Ileus In Rats Research Articles

Exploring the chemical components of Kuanchang-Shu granule and its protective effects of postoperative ileus in rats by regulating AKT/HSP90AA1/eNOS pathway

BackgroundPostoperative ileus (POI) is a common obstruction of intestinal content passage caused by almost all abdominal operations that seriously strokes the quality of life of patients. Kuanchang-Shu granule (KCSG), a classic modified prescription based on “Da-Cheng-Qi Decoction”, has obtained satisfactory efficacy in the clinical therapeutics of POI. However, its material basis and holistic molecular mechanism against POI have not been revealed.MethodsThe chemical ingredients of KCSG were first characterized by ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UHPLC-QTOF-MS). Subsequently, an integration strategy of the network pharmacology and molecular docking based on above identified ingredients was performed to unveil the potential targets involved in the treatment of KCSG on POI. Finally, intestinal manipulation induced rat POI model was constructed to verify the efficacy and predicted mechanism of KCSG against POI.ResultsIn total, 246 ingredients mainly including organic acids, flavonoids, quinones, alkaloids, terpenoids, phenylpropanoids and phenols were identified. 41 essential ingredients, 24 crucial targets as well as 15 relevant signaling pathways were acquired based on network pharmacology analysis. Pharmacodynamic research showed that KCSG treatment could protect intestinal histological damage, promote the recovery of measurement of gastrointestinal transit disorder and inhibit the secretion of myeloperoxidase in the distal ileum tissues. The up-regulated expression of p-AKT and down-regulated expression of p-eNOS and HSP9OAA1 predicted by molecular docking and validated by western blotting showed that AKT/eNOS/HSP90AA1 pathway may be one of the crucial mechanisms that mediates the protective effect of KCSG.

The role of beta-adrenoreceptors in postoperative ileus in rats

The aim of the research was to evaluate the influence of antagonists of specific beta-adrenergic receptor subtypes on bowel motility following abdominal surgery in rat model of postoperative ileus. Bowel motility was measured by the intestinal transit of Evans blue introduced via orogastric tube after surgical procedures of skin incision, laparotomy and laparotomy with gut manipulation. Male rats were given individual adrenergic receptor subtypes antagonists intraperitoneally, and the influence of administered agents on intestinal transit of Evans blue was then evaluated. No statistically significant differences in the length of intestine in tested rats were observed. Propranolol administered prior to surgical procedure has shown protective effect on Evans blue migration in rats undergoing laparotomy and gut manipulation. Intestinal dye transit for propranolol doses of 10, 30 and 45 mg/kg was 18.00 ± 1.88c m, 23.75 ± 1.71 cm and 22.5 ± 2.43 cm, respectively, and for last two doses, statistically significant increase of dye passage was noted, compared to Evans blue transit of 11.00 ± 2.43 cm in the control group. No acceleration of dye migration was seen following administration of beta1-, beta2- and beta3-selective adrenergic receptor antagonist metoprolol, ICI 118.551 and SR58894A, respectively. Our research confirmed that propranolol at high doses, as seen by other researchers, improved bowel motility in early phase of postoperative ileus. That slight acceleration of intestinal dye transit after surgery with gut manipulation is rather connected with membrane-stabilizing action, than the receptor blocking effect, as this effect was not observed after the application of selective antagonists of respective subtypes of beta-adrenergic receptor.

Phlorizin attenuates postoperative gastric ileus in rats.

Postoperative ileus (POI) is a major complication of abdominal surgery (AS). Impaired gut barrier mediated via Toll-like receptor 4 (TLR4) and interleukin-1 (IL-1) receptor is involved in the development of POI. Phlorizin is a nonselective inhibitor of sodium-linked glucose transporters (SGLTs) and is known to improve lipopolysaccharide (LPS)-induced impaired gut barrier. This study aimed to clarify our hypothesis that AS-induced gastric ileus is mediated via TLR4 and IL-1 signaling, and phlorizin improves the ileus. AS consisted of a celiotomy and manipulation of the cecum for 1 min. Gastric emptying (GE) in 20 min with liquid meal was determined 3 h after the surgery in rats. The effect of subcutaneous (s.c.) injection of LPS (1 mg kg-1 ) was also determined 3 h postinjection. AS delayed GE, which was blocked by TAK-242, an inhibitor of TLR4 signaling and anakinra, an IL-1 receptor antagonist. LPS delayed GE, which was also mediated via TLR4 and IL-1 receptor. Phlorizin (80 mg kg-1 , s.c.) significantly improved delayed GE induced by both AS and LPS. However, intragastrical (i.g.) administration of phlorizin did not alter it. As gut mainly expresses SGLT1, SGLT2 may not be inhibited by i.g. phlorizin. The effect of phlorizin was blocked by ghrelin receptor antagonist in the LPS model. AS-induced gastric ileus is mediated via TLR4 and IL-1 signaling, which is simulated by LPS. Phlorizin improves the gastric ileus via activation of ghrelin signaling, possibly by inhibition of SGLT2. Phlorizin may be useful for the treatment of POI.

Effect of DA-9701, a Novel Prokinetic Agent, on Post-operative Ileus in Rats.

Background/AimsPost-operative ileus (POI) is a common complication of abdominal surgery. DA-9701, an extract of Pharbitis Semen and Corydalis Tuber, is a new prokinetic agent that also alleviates visceral pain. The aim of this study was to investigate whether DA-9701 can ameliorate POI in rats.MethodsA total of 32 rats were divided into 4 groups: no surgery/no medication (NSNM), no surgery/medication (NSM), surgery/no medication (SNM), and surgery/medication (SM). Gastrointestinal transit (GIT), which is assessed by migration of charcoal, and cumulative stool weight were measured at 24 hours after surgery.ResultsGIT was significantly more delayed in the SNM group than in the other groups (SNM vs NSNM, P < 0.001; SNM vs NSM, P < 0.001; SNM vs SM, P = 0.005). Cumulative stool weight in that group was also lower than in the no surgery groups (SNM vs NSNM, P = 0.007; SNM vs NSM, P = 0.033), and there was no significant difference between the SM group and the no surgery groups (SM vs NSM, P = 0.703; SM vs NSNM, P = 0.347).ConclusionDA-9701 can ameliorate POI by reducing delayed GIT and improving defecation in a rat model of POI.

Enhanced Recovery Protocol after Radical Cystectomy for Bladder Cancer

Enhanced recovery after surgery protocols aim to improve patient care and decrease complications and hospital stay. We evaluated our enhanced recovery after surgery protocol, focusing on length of stay, early complication and readmission rates after radical cystectomy for bladder cancer. From May 2012 to July 2013 a perioperative protocol was applied in 126 consecutive patients who underwent open radical cystectomy and urinary diversion. Nonconsenting patients (2), those with previous diversion (2) and prolonged postoperative intubation (3), and those who underwent additional surgery (9) were excluded from study. The protocol focuses on avoiding bowel preparation and nasogastric tube, early feeding, nonnarcotic pain management and the use of cholinergic and μ-opioid antagonists. Outcomes were compared to those in matched controls from our bladder cancer database. A total of 110 patients with a median age of 69 years were included in analysis, of whom 68% underwent continent urinary diversion. Of the patients 82% had a bowel movement by postoperative day 2. Median length of stay was 4 days. The 30-day minor and major complication rates were 64% and 14%, respectively. The most common minor complication was anemia requiring transfusion in 19% of patients, urinary tract infection in 13% and dehydration in 10%. The latter 2 complications were the most common etiologies for readmission. The 30-day readmission rate was 21% (23 patients). Patients 75 years old or older had a longer length of stay (5 vs 4 days, p = 0.03) and a higher minor complication rate (72% vs 51%, p = 0.04) than younger patients. Our enhanced recovery after surgery protocol expedites bowel function recovery and shortens hospital stay after RC and urinary diversion without an increase in the hospital readmission rates.

Mo2107 Vagal Activation and Changes in Peptidergic Neurotransmission With Vasoactive Intestinal Polypeptide and Substance P During Postoperative Ileus in Rat

Introduction: Simultaneous manometry and intraluminal ultrasound imaging studies show that similar to contraction wave, distension wave traversing ahead of contraction wave is also peristaltic. Cross sectional area (CSA) of the esophagus is one of the several variables that determine intraluminal esophageal impedance value. Aim: We recorded simultaneous intraluminal US images, impedance and high resolutionmanometry to determine the relationship between esophageal CSA and intraluminal esophageal impedance values. Studies were conducted in 15 normal healthy subjects. Impedance and manometry were measured along the whole length of the esophagus (Sierra Scientific) and US images were recorded at 2 and 12 cm above the LES. Swallow induced primary peristalsis was recorded using 5 ml bolus of 0.5 N saline. Impedance data were exported to Excel and analyzed for the baseline and lowest impedance value at each level. Cross sectional area of the esophagus at 4 and 14 cm of the esophagus were measured from the US images. Results: Impedance recordings show that following a swallow, the onset of drop in impedance as well as nadir impedance traverses the esophagus in a sequential fashion in front of the contraction wave (figure, left panel). There is strong linear relationship between the location and nadir impedance value such that the lowest impedance values are located just above the LES, with a difference of approximately 100 ohms every 1 cm along the length of the esophagus (right panel). Atropine injected intravenously (10 μgm/kg) abolished esophageal contractions, reduced baseline esophageal impedance and abolished sequential progression of nadir impedance along the esophagus). US image analysis shows that peak distension corresponds with nadir impedance value. Similar to nadir impedance, peak distension recorded by US imaging traverses the esophagus in a peristaltic fashion. US images show greater esophageal distension at 4 cm compared to 14 cm above the LES, cross sectional area of 1400 versus 600 mm2 respectively. Conclusion: These data prove: 1) intraluminal distension and contraction wave during peristalsis are tightly linked and 2) intraluminal impedance recording is a relatively simple technique to record luminal distension of the esophagus.

Mo1884 Changes in Neurotransmission via α1- and α2-Receptors During Postoperative Ileus in Rat

Mo1884 Changes in Neurotransmission via α1- and α2-Receptors During Postoperative Ileus in Rat

Tu2061 Changes in Peptidergic Neurotransmission With VIP and Substance P During Postoperative Ileus in Rat

Tu2061 Changes in Peptidergic Neurotransmission With VIP and Substance P During Postoperative Ileus in Rat

Differential molecular and cellular immune mechanisms of postoperative and LPS-induced ileus in mice and rats

Ileus is caused by the initiation of a complex cascade of molecular and cellular inflammatory responses within the intestinal muscularis, which might be species specific. Our objective was to investigate a possible immunological divergence in the mechanisms of postoperative- and endotoxin-induced ileus in C57BL/6 mice and Sprague–Dawley rats.Gastrointestinal transit (GIT) was measured at 24h after the injurious stimulus. MPO-staining and F4/80 immunohistochemistry were used to quantify polymorphonuclear and monocyte infiltration of jejunal muscularis whole-mounts, and intestinal muscularis MCP-1, ICAM-1 and iNOS gene expression was assessed by RT-PCR. Intestinal muscularis subjected to in vivo surgical manipulation (SM) or LPS treatment was cultured for 24h, and the liberation of nitric oxide and chemokines/cytokines into the culture medium was analyzed by Griess reaction and Luminex multiplex assay.Intestinal SM and lipopolysaccharide (LPS) (15mg/kg) caused a significant delay in gastrointestinal transit, which was more severe in mice compared to rats in both injury models. Both SM- and LPS-triggered neutrophil and monocytic extravasation into the rat jejunal muscularis exceeded the cellular infiltration seen in mice. These results correlated with significantly greater increases in rat muscularis MCP-1 (syn. CCL2), ICAM-1 and iNOS message with more subsequent NO production after SM or LPS compared to mouse. The cultured muscularis obtained from SM mice released significantly more inflammatory proteins such as TNF-α, IL-1-α, IL-4 and GM-CSF compared to the manipulated rat muscularis. In contrast, LPS initiated the secretion of significantly more IL-1β by the inflamed rat muscularis compared to the mouse, but GM-CSF (syn. CSF2) liberation from mouse muscularis was markedly higher compared to LPS-treated rat muscularis.The data indicate that mechanistically the development of ileus in rat is mediated predominately through a leukocytic pathway consisting of chemotaxis, cellular extravasation and NO liberation. Whereas, the more intense mouse ileus evolves via a potent but injury-specific local cytokine response.

Interstitial Cells of Cajal in Abdominal Sepsis and Hypertension-Induced Ileus in Rats

Purpose: To evaluate injury to the myenteric interstitial cells of Cajal (ICC-MY) and assess the role of ICC-MY in gastrointestinal motility in rat models of abdominal sepsis and intra-abdominal hypertension (IAH). Materials and Methods: Sprague-Dawley rats were divided into 4 groups; group 1: sham group; group 2: sepsis induced by cecal puncture and ligation; group 3: IAH created by placing a catheter into the abdominal cavity; group 4: sepsis and IAH induced simultaneously. Small intestinal segments were resected 24 h after surgery. Ileum sections stained with HE were assessed pathologically. The spontaneous mechanical activity was evaluated using the organ bath technique. The alterations in ICC-MY networks by immunohistochemical staining for c-Kit and the ultrastructural changes in ICC-MY by transmission electron microscopy were evaluated. Results: There were significant differences in the frequency and amplitude of the bowel segment contractions between groups 1, 2, 3 and 4. These changes were associated with lesions of ICC-MY networks and ultrastructure. Conclusions: Abdominal sepsis and IAH resulted in damage to ICC-MY networks, leading to disordered intestinal rhythmicity. The combination of sepsis and IAH causes far more serious injury than either sepsis or IAH alone.

Gastric electrical stimulation modulates hypothalamic corticotropin-releasing factor–producing neurons during post-operative ileus in rat

High-frequency/low-energy gastric electrical stimulation (GES) is an efficient therapy to treat gastric emptying–related disorders but its mechanism of action remains poorly understood. We aimed to assess the effects of high-frequency/low-energy GES on corticotropin-releasing factor (CRF)–producing neurons in the paraventricular nucleus of the hypothalamus (PVN), which are involved in gastric ileus induced by laparotomy. Two electrodes were implanted in the rat gastric antrum during laparotomy, then stimulation (amplitude: 2 mA; pulse duration 330 μs; frequency: 2 Hz; 1 min ON/2 min OFF) or sham stimulation (control group) were applied. Using immunohistochemistry, the number of c-Fos protein-expressing neurons (c-Fos protein-immunoreactive cells, Fos-IR) was quantified in the PVN after 1 h of stimulation. The number of neurons expressing simultaneously c-Fos protein and CRF mRNA was measured by means of immunocytochemistry combined with in situ hybridization. Finally, c-Fos and CRF mRNA levels in the hypothalamus were determined by in situ hybridization or quantitative reverse transcriptase–polymerase chain reaction. Fos-IR in the PVN was significantly decreased 1 h after GES ( P<0.05) but was not affected by sub-diaphragmatic vagotomy. The number of neurons containing c-Fos protein and CRF mRNA was lower in the GES group compared with the control group ( P<0.05). In addition, c-Fos and CRF mRNA levels in the PVN were significantly decreased by GES ( P≤0.05). It is concluded that acute GES reduces the number of CRF-producing neurons and decreases CRF expression in the PVN during post-operative gastric ileus.

The selective mu opioid receptor antagonist, alvimopan, improves delayed GI transit of postoperative ileus in rats

Postoperative ileus (POI) is often exacerbated by opioid analgesic use during and following surgery, since mu opioid receptor activation results in a further delay of gastrointestinal (GI) transit. The effects of alvimopan, a novel, selective, and peripherally acting mu opioid receptor antagonist, and the reference compound methylnaltrexone, upon POI were investigated in rats. Under isoflurane anesthesia, POI was induced by laparotomy with intestinal manipulation. Immediately after the surgery, the rats received 51Cr by gavage. Three hours after the surgery, the rats were sacrificed and GI transit was estimated using the geometric center (GC) of 51Cr. Alvimopan (0.1–3 mg/kg) or methylnaltrexone (100 mg/kg) were administered by gavage either before or after the surgery, with or without morphine administration (1 mg/kg). GI transit was delayed by intestinal manipulation (GC = 2.92 ± 0.17). Alvimopan (1 and 3 mg/kg) significantly reversed this delayed GI transit when administered 45 min prior to surgery. However, the effects of alvimopan were less pronounced when administered following surgery. Morphine administration further delayed GI transit induced by intestinal manipulation (GC = 1.97 ± 0.11). Under these conditions, alvimopan (1 and 3 mg/kg) also significantly improved delayed GI transit when administered before surgery. Methylnaltrexone was inactive under all experimental conditions. These data suggest that mu opioid receptors play a role in the pathogenesis of POI, and that the clinical benefit reported to be afforded by alvimopan may be in part mediated via inhibition of an endogenous opioid release as well as blockade of the unwanted GI actions of analgesic agents.

Role of brain CRF signaling pathways in development of postoperative gastric ileus in rats

Abdominal surgery (AS) delays gastric emptying (GE) through CRF receptors (CRF-R). CRF-R1 contributes to central CRF-induced sympathetic activation. CRF1 knockout mice did not develop gastric ileus.

The role and interactions of nitric oxide (NO), carbon monoxide (CO), and prostanoids in the pathogenesis of postoperative ileus in rats.

The effects of heme oxygenase (HO) inhibitors, zinc-protoporphyrin-IX (ZnPP-IX), and tin protoporphyrin-IX (SnPP-IX) and their interactions with L-arginine/nitric oxide synthase (NOS) and cyclooxygenase (COX) pathways were investigated in postoperative ileus in rats. Intestinal transit was measured as Evans blue migration after skin incision, laparotomy or laparotomy plus gut evisceration and handling. Laparotomy and small intestinal manipulations increased blood plasma nitrites/nitrates level 1.88-fold. N(omega)-nitro-L-arginine methyl ester, indomethacin, a selective COX-1 blocker (resveratrol) and COX-2 antagonists (nimesulide, DuP-697, NS-398) reversed the additional inhibitory effects of gut manipulation subsequent to laparotomy. In contrast, N-(3-(aminomethyl)benzyl)acetamidine or S-methylisothiourea, highly selective inducible NOS blockers, remained ineffective. ZnPP-IX and SnPP-IX overturned the effects of laparotomy on dye propulsion, but were only partially effective after laparotomy and gut handling attenuating the additional inhibitory influences of gut manipulation, the intestinal transit reaching 89.21%, 92.87%, 53.46%, and 48.56% of respective controls transit. Salutary effects of L-NAME, ZnPP-IX, and SnPP-IX were dose-dependent, L-arginine or hemin (HO substrate) sensitive. Administration of indomethacin and resveratrol subsequent to SnPP-IX reversed the inhibitory effects of laparotomy and manipulation, amounting to 93.91% and 87.43% of controls. On the other hand, L-NAME injected after SnPP-IX abolished the salutary effects of the latter, study dye migration reached 25.18% of control rat. Therefore we demonstrated that nitric oxide, carbon monoxide, and prostanoids play a role in the pathogenesis of postoperative ileus albeit in different mechanisms. Laparotomy stimulated HO activity, whereas gut manipulation led to an excessive constitutive NOS stimulation accompanied by augmented prostanoid synthesis by COX-1. Unaffected synthesis of either NO or CO enables a return of gastrointestinal transit during postoperative period, whereas a pharmacological blockade of two complementary metabolic pathways provides a most effective measure against postoperative ileus development.

The longer and deeper abdominal incision causes prolonged postoperative ileus in rats

The longer and deeper abdominal incision causes prolonged postoperative ileus in rats

Mast cell stabilization by ketotifen or lodoxamide has distinct effects on gastrointestinal transit under control conditions or in postoperative ileus in rat

Mast cell stabilization by ketotifen or lodoxamide has distinct effects on gastrointestinal transit under control conditions or in postoperative ileus in rat

Differential salutary effects of nonselective and selective COX-2 inhibitors in postoperative ileus in rats

Background. Postoperative ileus (PI) is a common surgical complication, the treatment of which consists of supportive measures.Aim. The effects of several cyclooxygenase (COX) inhibitors and their interaction with l-arginine/nitric oxide synthase (NOS) pathway were tested in a rat PI model.Methods. Intestinal transit was measured as Evans blue migration after skin incision, laparotomy, or laparotomy followed by evisceration and gut handling.Results. In contrast to a selective inducible NOS (iNOS) blocker, l-N6-(1-iminoethyl)lysine hydrochloride (L-NIL), Nω-nitro-l-arginine methyl ester (L-NAME) reversed the additional inhibitory effects of gut manipulation after laparotomy on the gastrointestinal transit (GI) in a dose-dependent, l-arginine-sensitive manner. Laparotomy and manipulations of small intestine increased blood plasma nitrites and nitrates level (NOx), an effect preventable by L-NAME. Indomethacin, resveratrol (selective COX-1 blocker), and COX-2 antagonists, nimesulide, NS-398, DuP-697, and L-752860, attenuated the additional inhibitory effects of gut manipulation following laparotomy in a dose-dependent manner. In contrast, only nimesulide, NS-398, DuP-697, and L-752860 partly, but significantly, reversed the effects of laparotomy on the intestinal transit. Administration of L-NAME subsequent to COX inhibitors abolished the salutary effects of the latter, implying that at least the synthesis of either NO or prostanoids must remain unaffected to enable a return of GI transit during the postoperative period.Conclusion. In addition to NO synthesized by constitutive NOS (cNOS), prostaglandins produced by both COX-1 and COX-2 participate in the pathogenesis of PI, albeit in different pathological mechanisms. Thus laparotomy stimulated COX-2 activity, whereas gut manipulation led to an excessive cNOS activity and prostaglandin synthesis by COX-1.

Small intestinal transit does not adequately represent postoperative paralytic ileus in rats.

Small intestinal transit (SIT) has often been regarded as an index of pathophysiological state of postoperative ileus (PI) in rats. The reliability of SIT as an index of PI was examined in the present study. PI was induced via abdominal surgery (i.e., laparotomy with evisceration and manipulation) in rats. For one group of PI-induced rats, SIT of a charcoal test meal was measured. When necessary, the physical state (i.e., severity and site of distension) of the gastrointestinal (GI) tract in each rat was visually examined. For another group of PI-induced rats, abdominal X-ray radiographs were obtained after introducing the barium sulfate suspension. The abdomen was then opened and the physical state of the GI tract was visually examined. The SIT was decreased in most of the PI-induced rats, and the GI distension was observed, with substantial intersubject variations, in all of the PI-induced rats. However, no linear relationship was evident between the SIT and the severity of GI distension (e.g., at 20 h after PI induction). Instead, the severity and site of GI distension could be monitored by the X-ray radiology. Therefore, the use of SIT as an index of Pi should be substantially limited.

Ghrelin/motilin-related peptide is a potent prokinetic to reverse gastric postoperative ileus in rat.

A novel peptide called ghrelin or motilin-related-peptide (MTLRP) was found in the stomach of various mammals. We studied its effect on the motor function of the rat gastrointestinal tract. In normal, conscious unoperated animals, ghrelin/MTLRP (5 or 20 microg/kg iv) significantly accelerated the gastric emptying of a methylcellulose liquid solution (gastric residue after 15 min: 57 +/- 7, 42 +/- 11, 17 +/- 4, and 9 +/- 3% of the ingested meal with doses of 0, 1, 5, and 20 microg/kg iv, respectively) Transit of the methylcellulose liquid solution was also accelerated by ghrelin/MTLRP in the small intestine but not in the colon. Des-[Gln(14)]ghrelin, also found in the mammalian stomach, was as potent as ghrelin in emptying the stomach (gastric residue after 15 min: 12 +/- 3% at a dose of 20 microg/kg iv). In rats in which postoperative gastrointestinal ileus had been experimentally induced, ghrelin/MTLRP (20 microg/kg iv) reversed the delayed gastric evacuation (gastric residue after 15 min: 28 +/- 7% of the ingested meal vs. 82 +/- 9% with saline). In comparison, the gastric ileus was not modified by high doses of motilin (77 +/- 7%) or erythromycin (82 +/- 6%) and was only partially improved by calcitonin gene-related peptide (CGRP) 8-37 antagonist (59 +/- 7%). Ghrelin/MTLRP, therefore, accelerates the gastric emptying and small intestinal transit of a liquid meal and is a strong prokinetic agent capable of reversing the postoperative gastric ileus in rat.

Effects of lanreotide on the healing of small bowel anastomoses following obstructive ileus in rats.

PURPOSE: Lanreotide, a long-acting somatostatin analogue, inhibits intestinal, bile and pancreatic secretions and decreases intestinal motility. The purpose of this experimental study was to evaluate the effects of lanreotide on the healing of intestinal anastomoses following small bowel obstruction. METHODS: Two groups of 16 Wistar rats (average weight 310 g) were used. Basal diameters of ileus were measured prior to the ligation of the bowel, 15 cm from the ileocecal valve. Luminal fluid was also withdrawn proximal to the obstructed bowel for sodium and potassium analysis. Lanreotide was administered intramuscularly in a single dose (5.4 mg/kg) in the first group, while the same volume of saline was used in the control group. 48 h later rats were re-operated upon. Diameters of the obstructed segments were measured, and luminal fluid of the obstructed bowel was withdrawn and sodium and potassium levels were measured. A segment of 1 cm of the obstructed bowel was resected and end-to-end intestinal anastomosis was performed. Rats were sacrificed on day 7 following the second operation. Anastomoses were examined macroscopically and resected including a 2.5 cm of small bowel on either side. Bursting pressures were measured and the specimens were send for histological examination. RESULTS: The diameter of obstructed bowel increased significantly in both groups. The increase was more prominent in the control group (P < 0.001). Total luminal electrolyte contents for sodium and potassium were stastistically higher in the control group compared to the lanreotide group (P < 0.001). Adhesion formation was more extensive in the control group. Bursting pressures were significantly higher in the lanreotide group compared to the control group (P=0.003). Histological examination of anastomoses showed a more profound inflammatory reaction in the control group compared to the lanreotide group while microscopical healing of the anastomoses was almost the same in both groups. CONCLUSIONS: Lanreotide administration in rats with small bowel obstruction decreases significantly distension and electrolyte losses and seems to improve strength of small bowel anastomoses.