Conventional Rats Research Articles

Small intestinal growth caused by feeding red kidney bean phytohemagglutinin lectin to rats

Background: Plant lectins are present in significant quantity in a variety of food sources. The aim of this study was to determine if they stimulated growth of the intestine. Methods: Germ-free and conventional rats were pair fed purified phytohemagglutinin lectin (PHA) or equivalent casein in a fully nutritious diet. PHA was instilled into in situ jejunal and ileal loops. Organ weight, length, DNA, protein content, morphometry, and [3H]thymidine uptake into jejunal crypt cells were measured. Results: A trophic response occurred in the small intestine (jejunum greater than ileum) because of PHA (P < 0.001), was sustained by continued exposure, and was reversible on reinstitution of the control diet (P < 0.05). The intestinal microbial flora in conventional animals that were fed PHA augmented the growth-stimulatory effects of PHA on intestinal weight (P < 0.01). PHA caused fecal protein, fat, and mucous glycoprotein levels (P < 0.001) to increase in germfree animals. PHA increased jejunal mucosal crypt depth and crypt mitotic activity (P < 0.05); DNA content (P < 0.05) and [3H]thymidine uptake (P < 0.01) into crypt cells was increased. No increase in plasma or tissue content of gastrin, enteroglucagon, or peptide YY was observed on PHA exposure, and there was no increase in organ weight of the liver, kidney, or colon. Conclusions: PHA stimulated growth of rat small intestine when present in the diet or instilled in the bowel lumen.

Effects of galacto-oligosaccharide and bacterial status on mucin distribution in mucosa and on large intestine fermentation in rats

The purpose of the present paper was to study the effects of a dietary undigestible carbohydrate and intestinal microflora on mucin distribution (neutral, acid, sulphonated), glycolytic activities: beta-D-galactosidase (EC 3.2.1.23), N-acetyl-beta-D-galactosaminidase (EC 3.2.1.43), N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30), alpha-L-fucosidase (EC 3.2.1.51) and bacterial metabolism (gas production, short-chain fatty acids (SCFA) and lactic acid caecal concentration) in germ-free (GF), conventional (CV) and heteroxenic (HE) rats (GF rats associated with a human flora). Rats were fed on either a control diet or a diet containing 40 g trans-galactosylated oligosaccharide (TOS)/kg. In GF rats fed on the control diet caecal pH was almost neutral and glycolytic activities negligible. The number of mucus-containing cells increased from the caecum to the colon for the three types of mucin. TOS had no effect in the caecum but it modified mucin cell repartition in the colon. In CV and HE rats fed on the control diet caecal pH was similar (6.8), but caecal SCFA and lactic acid concentrations (mumol/g) and gas production (ml/24 h) were higher in CV (70, 5.9 and 2.3 respectively) than in HE rats (32, 4.6 and 0.4 respectively). In CV, as in HE rats, acid-mucin-containing cells increased from the caecum to the colon and glycolytic activities were similar. TOS reduced acid-mucin-containing cells in the caecum of CV rats by twofold but had no effect in either the caecum or the colon of HE rats. TOS strongly increased beta-galactosidase activity and slightly modified the other glycolytic activities. Its effect on bacterial metabolites depended on bacterial status. However, comparison between CV and HE rats showed no evident relationship between the number of mucus-containing cells and measured bacterial metabolites. Differences between CV and HE rats might be due to bacterial microflora specificity. TOS had an intrinsic effect on mucus cell distribution in the colon of GF rats. In CV and HE rats the presence of the flora abolished this effect.

Protective salivary immunoglobulin A responses against Streptococcus mutans infection after intranasal immunization with S. mutans antigen I/II coupled to the B subunit of cholera toxin

The B subunit of cholera toxin (CTB) has been shown to augment mucosal responses to microbial virulence antigens, including those of Streptococcus mutans, which is the principal etiologic agent of dental caries. In the present study, the surface fibrillar protein antigen of S. mutans, antigen I/II (Ag I/II), was chemically coupled to CTB (Ag I/II-CTB), and the conjugate was examined for its effectiveness in inducing salivary immune responses protective against S. mutans infection. Weanling Fischer rats were given Ag I/II-CTB (50 micrograms) by the intranasal route and then orally infected with a virulent strain of S. mutans. Gnotobiotic or conventional rats were given two or three additional immunizations, respectively, at about 2-week intervals. One week after each immunization, individual serum, saliva, and fecal samples were collected and stored frozen until assayed for antibody activity to Ag I/II and cholera toxin (CT) by an enzyme-linked immunosorbent assay. The rats were sacrificed 1 week after the last immunization, when mandibles were also collected from individual rats for assessment of S. mutans levels in plaque and caries activity. Rats immunized only or both immunized and infected showed a salivary immunoglobulin A (IgA) anti-Ag I/II response which reached significantly (P < 0.05) higher levels than those seen in nonimmunized, infected controls. A salivary IgA anti-Ag I/II response was also seen in rats infected only with S. mutans. Essentially no salivary antibody activity to CT was detected. Some serum anti-Ag I/II and anti-CT responses were seen in immunized animals. Serum IgG anti-Ag I/II responses were seen in immunized, infected rats and also in infected-only rats, suggesting that the responses were a result of infection with S. mutans. The immunized and infected rats had significantly (P < 0.05) lower levels of S. mutans in plaque and lower caries activity than nonimmunized, infected rats. These results indicated that intranasal immunization of rats with Ag I/II-CTB induced a protective salivary immune response which was associated with a reduction in S. mutans colonization and S. mutans-induced dental caries.

Sulphated bile acid per se inhibits colonic carcinogenesis in mice

Peroral sulpholithocholic acid (SLC) promoted colonic tumorigenesis in conventional rats. We then tested this compound in the mouse, a species with different bile acid metabolism from the rat. Female conventional ICR mice received 0.5 mg of N-methyl-N-nitrosourea (MNU) three times in one week intrarectally or 16 mg/kg body weight of 1,2-dimethylhydrazine (DMH) subcutaneously once a week for 10 weeks, followed by a basal diet (CE-2), or CE-2 containing SLC or lithocholic acid (LC) (both at 0.5 mmol/100 g CE-2) for 40 weeks. At autopsy, numbers of mice bearing colonic neoplasms were 4/26 (15%) in the MNU + CE-2, 4/23 (17%) in the MNU + SLC, 5/28 (18%) in the MNU + LC, 12/24 (50%) in the DMH + CE-2, 6/23 (26%) in the DMH + SLC and 11/27 (41%) in the DMH + LC group. The DMH + SLC group had less adenocarcinomas than did the DMH + CE-2 and the DMH + LC group (P < 0.05). Total faecal bile acids in the mice fed on bile salts showed threefold increases compared with those on the basal diet. Sulphates constituted an average 7% and 19% of faecal bile acids in the MNU + SLC and DMH + SLC group, respectively. These results indicated that effects of peroral SLC on colonic carcinogenesis correlated with the degree of desulphation of SLC in the intestine and sulphates per se inhibited colonic carcinogenesis.

Effect of LongoVital treatment on development of periodontal disease in rats.

LongoVital is a herbal tablet with documented immunostimulatory effects in man. In the present study the effect of LongoVital on development of periodontal disease was investigated in a rat model. Fifty-four conventional rats, 5 wk old, were distributed into the following groups: A) untreated, uninfected; B) untreated, infected with Actinomyces viscosus and Porphyromonas gingivalis wk 8; C) treated with LongoVital 80 mg x 3/wk, wk 5-14, uninfected; D) treated with LongoVital 80 mg x 3/wk, wk 5-14, infected with A. viscosus and P. gingivalis wk 8; E) treated with LongoVital 200 mg x 1 in wk 8 and 80 mg wk 9-14, uninfected; F) infected with A. viscosus and P. gingivalis wk 8, subsequently treated with LongoVital 200 mg x 1 in wk 8 and 80 mg wk 9-14. All animals were killed when they were 15 wk old, and periodontal bone support was assessed radiographically. Statistically significant bone loss was found in untreated, infected rats, as compared with untreated, uninfected rats. In LongoVital-treated animals, no significant difference was seen in bone level between infected and uninfected rats. These results indicate that LongoVital-treated rats were protected against periodontal bone loss caused by infection with A. viscosus and P. gingivalis. Furthermore, the protection seemed effective both when LongoVital was administered prophylactically and after exposure to periodontal pathogens. The active components of LongoVital, as well as the mechanisms responsible for the protection, remain obscure.

In vitro evaluation of dexamethasone-beta-D-glucuronide for colon-specific drug delivery.

Dexamethasone-beta-D-glucuronide is a potential prodrug for colonic delivery of the antiinflammatory corticosteroid dexamethasone. Previous studies [T. R. Tozer et al., Pharm. Res. 8:445-454 (1991)] indicated that a glucoside prodrug of dexamethasone was susceptible to hydrolysis in the upper gastrointestinal tract. Resistance of dexamethasone-beta-D-glucuronide to hydrolysis in the upper gastrointestinal tract was therefore assessed. Conventional, germfree, and colitic rats were used to examine enzyme levels along the gastrointestinal tract to compare the stability of two model substrates (p-nitrophenyl-beta-D-glucoside and -beta-D-glucuronide) and to evaluate the prodrug dexamethasone-beta-D-glucuronide. Hydrolytic activity was examined in the luminal contents, mucosa, and underlying muscle/connective tissues in all three types of rats. Enzymatic activity (beta-D-glucosidase and beta-D-glucuronidase) was greatest in the lumen of cecum and colon of conventional rats. In contrast, germ-free rats exhibited relatively high levels of beta-D-glucosidase activity (about 80% of total activity in the conventional rats) in the proximal small intestine (PSI) and the distal small intestine (DSI). Rats with induced colitis (acetic acid) showed reduced levels of luminal beta-D-glucuronidase activity in the large intestine; however, beta-D-glucosidase activity was relatively unchanged relative to that of the conventional rat. Mucosal beta-D-glucuronidase activity was significantly lower in the colitic rats compared with that in the conventional animals. Despite reduced luminal levels of beta-D-glucuronidase activity in the colitic rats, there was still a sharp gradient of activity between the small and the large intestines. Permeability of the glucoside and glucuronide prodrugs of dexamethasone through a monolayer of Caco-2 cells was relatively low compared to that of dexamethasone. The results indicate that dexamethasone-beta-D-glucuronide should be relatively stable and poorly absorbed in the upper gastrointestinal tract. Once the compound reaches the large intestine, it should be hydrolyzed to dexamethasone and glucuronic acid. Specificity of colonic delivery in humans should be even greater due to lower levels of beta-D-glucuronidase activity in the small intestine compared with that in the laboratory rat.

Steroid-Induced Depletion of Mucosal Mast Cells and Eosinophils in Intestine of Athymic Nude Rats

In conventional rats, we have previously demonstrated that corticosteroid treatment caused macrophage engulfment and destruction of intestinal mucosal mast cells and eosinophils by 24 h without evidence of local tissue destruction, inflammation or secretion of rat mast cell protease II. As the growth and survival of these cells appear to be dependent on factors derived from T lymphocytes, we examined the response in congenitally athymic rnu/rnu rats and euthymic rnu/+ rats 35 days after parasitic infection. Rats were injected intraperitoneally with 1 mg dexamethasone and sections of jejunum were examined at 0, 7, 13 and 24 h. The numbers of mucosal mast cells significantly decreased in both groups and became less than 30% of the original values at 24 h. Tissue mast cell protease decreased similarly. However, protease in serum did not increase and there were no inflammatory changes at any time. The numbers of eosinophils also rapidly decreased and became less than 20% at 24 h in both rnu/rnu and rnu/+ rats. By electron microscopy, we saw granular changes (fusion) in mast cells and nuclear changes (apoptosis) in eosinophils by 7 h after corticosteroid in athymic rats. Macrophage engulfment of these cells was observed at 7 and 13 h. Our results suggest that inflammatory cell depletion by macrophages is not dependent on suppression of typical thymus-derived T lymphocytes, and may be due either to direct effects of steroids on the cells themselves, or indirectly upon cells other than T cells which normally supply maintenance and growth factors for them.

Serological evidence of pneumonia virus of mouse (PVM) infection in laboratory rats.

PVM specific antibody was determined using 3 serological tests (Parker's original hemagglutination-inhibition [HI] test, modified HI test, and indirect fluorescent antibody [IFA] test). IFA test was found to be the most sensitive method, so that IFA test was considered to be the method of choice for a small scale microbiological monitoring in animal facilities. A total of 1,280 sera including rats, mice, hamsters and rabbits were tested for PVM antibody. The prevalence of PVM antibody was 17.2% (116/674) in conventional rats and 30.0% (160/200) in SPF rats obtained from commercial breeders and research facilities. Furthermore, two samples of 144 conventional rabbits (1.4%) were showed specific antibody positive to the virus. However, hamsters and mice showed no evidence of PVM infection. These results suggest that PVM infection is prevalent, especially in laboratory rats in Japan.

The development of Pneumocystis carinii pneumonia in germ-free rats requires immunosuppression and exposure to the Pneumocystis carinii organism

Adult germ-free rats treated with dexamethasone and exposed to a non-sterile environment did not harbor or develop Pneumocystis carinii cysts or trophozoites after 10 weeks of immunosuppression. Only when they were exposed to infected, conventional rats and treated with dexamethasone for 8 weeks or longer, did adult germ-free rats develop P. carinii infection.

Prevalência do nematóide Trichosomoides crassicauda em uma colônia convencional de ratos Wistar

Determinou-se a prevalência do nematóide Trichosomoides crassicauda na colônia convencional de ratos Wistar do Biotério Central (DTAEP) da Faculdade de Medicina da USP. Foram examinadas as bexigas urinárias de 365 ratos sendo 130 machos e 133 fêmeas, de 8 a 19 semanas de idade; e 51 machos e 51 fêmeas, com idade acima de 20 semanas, retirados da reprodução. Foi também determinada a prevalência de cálculos urinários, os quais têm sido associados à presença do parasita. Os resultados obtidos indicaram que a prevalência do T. crassicauda na colônia foi de 48% (43% em machos e 53% em fêmeas), sendo que o máximo valor observado foi 80%, em machos de 16 semanas de idade. O número médio de parasitas por rato não ultrapassou o limite de 2,5 em fêmeas de 16 semanas de idade. Não houve diferença na prevalência de cálculos urinários entre animais parasitados e não parasitados (10% e 16%, respectivamente), mas esta diferença foi significante entre machos e fêmeas (23% e 4%). Além disso, os cálculos encontrados nos machos (mucóides) foram diferentes daqueles encontrados nas fêmeas (cristais).

A Method for Estimating the Available Energy of Incompletely Digested Carbohydrates in Rats

We developed a method to estimate the available energy from carbohydrates that are unavailable or partially unavailable through direct digestion and absorption. Radiolabeled bacterial and plant cellulose and polydextrose were administered orally to germfree and conventional rats. Label in breath, feces, intestinal contents and carcass were determined with excellent total recovery of the administered label. Comparison of these measurements in germfree and conventional rats was used to calculate the energy directly available by digestion and that available only after fermentation. Although the method overestimates available energy because of the more efficient digestive metabolism of the germfree rat, it provides a reliable, maximum energy value based upon fewer assumptions than previous methods. In conventional rats, 65% of the administered cellulose and 54% of the administered polydextrose were recovered in feces. In conventional rats, appreciable amounts of cellulose were fermented and an available energy value of 3.5 kJ/g was calculated. Calculation of the total availability of polydextrose, taking into account the direct absorption of small amounts of monomers present and the efficiency of fermentation, indicates an available energy value of 4.7 kJ/g.

Chronic peroral immunization of conventional laboratory rats with mutans streptococci leads to stable acquired suppression of salivary antibodies.

Prior investigations have demonstrated that salivary antibody responses to mutans streptococci are dose-dependent and temporary. The purpose of this study was to evaluate the stability of antibody suppression established by mutans streptococci. Streptococcus mutans 6715-15 was provided in food to conventional rats for 18 weeks. Antigen was withdrawn for 10 weeks and then resumed for an additional 6 weeks. Saliva and serum from nonimmunized controls and from experimental rats were tested with a quantitative enzyme-linked immunosorbent assay for IgA and IgG antibodies to whole bacterial cells and to soluble antigen. Results show that salivary antibodies were stimulated by primary peroral immunization, that IgA was the dominant isotype and that IgA antibodies were primarily directed against soluble antigen. This study also shows that immunity is not maintained, even while challenge continues, and that once suppression is established, immunized animals do not recover their ability to respond, even if exposure is stopped for 10 weeks before re-exposure.

Contribution of the digestive tract microflora to amylomaize starch degradation in the rat.

To study in vivo the contribution of the bacterial flora to amylomaize starch degradation in the rat, germ-free and conventional rats were fed on a diet containing either a normal maize starch or an amylomaize starch. In germ-free rats maize starch was almost totally digested in the small intestine, whereas 40% of the ingested amylomaize starch reached the caecum and 30% was excreted, despite the very high endogenous amylase activity. Study by transmission electron microscopy of germ-free caecal contents showed an endocorrosion of the starch granule. In conventional rats, as in germ-free rats, digestibility of maize starch reached 98% in the small intestine, whereas that of amylomaize starch was only 60%. In the caecum of these rats amylomaize starch was fermented, and this led to a decrease in caecal pH and to formation of short-chain fatty acids (SCFA), especially propionate. Comparison between conventional rats fed on maize starch or amylomaize starch showed that caecal SCFA concentrations during a circadian cycle varied in the same way whereas total SCFA and lactic acid concentrations were much higher in rats fed on amylomaize starch. Amylase (EC 3.2.1.1) activity was similar in the caecal contents of conventional rats whatever the ingested starch. It was lower in conventional than in germ-free rats, but no starch granule remained in the caecum of conventional rats. These results showed that bacterial amylase was more efficient at degrading resistant amylomaize starch than endogenous amylase.

Class II MHC Molecules and Monocytes/Macrophages in the Respiratory System of Conventional, Germ-Free and Interferon-Gamma-Treated Rats

The localization of I-A-like class II major histocompatibility complex (MHC) molecules and cells of the monocyte/macrophage lineage was studied immunohistologically in the trachea and lungs of conventional, specified pathogen-free (SPF) and germ-free rats. In the three groups of animals I-A-like class II MHC molecules occurred in epithelia of the bronchus-associated lymphatic tissue (BALT), in B lymphocytes, in dendritic-shaped and elongated interstitial cells and in type II pneumocytes. Conventional and SPF rats were distinguished from germ-free animals only by the larger number of class II MHC-positive respiratory epithelial cells in the lower trachea and main bronchi. The distribution of monocytes/macrophages (ED1-positive cells) did not differ between the groups. After systemic treatment of SPF rats with interferon-gamma class II MHC molecules were newly induced in all respiratory epithelia and in the endothelium of large vessels. In addition, interferon-gamma sometimes led to pulmonary infiltration and caused class II-positive activated monocytes to accumulate in medium-sized pulmonary vessels and in alveolar capillaries. It is concluded that the microbial status does not qualitatively alter the distribution of class II MHC molecules and monocytes/macrophages in rat respiratory organs. Interferon-gamma can, however, provoke profound changes.

Effect of spontaneous pathology and thrombin on leukocyte adhesion to rat aortic endothelium

Leukocyte adhesion and other injury parameters have been studied in the aortic endothelium of Sprague-Dawley rats in two situations: (1) spontaneous pathology in conventional rats with antibodies to Mycoplasma pulmonis and/or Kilham or Sendai viruses, and (2) intravascular coagulation by thrombin administration in SPF rats. Adhesion (esterase (+) leukocytes/mm 2) in SPF rats was 8 ± 5 ( n = 12). Adhesion in 38% of the conventional rats was 54 ± 27 ( n = 8), half of them being non-analyzed and the rest having antibodies to M. pulmonis and/or Kilham rat virus. In 19 rats with antibodies to M. pulmonis and/or Kilham or Sendai viruses, AgNO 3 and hematoxylin staining of the aortic endothelium showed an increase in leukocyte adhesion, and the presence of argyrophilic cells, stigmata and granularity — severe endothelial lesions being observed in some cases. Adhesion in rats after 0.25, 1, 3 and 6 h of thrombin administration (30 units/100 g) was not different from controls. Adhesion after 24 h was 108 ± 53 ( n = 10) and 60 ± 59 ( n = 10), and 22 ± 20 ( n = 10) in rats treated with thrombin plus heparin or hirudin, respectively. Thrombin produced endothelial lesions at all times studied, and these included membrane blebs, platelet and erythrocyte adhesion and alterations in the pattern of endothelial esterase activity.

Introduction of conventional microbial flora to germfree rats increases the frequency of migrating myoelectric complexes

AbstractThe present study demonstrates a direct stimulating influence of the viable conventional microbial flora on fasting myoelectric activity of the small intestine. Ten germfree AGUS rats were operated upon within sterile stainless steel isolators. Three bipolar electrodes were implanted into the muscular wall of the proximal small intestine, and fasting myoelectric recordings were performed one week later. Subsequently, the rats were transferred to the external conventional environment, and caecel content from conventional AGUS rats was given perorally and rectally. One week later, when the intestinal tract was colonized, myoelectric recordings were repeated. The frequency of activity fronts in proximal jejunum increased after introduction of conventional intestinal microflora, reflected by a decrease of the interval between activity fronts from median 17.6 min (15.2–23.4 min) (10th and 90th percentiles) to 13.9 min (11.4–17.6 min) (P &lt; 0.05). The duration of activity fronts in proximal jejunum decreased from 4.9 min (3.8–5.9 min) to 3.6 min (3.2–3.9 min), respectively (P &lt; 0.05). The propagation velocity of activity fronts was not significantly different. Stimulation of the fasting motility in the small intestine by conventional microbial flora may reflect activation of a physiological defense response in the host, in order to restrict bacterial colonization and avoid bacterial overgrowth of the small intestine.

Serum Zinc in Aging Germ-Free and Conventional Rats

Zinc nutritional status appears to decline with age in humans and rodents. Since germ-free rats outlive their conventional counterparts in better health, serum Zn levels were determined in male germ-free and conventional Lobund Wistar rats in samples originating from the Lobund Aging Study. Starting at 5 months of age, germ-free rats showed significantly higher serum Zn levels than did their conventional counterparts. In conventional rats sacrificed up to 30 months of age in apparently good health, serum Zn levels showed no effect of age, while a slight but significant increase with age was observed in the germ-free rats. In healthy germ-free adults (6-24 months of age), serum Zn concentrations were approximately 25% higher than those in comparable conventional animals. In conventional rats 18-30 months of age (average, 24.5 months), sacrificed because of an obvious moribund condition, serum Zn levels were significantly lower than those in rats of the same age range (average, 24.9 months) that were obviously healthy. Results suggest that the often observed higher absorptive capacity of the germ-free gut might have contributed to higher serum Zn levels, and that a decline in serum Zn concentration with age may be a consequence, rather than a causative factor, of declining health.

Intestinal mucosal morphometry and ileal epithelial renewal in conventional and germ-free rats fed an amylomaize starch diet.

Intestinal mucosal morphometry and ileal epithelial renewal were studied in conventional (CV) and germ-free (GF) rats fed either poorly digestible amylomaize or normal maize starch diets. Intestinal morphometry and position of labelled enterocytes were studied at various times after tritiated thymidine injection. With amylomaize starch diet, no difference was observed in the size of crypts (C), villi (V) and C + V between duodenum and jejunum both in CV and GF rats. In the ileum, however, values were significantly lower than those in the duodenum and jejunum. Furthermore, the presence of the microbial flora led to higher values when compared with GF values. Despite the morphological modifications in the ileum, no significant difference was detected in the labelled cell positions and epithelial renewal time between CV and GF values. This suggests that the resistant part of amylomaize starch was responsible for the modification in mucosal morphometry and the longer ileal epithelium renewal time in CV rats which then becomes similar to that in GF rats.

Preventive Effect of Green Tea Polyphenols against Dental Caries in Conventional Rats.

The effects of green tea polyphenols, inhibitors of various biological activities of cariogenic bacteria in vitro, on caries development were examined using conventional rats. A total of 96 male rats were divided into 8 groups and the rats in the test groups were given tea polyphenols ranging from 0.1% to 0.5% in their cariogenic diet or drinking water for 40 days. Total fissure caries lesions was significantly reduced by the addition of tea polyphenols to the diet or in the drinking water. Diet containing 0.1% tea polyphenols demonstrated about 40% reduction of total fissure caries lesions. No toxic effect of tea polyphenols on rats were observed under these experimental conditions.

The role of the gastrointestinal microflora in postsurgical adhesion formation--a study in germfree rats.

The elucidation of the pathogenesis of postsurgical adhesion formation is still lacking. In this study experimental adhesion formation was studied in germfree (i.e. void of bacteria) and conventional rats (intestinal flora comprising over 400 species) using a caecal crush model. The germfree rats responded significantly weaker to the same stimuli, forming adhesions in only 20% of the cases as compared to the conventional rats 87.5% (p = 0.0076). The findings indicate that the bowel flora is of importance but not essential for postsurgical adhesion formation in rats.