GLP-I) as a major physiological incretin would seem to be associated with production in proximal small bowel. To better characterize the sites of production of proglucagon and GLP-I in the small intestine and evaluate nutrient regulation of small bowel proglucagon and derived peptides, we evaluated the effects of fasting for 72 h and subsequent refeeding or jejunal infusion of long-chain triglyceride (LCT) for 24 h on local expression of proglucagon in proximal and distal small bowel. Proglucagon mRNA abundance and cellular localization were determined and correlated with wet weight of bowel. In jejunum, proglucagon mRNA abundance decreased by 40% with fasting (P < 0.005) and increased with refeeding to levels similar to those of ad libitum-fed animals. In ileum, fasting resulted in a 20% decrease in proglucagon mRNA (P < 0.005); in contrast to jejunum, refeeding did not result in a significant rise in ileal proglucagon mRNA abundance from fasting values. In jejunum, signal intensity of proglucagon mRNA per cell, determined by in situ hybridization, decreased with fasting (P < 0.05) and increased with refeeding (P < 0.005) in proportion to changes in mRNA abundance. Plasma enteroglucagon and GLP-I levels correlated with jejunal proglucagon mRNA. Intrajejunal infusion of LCT increased expression of proglucagon to a greater extent in jejunum than in ileum. In conclusion, enteral nutrient intake stimulates small bowel proglucagon expression; this effect is greater in jejunum than ileum, consistent with greater intraluminal nutrient exposure and the role of jejunum as a source of the major incretin GLP-I.

Animals↗

Segmental difference in epithelial and mucosal barrier functions between the jejunum and the ileum in cold storage small bowel grafts in the rat.

The purpose of this study was to determine the differences in epithelial and mucosal barrier function between the jejunum and the ileum at transplantation. Rat small bowel was preserved in cold University of Wisconsin solution for 0, 12 or 24 hrs. Time-related segmental differences in the potential differences, at rest (rPD) and upon glucose stimulation (PDgs), and in the permeation rates of phenolsulfonphtalein (PSP) and polyethylene glycol 4000 (PEG) as non-absorbable markers were studied after a 20-min reoxygenation period following cold preservation. Time-related histologic damage during cold preservation was also evaluated. After 24 hrs of preservation, when the villi were denuded both in jejunum and ileum, the rPD (1.4 +/- 0.3 mV/cm2) and PDgs (1.4 +/- 0.3 mV/cm2) of the jejunum were significantly lower than those of the ileum (1.9 +/- 0.3 mV/cm2 and 2.1 +/- 0.3 mV/cm2, respectively). A difference in PEG permeation rates occurred after 24 hrs of preservation. The permeation rate of PSP in the jejunum was 10.5 +/- 1.0%, which was significantly higher than that in the ileum (8.6 +/- 1.0%) after 12 of preservation, when subepithelial edema occurred both in the jejunum and ileum. Our functional study demonstrated that, in the rat small bowel, the ileumis more resistant than the jejunum to cold preservation.

Animals↗

Role of extrinsic and intrinsic nerves in hormonal induction of the migrating motor complex in the jejunum.

The mechanism of induction of the migrating motor complex (MMC) by neural or humoral agents and their role in the control of fasting motility are not well understood. Our aim was to determine the role of extrinsic and intrinsic nerves in mediating the induction of the MMC by motilin. Three groups of dogs were studied. Group I consisted of neurally intact control dogs. In group II, intrinsic neural continuity between the duodenum and the jejunum was interrupted by transection and reanastomosis of the distal duodenum. Dogs in group III underwent disruption of all intrinsic and extrinsic neural input to the entire jejunoileum. Serosal electrodes were sewn to duodenum and jejunum in all dogs. After a 2-week recovery, fasting myoelectric activity was recorded on four or more occasions. Motilin (0.1 microgram/kg iv) was given 30 min after a spontaneous duodenal phase III. In group I (controls), motilin induced a premature MMC, which originated in the duodenum and migrated along the small intestine. In group II (intrinsic neural disruption), motilin induced a premature MMC, which began simultaneously in the proximal duodenum and proximal jejunum. In group III (intrinsic and extrinsic neural disruption), motilin induced a premature MMC in the duodenum but not in the jejunum; rather, a short, nonmigrating burst of spike potentials occurred simultaneously in all jejunal electrodes. These observations suggest that extrinsic innervation is necessary for motilin to induce phase III activity in the jejunum. Extrinsic neural pathways appear to mediate motilin-induced MMC activity in the jejunum.

Animals↗