[Irrigation of the cecum and of the appendix; problems in necrosis of the cecum].
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The existence of disaccharidases and an enzyme that hydrolyzes maltitol were investigated in the large intestine of rats. In addition, the properties of disaccharidases were studied in the cecum and colon with hyperplasia induced by the ingestion of nondigestible carbohydrates such as maltitol and glucomannan. Maltase activity was detected in the cecal and colonic mucosa of rats fed a regular diet, although it was a very low level as compared with that in the small intestinal mucosa. Maltitol hydrolysis was notably lower in the cecum and colon than in the small intestine. The Km of maltose was 5.56 mM in the small intestine and 5.59 mM in the cecum, while that in the colon was 2.56 mM. The Vmax of maltose was at very low levels in the cecum (0.38 mumol/mg protein/h) and colon (0.37 mumol/mg protein/h) in comparison with that in the small intestine (30.3 mumol/mg protein/h). With regard to the maltitol hydrolyzing enzyme, Km and Vmax were 2.00 mM and 2.51 mumol/mg protein/h in the small intestine, respectively. Km and Vmax in the cecum and colon could not be measured because the level was too low. The tissue weights of the cecum and colon increased significantly in both the maltitol (p < 0.01, p < 0.05) and glucomannan (p < 0.01, p < 0.05) groups in comparison with that of the control group. The specific activity of maltase decreased significantly in the small intestine of the maltitol (p < 0.05) and glucomannan (p < 0.01) groups. However, maltase activity in the cecum and colon was not lowered by maltitol ingestion, although it decreased significantly in the cecum of the glucomannan group (p < 0.01). Sucrase activity in the small intestine and cecum was decreased significantly by maltitol (p < 0.05, p < 0.01) or glucomannan (p < 0.01, p < 0.01) ingestion, whereas it was not decreased in the colon. Maltitol hydrolyzing activity did not decrease significantly in the small intestine of the maltitol group, although that in the cecum and colon was not measured exactly by the methods used here. These results demonstrate that disaccharidases exist in the cecal and colonic mucosa of rat, and that they are not induced even in the tissue with hyperplasia, which is caused by maltitol ingestion.
Sepsis in short bowel syndrome (SBS) is due in part to bacterial translocation (BT). Parenteral nutrition (PN) is often necessary in SBS and promotes BT. The presence of ileocecal valve (ICV) has been considered as a good prognostic factor in the outcome of this children. The aim of this study was to asses the effect of the presence or absence of ICV and cecum in five different models of gut resection in the rat. Fifty-five adult Wistar rats were randomly assigned to one of five groups: Group 1 (N = 14): standard rat chow + 80% small bowel resection. Group 2 (N = 10): standard rat chow + 80% small bowel resection including cecum. Group 3 (N = 10): standard rat chow + 80% small bowel resection including ICV. Group 4 (N = 11): NP + 80% small bowel resection. Group 5 (N = 10): NP + 80% small bowel resection including ICV and cecum. Ten days after surgery they were sacrificed and mesenteric lymph nodes (MLN), spleen and peripheral (PBL) and portal blood (POBL) specimens were recovered and cultured. Groups 3 (without ICV, with cecum) and 5 (without ICV, without cecum) showed 60% BT in MLN and POBL, and groups 1 and 4 (with ICV, without cecum) 93% and 91% respectively (p < 0.05). In PBL, group 3 (without ICV, with cecum) showed also less BT than groups 1 and 4 (10% vs 43% and 55% respectively, p < 0.05) and group 5 (without ICV and cecum) had less BT than groups 1, 2 and 4 (0% vs 43%, 30% and 55%, p < 0.01). In conclusion, these results suggest that the absence of ICV decreases BT and that the cecum does not seems to play a role on his.
Pectin is a soluble indigestible polysaccharide that stimulates cecal polyamine formation in rats. Bacteroides and fusobacteria, two numerically dominant bacterial population groups in the large intestine, were found to synthesize in vitro high amounts of spermidine and putrescine. The purpose of this study was to elucidate the effect of pectin on the polyamine production by defined bacterial species in vivo. Germfree male Wistar rats (n = 18) were randomly assigned to one of three treatments: (i) monoassociation with Bacteroides thetaiotaomicron + fiber-free diet; (ii) diassociation with B. thetaiotaomicron + Fusobacterium varium + fiber-free diet or (iii) diassociation with B. thetaiotaomicron + F. varium + fiber-free diet + 10% pectin. The cecal contents of monoassociated rats fed fiber-free diet contained large amounts (1.51+/-0.21 micromol/dry total cecum content) of spermidine which was the major polyamine. The cecum of diassociated rats fed the fiber-free diet contained even higher concentrations of spermidine (2.53+/-0.21 micromol/dry total cecum content) and also putrescine, which was now the dominant polyamine (putrescine 0.32+/-0.28 vs. 3.01+/-0.28 micromol/dry total cecum content; monoassociation vs. diassociation). Pectin consumption by diassociated rats led to an additional increase in the cecal concentrations of all polyamines: putrescine, spermidine and spermine were 40, 37 and 100%, respectively, higher in the diassociated rats consuming the pectin diet than in those consuming the pectin-free diet. Since the microbial counts in the cecum did not differ in the diassociated treatment groups, the elevated concentrations of polyamines observed in the pectin group must have been due to stimulated bacterial polyamine synthesis. The decline of individual polyamines from cecum to feces detected at the end of the study in all treatment groups and the high microbial counts in the cecum and in feces suggest that bacterial polyamines are absorbed in cecum and colon. Pectin stimulates intestinal microbes to synthesize large amounts of polyamines which may be utilized by the host.
OBJECTIVE: To analyze myoelectric activity of the cecum and proximal loop of the ascending colon (PLAC) in cows after spontaneous cecal dilatation/dislocation (CDD) and compare it with that in healthy cows after surgical evacuation of the cecum. ANIMALS: 12 cows with spontaneous CDD and 6 healthy cows (group C). Cows with spontaneous CDD were retrospectively assigned to 2 groups: delayed recovery from surgery or recurrence (group A; n = 3), and normal recovery (group B; n = 9). PROCEDURE: After surgical evacuation of the cecum, 8 pairs of bipolar, retrievable electrodes were implanted in the ileum, cecum, and PLAC. Cows were evaluated daily from postoperative day 1 to 7, using routine clinical methods and computer-based analysis of myoelectric activity of the cecum, and PLAC. Parameters of myoelectric activity included rate of spike bursts, duration of individual spike bursts, duration of overall spike burst activity per electrode, rate of propagated spike burst sequences, and ratio of orally propagated spike burst sequences. RESULTS: Rate of spike bursts, duration of cecocolic spike burst activity, and ratio of orally to aborally propagated spike burst sequences did not vary among groups during the 7-day recording period. However, cows with delayed recovery had a typical, uniform pattern of myoelectric activity of the cecum and PLAC at days 1 and 2 after surgery that consisted of repeated, propagated spike burst sequences, made up of spike bursts of significantly (P < 0.05) increased duration at postsurgical day 1 and substantially prolonged duration at postsurgical day 2, interrupted by periods of little or no activity. CONCLUSION: Delayed recovery and recurrence of CDD in cows after spontaneous CDD is not caused by hypomotility of the cecum and PLAC. CLINICAL RELEVANCE: Postoperative treatment, intended to reduce recurrence of CDD or delayed recovery after surgical evacuation of the cecum, should address propagation of digesta in the spiral colon.
We have investigated the possible relation between the phloridzin-sensitive influx of alpha-methyl-D-glucoside (concentration 5 mmol/l) and the brush border surface area, in chicken isolated enterocytes. The intestinal regions studied were: jejunum and proximal cecum (both with high affinity sugar transport sites), medial cecum (with a low affinity transport system) and distal cecum (which lacks any transport ability). Cell apical surface measured by electron microscopy gave the following results; jejunal cells (0.41 micron 2) greater than proximal cecal cells (0.23 micron 2) greater than medial cecal cells (0.15 micron 2) = distal cecal cells (0.14 micron 2). This parameter is mainly determined by the length of microvilli. Sugar influx studies showed that the concentration of the substrate in cell water (in mmol/l) was jejunum (7.1) greater than proximal cecum (2.9) greater than medial cecum (1.7) greater than distal cecum (not different from zero). The decline in influx rate from proximal to distal cecum may be explained both by changes in surface and by the different carriers involved (different Km). Results of sugar concentration in the distal cecal cells do not correlate with the other segments studied since the substrate enters in these cells by a passive process. It is concluded that the degree of development of microvilli should be taken into account when estimating nutrient transport rates in different intestinal segments.
This study was conducted to determine the ion transport mechanisms in the normal mouse cecum and compare them to an inbred mouse model of colitis. The Ussing chamber-voltage clamp technique was used to monitor the short circuit current (I(sc)). The basal I(sc) in the normal cecum was 82.6 +/- 5.8 microA/cm2. It was not affected by bumetanide, 9-anthracene carboxylate, amiloride, and phenamil or by removal of Cl- ions; but was abolished by the removal of Na+ ions. Flux measurements revealed the presence of neutral NaCl transport. In the colitic cecum, the basal current was significantly higher than the normal cecum. Basal current in the normal cecum was due primarily to Na+ absorption through a Na+ channel, while in the colitic cecum it was due to Cl- ion secretion. cAMP addition in colitic cecum did not increase Cl- secretion, further suggesting that the tissue is already secreting at a maximal rate.
The acute effects of both cigarette smoking and nicotine on postprandial mouth-cecum transit were studied in 20 habitual smokers, 10 males and 10 females. Mouth-cecum transit time was measured by the breath hydrogen technique, following ingestion of a standard mixed liquid meal. Each subject was studied on four separate occasions, either (1) sham or actively smoking two standard cigarettes, commencing 20 min after the meal, or (2) chewing two placebo or nicotine tablets over a 60-min period, commencing immediately after the meal. The time of administration of these stimuli was designed to minimize the effects on mouth-cecum transit time of alterations in gastric emptying. Mouth-cecum transit time was prolonged in response to both smoking [median and interquartile range: 120 (95, 150) min vs 100 (75, 140) min, P = 0.01] and nicotine [120 (80, 170) min vs 100 (70, 140) min, P = 0.002]. No difference was observed between sexes with respect to nicotine; the effect of smoking on mouth-cecum transit time, however, was less pronounced in females compared to males [difference active-placebo: 10 (10, 20) min vs 35 (20, 60) min, P = 0.01]. We conclude that acute cigarette smoking delays mouth-cecum transit time, an effect most likely due to nicotine.
Addition of penicillin, Terramycin, or kanamycin to the drinking water of adult mice rapidly induced in them an enlargement of the cecum. In all animals, this occurred within 12 hr after the beginning of drug administration-the effect being most pronounced with penicillin. The cecums remained enlarged and generally continued to increase in size as long as the antibacterial drugs were administered. The increase in wet weight of the cecums was due primarily to an accumulation of water in the lumens during the first 24-48 hr of drug administration. At that time, there were no detectable histological changes in any case, but the bacteriological picture differed from drug to drug. The cecums were free of bacteria in animals receiving penicillin, fusiform-shaped bacteria and bacteroides were present in those receiving Terramycin, and lactobacilli and bacteroides in those receiving kanamycin. After the initial 48 hr, an abundant and complex secondary microflora developed in all treated animals, its composition being characteristic for each type of antibacterial drug. When penicillin was administered for 2 wk, the cecal weights and microbial populations did not return to normal levels for over 14 days after discontinuance of the drug. This recovery period could be shortened to 10 days by giving the mice food contaminated with cecal homogenates prepared from normal animals. A period of 7 or 8 days was required for the cecal weights and microflora to reach normal levels when the administration of penicillin lasted only 24 hr; this period could not be shortened by giving the animals contaminated food. The effects of drugs on the size and bacterial contents of the cecum have been discussed in the light of earlier findings concerning the characteristics of the huge cecums uniformly found in germfree mice. Taken together, these observations support the hypothesis that certain elements of the intestinal microflora-not yet completely identified-play an essential role in maintaining the integrity of the water-transport mechanism in the intestinal epithelium.
Six Jersey cows were implanted with 8 pairs of bipolar electrodes: 1 in the jejunum, 1 in the ileum, 3 in the cecum, and 3 in the proximal loop of the ascending colon (PLAC). Myoelectric activity was recorded at 2- to 3-day intervals, 3 times for 8 hours or 4 times for 6 hours, using a computer-based oscillograph and data-acquisition program. Mean (+/- SD) duration of the migrating myoelectric complex (MMC) in the ileum was 84.52 +/- 4.87 minutes. Phases I and II of the MMC lasted significantly (P < 0.05) longer than phase III. Two types (A and B) of cyclic activity were found in the cecum and PLAC. Cyclic activity type A was observed predominantly in the cecum, and type B was observed exclusively in the PLAC. Phase III of the MMC in the ileum was accompanied by hyperactivity type A at the level of the ileocecocolic junction in 60.90 +/- 12.65% of the MMC. Twenty-seven types of orally and aborally propagated spike sequences, involving the cecum and PLAC, were found. They were most frequent when an MMC phase III was observed in the ileum, and least frequent when an MMC phase I was observed in the ileum (P < 0.05). All electrode sites of the cecum and PLAC served as pacemaker areas. Propagated and nonpropagated spikes were found at all electrode sites of the cecum and PLAC. Although propagated spikes lasted significantly (P < 0.05) longer than nonpropagated spikes, a clear distinction on the basis of duration could not be defined between the 2 spike types because broad overlapping of duration existed.(ABSTRACT TRUNCATED AT 250 WORDS)