OBJECTIVETo establishment and verify pelvic nerve denervation (PND) model in mice.

METHODS(1) Establishment of models. Seventy-two healthy male SPE class C57 mice with age of 7 weeks and body weight of (25±1) g were chosen. These 72 mice were randomly divided into PND group containing 36 mice and sham operation group containing 36 mice. Referring to the establishment method of PND rats, after anesthesia, a laparotomy was performed on the mouse with an abdominal median incision. Under the dissection microscope, the pelvic nerves behind and after each sides of the prostate gland were bluntly separated with cotton swabs and cut with a dissecting scissor. After the operation, the urination of mice was assisted twice every day. For the mice of sham operation group, the pelvic nerves were only exposed without cutting. (2) Detection of models. Colonic transit test was performed in 18 mice chosen randomly from each group to detect the colonic transit ratio (colored colon by methylene blue/ whole colon) and visceral sensitivity tests was performed in the rest mice to observe and record the changes of electromyogram.

RESULTSThree mice died of colonic transit test in each group. Uroschesis occurred in all the mice of PND group and needed bladder massage to assist the urination. Colonic transit test showed that the colonic transit ratios of sham operation group at postoperative day (POD) 1, 3 and 7 were (0.4950±0.3858)%, (0.6386±0.1293)% and (0.6470±0.1088)% without significant difference (F=0.3647, P=0.058), while in PND group, the colonic transit ratio at POD 7 [(0.6044±0.1768) %] was obviously higher than that both at POD 3[(0.3876±0.1364)%, P=0.022] and POD 1[(0.2542±0.0371)%, P=0.001], indicating a recovery trend of colonic transit function (F=9.143, P=0.004). Compared with the sham operation group, the colonic transit function in PND group decreased significantly at POD 1 and POD 3(both P<0.05), and at POD 7, there was no significant difference between two groups. Visceral sensitivity test showed that the visceral sensitivity of sham operation group at POD 1, 3 and 7 was 24.2808±9.5566, 33.6725±7.9548 and 43.9086±12.1875 with significant difference (F=5.722, P=0.014). The visceral sensitivity of PND group at POD 1, 3 and 7 was 11.7609±2.1049, 21.8415±8.1527 and 26.2310±4.2235 with significant difference as well (F=11.154, P=0.001). The visceral sensitivity at POD 3 and POD 7 was obviously higher than that at POD 1 (P=0.006, P<0.001), and there was no significant difference between POD 3 and POD 7 (P=0.183). Compared with sham operation group, the visceral sensitivity of PND group decreased significantly at POD 1, 3 and 7(all P<0.05).

CONCLUSIONSDenervation of pelvic nerves can obviously decrease the colonic transit function and the visceral sensitivity of mice, but these changes can recover over time, which suggests that the establishment of PND model in mice is successful.

Abdominal Pain ; physiopathology ; Animals ; Autonomic Pathways ; growth & development ; physiopathology ; surgery ; Colon ; innervation ; physiopathology ; Denervation ; methods ; Disease Models, Animal ; Gastrointestinal Transit ; physiology ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue ; growth & development ; physiopathology ; surgery ; Pain, Postoperative ; physiopathology ; Pelvis ; innervation ; physiopathology ; surgery ; Prostate ; innervation ; Recovery of Function ; physiology

OBJECTIVETo study the effects of sacral nerve root electrostimulation (SNS) on the colon function and its mechanisms in rats with spinal cord injury (SCI).

METHODSOne hundred and four Wistar rats were divided into three groups: A, B and C. A group ( n = 24) was divided into three subgroups (n = 8) for studying the bioelectricity: Normal group (NG), SCI group (SCI) and SCI group with SNS(SNS); B group( n = 24) was divided into three subgroups( n = 8) for studying the colon motility: NG, SCI and SNS. C group( n = 56) were divided into three groups for studying the change of morphology and neurotransmitters(SP and VIP): NG (n = 8), SCI (n = 24), and SNS (n = 24) . In SCI and SNS, included of three subgroups: 24, 48, 72 h after spinal cord injury (n = 8).

RESULTSIn SCI group, the activity of bioelectricity in proximal and distal colon was reduced; the colon motility was lessened, and colon mucosa appeared different degree of damage; cell-cell connections between intestinal epithelial cells were destroyed. The expressions of substance P(SP) and vasoactive intestinal peptide (VIP) in colon were decreased obviously. SNS was found to activate the bioelectricity, promote the colon motility, improve the intestinal mucosal, and increase the expressions of SP and VIP. Conclusion: SNS can activate the peristalsis, rehabilitate the motility of denervated colon, protection of the intestinal mechanical barrier between intestinal epithelial cells and tight junction, rebuild the colon function through activating the bioelectricity and increase the expressions of SP and VIP.

Animals ; Colon ; physiopathology ; Electric Stimulation Therapy ; Epithelial Cells ; drug effects ; Intestinal Mucosa ; drug effects ; Lumbosacral Region ; innervation ; Neurotransmitter Agents ; metabolism ; Rats ; Rats, Wistar ; Spinal Cord Injuries ; therapy ; Substance P ; metabolism ; Vasoactive Intestinal Peptide ; metabolism

In recent years, according to the etiology and pathology researches of slow transit constipation (STC) STC is considered as a kind of "enteric neuropathy", indicating it is a kind of disease caused by abnormity of the enteric nervous system (ENS). Through reviewing the mechanism of acupuncture to regulate STC, it is found out that there is a close relationship between acupuncture regulating STC and ENS. Through various channels including ganglion cells, nerve plexus, neurotransmitter and TRPV1 (the primary sensory neurons receptor of the ENS) of the ENS, acupuncture is likely to make comprehensive adjustment on STC.
Acupuncture Therapy ; Colon ; innervation ; physiopathology ; Constipation ; physiopathology ; therapy ; Enteric Nervous System ; physiopathology ; Humans

Successful assessing intestinal lumen content with ultrasound signals might lay a strong basis for the development of the artificial anal sphincter. In the present study, we utilized a modified MLU02-212 ultrasonic gas bubble detector to test the distal part of proximal colon in each rabbit, for the group of twenty healthy New Zealand rabbits. Voltage signals of solid, liquid, gas and empty content of the lumen were collected and compared. The results indicated that there were significant differences among the voltage signals in the 4 conditions (P = 0.000), respectively. Multiple comparison showed significant differences existed in any pair of the four conditions (P = 0.000). Three signal non-overlapping regions existed in these 4 conditions. Thus it seemed that ultrasound could be utilized to distinguish various contents inside the intestinal lumen and could act as "artificial sensory nerve".
Anal Canal ; innervation ; physiology ; Animals ; Artificial Organs ; Colon ; diagnostic imaging ; Enteric Nervous System ; physiology ; Fecal Incontinence ; surgery ; Female ; Gastrointestinal Contents ; Gastrointestinal Motility ; physiology ; Male ; Rabbits ; Sensory Receptor Cells ; physiology ; Ultrasonography

Abdominal Muscles ; physiology ; Abdominal Pain ; diagnosis ; physiopathology ; Animals ; Animals, Newborn ; Colon ; innervation ; Electrodes ; Electromyography ; Female ; Pain Measurement ; methods ; Pain Threshold ; physiology ; Rats ; Rats, Sprague-Dawley ; Viscera ; Visceral Afferents ; physiology

OBJECTIVETo evaluate the roles of enteric nervous system neurotransmitters, nitric oxide (NO), substance P (SP) and vasoactive intestinal polypeptide (VIP), and interstitial cells of Cajal (ICC) in the colon in slow transit constipation in rats.

METHODSThirty-two healthy Wistar rats were randomly assigned to control and constipated groups. In the constipated group, the rats were daily administered with diphenoxylate (8 mg/kg) to develop slow transit constipation, while the control rats were fed with water. The number and the weight of fecal granule and the body weight of rats were recorded every 5 days for 90 days. Transit functions of intestinal movement were examined by an activated charcoal suspension pushing test one week after stopping the administration of diphenoxylate. The levels of NO and SP in the colonic mucosa were measured by nitrate reductase methods and ELISA respectively. The distribution of VIP and ICC positive cells confirmed with symbolic c-kit+ cells in the colonic wall were observed by immunohistochemical methods.

RESULTSThe daily number of fecal granule in the constipated group was significantly less than that in the control group (P<0.01). The mean weight of each fecal granule in the constipated group was significantly higher than that in the control group (P<0.01). The discharge time of the first granule of black faeces in the constipated group (430.2+/- 132.1 min) was significantly longer than that in the control group (337.2+/- 74.7 min; P<0.05). There were no significant differences in NO and SP levels and the density of VIP positive cells in the distal colonic segment between the two groups. The number of c-kit+ cells in the distal colonic wall in the constipated group was significantly reduced compared with that in the control group (P<0.05).

CONCLUSIONSThe reduction of ICC number in the distal colon may be contributed to the pathogenesis of slow transit constipation in rats.

Animals ; Body Weight ; Coiled Bodies ; Colon ; cytology ; innervation ; Constipation ; etiology ; Male ; Neurotransmitter Agents ; physiology ; Nitric Oxide ; analysis ; physiology ; Proto-Oncogene Proteins c-kit ; analysis ; Rats ; Rats, Wistar ; Substance P ; analysis ; physiology ; Vasoactive Intestinal Peptide ; analysis ; physiology

To study the acute and long-term effects of local gut inflammation on the sensitivity of the spinal sensory neurons, the expressions of vanilloid receptor 1 (VR1) and calcitonin gene-related peptide (CGRP) in the colon-innervated primary sensory neurons in dorsal root ganglia (DRG) were examined in rats with trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis. The neurons projecting to the distal colon were identified by DiI(3) retrograde labelling. Macroscopic examination, mean damage score and myeloperoxidase (MPO) activity were determined to assess the inflammatory status of the colon tissue. The number of CGRP and VR1 immunoreactive neurons at different stages of inflammation (on days 7, 21 and 42 after TNBS treatment) were compared. On day 7 after TNBS treatment, macroscopic damage of the mucosa could be easily detected and the percentage of colon-innervated DRG neurons expressing CGRP and VR1 increased nearly two folds respectively [(95.38±9.45)% vs (42.86±.02)% for CGRP, (89.23±8.21)% vs (32.54±4.58)% for VR1]. When the colon inflammatory reaction was resolved on days 21 and 42 after TNBS treatment, the percentage of colon-innervated DRG neurons expressing CGRP and VR1 were still higher than that in the control group [(86.25±8.21)%, (68.28±7.12)% vs (42.86±5.02)% for CGRP; (67.22±6.52)%, (56.25±4.86)% vs (32.54±4.58)% for VR1]. These results suggest that the local gut inflammation increases the expressions of CGRP and VR1 in gut-innervated DRG sensory neurons. More importantly, this abnormal status persists even after the gut inflammatory reaction has been resolved for certain time.
Animals ; Calcitonin Gene-Related Peptide ; metabolism ; Colitis ; physiopathology ; Colon ; innervation ; Ganglia, Spinal ; cytology ; Inflammation ; physiopathology ; Neurons, Afferent ; cytology ; Rats ; Rats, Sprague-Dawley ; Sensory Receptor Cells ; cytology ; Spinal Cord ; cytology ; TRPV Cation Channels ; metabolism

Intestinal neuronal dysplasia (IND) type B is a disease of the submucosal plexus of intestine manifesting chronic intestinal obstruction or severe chronic constipation. IND is one of intestinal dysganglionoses and clinically closely associated with Hirschsprung's disease. Until recently, it is not fully clear whether IND is a congenital malformation or an acquired secondary condition related to some gastrointestinal problems. However, recently published data and consensus reports have enhanced our understanding of the pathogenesis and management of IND. The aim of this paper was to review the current state of knowledge regarding the controversial issues of IND including the etiology, classification, diagnostic criteria, and available therapeutic intervention.
Child ; Colon/*innervation/radiography ; Constipation/etiology ; Enteric Nervous System/*abnormalities ; Ganglia/pathology ; Gastrointestinal Motility ; Hirschsprung Disease/pathology ; Humans ; Immunohistochemistry ; Intestinal Diseases/*diagnosis/pathology ; Intestinal Mucosa/pathology

Nitric oxide (NO) is a non-adrenergic, non-cholinergic neurotransmitter found in the enteric nervous system that plays a role in a variety of enteropathies, including inflammatory bowel disease. Alteration of nitrergic neurons has been reported to be dependent on the manner by which inflammation is caused. However, this observed alteration has not been reported with acetic acid-induced colitis. Therefore, the purpose of the current study was to investigate changes in nitrergic neuromuscular transmission in experimental colitis in a rat model. Distal colitis was induced by intracolonic administration of 4% acetic acid in the rat. Animals were sacrificed at 4 h and 48 h postacetic acid treatment. Myeloperoxidase activity was significantly increased in the acetic acid-treated groups. However, the response to 60 mM KCl was not significantly different in the three groups studied. The amplitude of phasic contractions was increased by Nomega-nitro-L-arginine methyl ester (L-NAME) in the normal control group, but not in the acetic acid-treated groups. Spontaneous contractions disappeared during electrical field stimulation (EFS) in normal group. However, for the colitis groups, these contractions initially disappeared, and then reappeared during EFS. Moreover, the observed disappearance was diminished by L-NAME; this suggests that these responses were NO-mediated. In addition, the number of NADPH-diaphorase positive nerve cell bodies, in the myenteric plexus, was not altered in the distal colon; whereas the area of NADPH-diaphorase positive fibers, in the circular muscle layer, was decreased in the acetic acidtreated groups. These results suggest that NO-mediated inhibitory neural input, to the circular muscle, was decreased in the acetic acid-treated groups.
Acetic Acid/toxicity ; Animals ; Colitis/chemically induced/*pathology/*physiopathology ; Colon/drug effects/enzymology/*innervation/pathology ; Indicators and Reagents/toxicity ; Male ; Muscle Contraction/drug effects ; Muscle, Smooth/drug effects/metabolism ; Myenteric Plexus/pathology ; NADPH Dehydrogenase/metabolism ; NG-Nitroarginine Methyl Ester/pharmacology ; Neuromuscular Junction/drug effects/*metabolism ; Nitrergic Neurons/drug effects/*metabolism ; Nitric Oxide/*metabolism ; Peroxidase/metabolism ; Potassium Chloride/pharmacology ; Rats ; Rats, Sprague-Dawley

Gastrointestinal (GI) motility has a crucial role in the food consumption, digestion and absorption, and also controls the appetite and satiety. In obese patients, various alterations of GI motility have been investigated. The prevalence of GERD and esophageal motor disorders in obese patients are higher than those of general population. Gastric emptying of solid food is generally accelerated and fasting gastric volume especially in distal stomach is larger in obese patients without change in accommodation. Contractile activity of small intestine in fasting period is more prominent, but orocecal transit is delayed. Autonomic dysfunction is frequently demonstrated in obese patients. These findings correspond with increased appetite and delayed satiety in obese patients, but causes or results have not been confirmed. Therapeutic interventions of these altered GI motility have been developed using botulinum toxin, gastric electrical stimulation in obese patients. Novel agents targeted for GI hormone modulation (such as ghrelin and leptin) need to be developed in the near future.
Botulinum Toxins/therapeutic use ; Colon/*physiopathology ; Eating ; Electric Stimulation Therapy ; Esophageal Motility Disorders/etiology/*physiopathology/therapy ; *Gastrointestinal Motility ; Ghrelin/therapeutic use ; Humans ; Intestine, Small/*physiopathology ; Leptin/therapeutic use ; Obesity/*complications ; Satiety Response ; Stomach/innervation/*physiopathology