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PubMed1994

Reversal of CRF- and dopamine-induced stimulation of colonic motility by CCK and igmesine (JO 1784) in the rat.

1. The role of dopamine in the genesis of corticotropin releasing factor (CRF)- and emotional stress (ES)-induced stimulation of colonic motility, as well as the mechanism of antagonistic action of cholecystokinin octapeptide (CCK-8s) and igmesine (alpha sigma receptor ligand, formerly JO 1784) on dopamine-induced colonic hypermotility, have been investigated in the rat. 2. ES and i.c.v. injection of CRF (0.5 microgram kg-1) increased the frequency of colonic spike bursts by 63% and 114%, respectively. Prior i.c.v. administration of (+)-SCH 23390 (a D1 receptor antagonist, 10 micrograms kg-1) significantly (P < 0.05) reduced the CRF- and ES-induced increase in colonic spike burst; whereas, sulpiride (a D2 receptor antagonist, 10 micrograms kg-1) blocked the CRF-induced stimulation of colonic spike bursts but had no effect on the colonic response to stress. 3. I.c.v. injection of dopamine (100 micrograms kg-1), increased colonic spike burst frequency by 54%. (+)-SKF 38393 (5 micrograms kg-1), a selective D1 receptor agonist, and quinpirole (5 micrograms kg-1), a selective D2 receptor agonist, increased colonic spike burst frequency by 71% and 70% respectively. CCK-8s (0.1 microgram kg-1) and igmesine (0.1 microgram kg-1) injected i.c.v. completely prevented the stimulatory effects of dopamine, (+)-SKF 38393 and quinpirole. 4. Previous i.c.v. injection of devazepide, a CCKA receptor antagonist, (10 micrograms kg-1) antagonized the inhibitory effects of both CCK-8s and igmesine injected i.c.v. on dopamine-induced colonic hyperkinesia. 5. These results show that CRF stimulates colonic motility through activation of central dopaminergic mechanisms in response to stress; furthermore, CCK-8s inhibits dopamine-induced colonic hyperkinesia through a mechanism involving D1 and D2 receptors. The sigma receptor ligand igmesine, blocks the CRF and ES-induced colonic hyperactivity via an interaction with central CCK mechanisms.

Action Potentials↗
PubMed2002

Effects of butyrate on active sodium and chloride transport in rat and rabbit distal colon.

Short chain fatty acids, particularly butyrate, stimulate electroneutral NaCl absorption from the colon. Their effect in colonic epithelia lacking basal electroneutral NaCl absorption is unknown. Butyrate is also reported to inhibit active Cl- secretion in the colon. The present studies were undertaken to investigate the inter-relationships between the effects of butyrate on active Na+ and Cl- transport in the colon. Studies were carried out in rabbit distal colon (known to have predominant electrogenic Na+ absorption), rat distal colon (characterised by electroneutral Na+ absorption), and hyperaldosteronaemic rat distal colon (characterised by electrogenic Na+ absorption). The effect of cholera toxin (CT) was also noted. Potential difference, short-circuit current (I(SC)) and fluxes of Na+ and Cl- were measured in stripped mucosa under voltage-clamp conditions. Butyrate stimulated electroneutral Na+ and Cl- absorption in distal colon of normal and salt-depleted rats, and stimulated Na+ absorption in rabbit distal colon. Amiloride (10(-4) M) or CT did not inhibit this process. In rabbit distal colon, stimulation of Na+ absorption by butyrate was not dependent on the presence of Cl- in the medium. Butyrate significantly decreased conductance, decreased flux of sodium from serosa to mucosa (particularly in rabbit distal colon), and decreased I(SC). Net Cl- secretion, induced by CT, was completely inhibited by butyrate. Stimulation of Na+ absorption was independent of exposure to CT. Bumetanide reversed net Cl- secretion to net absorption, but did not alter Na+ or Cl- fluxes in tissues exposed to butyrate. Thus butyrate stimulates active Na+ absorption in colonic epithelia, with or without expression of basal Na+-H+ exchange. Independently, butyrate inhibits active Cl- secretion induced by cAMP in these epithelia.

Absorption↗
PubMed2005

Synchronization of enteric neuronal firing during the murine colonic MMC.

DiI (1,1'didodecyl-3,3,3',3'-tetramethylindocarbecyanine perchlorate) retrograde labelling and intracellular electrophysiological techniques were used to investigate the mechanisms underlying the generation of spontaneously occurring colonic migrating myoelectric complexes (colonic MMCs) in mice. In isolated, intact, whole colonic preparations, simultaneous intracellular electrical recordings were made from pairs of circular muscle (CM) cells during colonic MMC activity in the presence of nifedipine (1-2 microm). During the intervals between colonic MMCs, spontaneous inhibitory junction potentials (IJPs) were always present. The amplitudes of spontaneous IJPs were highly variable (range 1-20 mV) and occurred asynchronously in the two CM cells, when separated by 1 mm in the longitudinal axis. Colonic MMCs occurred every 151 +/- 7 s in the CM and consisted of a repetitive discharge of cholinergic rapid oscillations in membrane potential (range: 1-20 mV) that were superimposed on a slow membrane depolarization (mean amplitude: 9.6 +/- 0.5 mV; half-duration: 25.9 +/- 0.7 s). During the rising (depolarizing) phase of each colonic MMC, cholinergic rapid oscillations occurred simultaneously in both CM cells, even when the two electrodes were separated by up to 15 mm along the longitudinal axis of the colon. Smaller amplitude oscillations (< 5 mV) showed poor temporal correlation between two CM cells, even at short electrode separation distances (i.e. < 1 mm in the longitudinal axis). When the two electrodes were separated by 20 mm, all cholinergic rapid oscillations and IJPs in the CM (regardless of amplitude) were rarely, if ever, coordinated in time during the colonic MMC. Cholinergic rapid oscillations were blocked by atropine (1 microm) or tetrodotoxin (1 microm). Slow waves were never recorded from any CM cells. DiI labelling showed that the maximum projection length of CM motor neurones and interneurones along the bowel was 2.8 mm and 13 mm, respectively. When recordings were made adjacent to either oral or anal cut ends of the colon, the inhibitory or excitatory phases of the colonic MMC were absent, respectively. In summary, during the colonic MMC, cholinergic rapid oscillations of similar amplitudes occur simultaneously in two CM cells separated by large distances (up to 15 mm). As this distance was found to be far greater than the projection length of any single CM motor neurone, we suggest that the generation of each discrete cholinergic rapid oscillation represents a discreet cholinergic excitatory junction potential (EJP) that involves the synaptic activation of many cholinergic motor neurones simultaneously, by synchronous firing in many myenteric interneurones. Our data also suggest that ascending excitatory and descending inhibitory nerve pathways interact and reinforce each other.

Action Potentials↗
PubMed2026

Difficult-to-treat resistant Gram-negative bacteria and genomic resemblances between colonization and infection among patients in an intensive care unit of a tertiary care hospital in Bangladesh.

Colonization with difficult-to-treat-resistant Gram-negative bacteria (DTR-GNB) increases the risk of subsequent infections with limited treatment options. This study aimed to assess the burden of DTR-GNB colonization in ICU patients, explore its association with clinical outcomes, and examine genomic similarities. This secondary analysis included patients enrolled within 24 h of ICU admission between July 2023 and January 2024. Rectal swabs were collected at enrollment, on days 3, 7, and weekly during ICU stay to detect colonization. Bacterial isolates grown on selective chromogenic agar media were identified and tested for antimicrobial susceptibility using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) and automated broth microdilution, respectively. Blood, urine, and/or tracheal aspirate cultures were performed if clinically suspected sepsis. Whole-genome sequencing (WGS) was performed on paired colonization and infection isolates, and genomic relatedness was assessed using FastANI, core-genome single-nucleotide polymorphism (SNP) analysis, and phylogenetic reconstruction. Among 373 patients, 181 (48.5%) were colonized with DTR-GNB; 76 (20.4%) at enrollment, and 105 (53.0%) acquired during hospital stay. Among 52 (13.9%) patients evaluated for suspected infection, 30 (57.7%) had positive cultures, predominantly Acinetobacter baumannii (n = 15) and Klebsiella pneumoniae (n = 11) of DTR-phenotypes. Compared to non-colonized patients, patients colonized with DTR-GNB had higher risks of infections (risk ratio [RR]: 2.18, 95% CI: 1.27-3.76) and longer ICU stays (median 7 vs 2 days, P < 0.001). DTR-GNB-infected patients had a higher risk of death (RR: 1.57, 95% CI: 1.34-1.84) compared to patients without DTR-GNB infection. WGS revealed that 13 of 14 paired colonization-infection isolates were conspecific, with three pairs being highly clonal; whereas the remaining pairs showed greater genomic divergence, consistent with the SNP and phylogenetic analyses. While common, more than half acquired DTR-GNB colonization from the ICU. Its association with subsequent infection and prolonged ICU stays underscores the need for enhanced infection prevention and control measures to mitigate nosocomial transmission and improve patient outcomes.IMPORTANCEThis study underscores the growing threat posed by difficult-to-treat resistant Gram-negative bacteria (DTR-GNB) in intensive care units. Nearly half of critically ill patients were colonized, with a considerable proportion acquiring these multidrug-resistant organisms during their ICU stay. Colonization with these pathogens substantially increased the risk of subsequent infections, even by the same colonizing strain, prolonged ICU stays, and likely worsened clinical outcomes due to the unavailability of susceptible antibiotics. Alarmingly, more than 90% of patients infected with DTR-GNB expired in the hospital. These findings highlight the urgent need for robust infection prevention and control strategies to curb nosocomial transmission and mitigate the impact of DTR-GNB on vulnerable patient populations. Addressing this emerging resistance phenotype is critical to improving patient safety and reducing the burden on healthcare systems.

Humans↗
PubMed1979

Effects of age, antigen deprivation, and allograft rejection on epithelial cell kinetics in mouse colon.

A technique of microdissection of colonic mucosa has allowed the study of mitotic activity, measured by metaphase accumulation following colchicine blockade, in individual crypts of mouse colon. The changes occurring during growth and development of normal colon have been studied and compared with changes found in antigen free colon (colonic isografts) and in cell-mediated immune damage of the bowel (allograft rejection). Metaphase accumulation was steady at two metaphases per hour in baby mouse colon until 18 days after birth. Between 18 and 24 days a rapid, and significant increase in mitotic activity occurred (P less than 0.01), reached adult values, and changed no further. Metaphase accumulation in isografts was similar to normal colon for the first two weeks after transplantation but the rise in mitotic activity in the third week did not occur. Allografts of colon showed two- to three-fold increases in metaphase accumulation when compared with both normal colon and isografts (P less than 0.01). When crypt mitotic activity was compared with the length of crypts measured in histological sections of normal colon, isografts, and allografts, no clear relationship was observed. Both changes in the luminal environment of the gut at the time of weaning and cell-mediated immune reactions in the colonic wall appeared to be associated with increased mitotic activity in colonic crypts.

Age Factors↗
PubMed1993

Cephalic phase of colonic pressure response to food.

A cephalic phase of colonic pressure response to food was sought in five normal subjects (mean age (22.6) years, 22-24), studied on six separate occasions by recording intraluminal pressures in the unprepared sigmoid colon. Gastric acid secretion was measured simultaneously by continuous aspiration through a nasogastric tube. After a 60 minute basal period, one of five 30 minute food related cephalic stimuli, or a control stimulus was given in random order; records were continued for a further 120 minutes. The cephalic stimuli were: food discussion, sight and smell of food without taste, smell of food without sight or taste, sight of food without smell or taste, and modified sham feeding; the control stimulus was a discussion of neutral topics. Colonic pressures were expressed as study segment activity index (area under curve, mm Hg.min) derived by fully automated computer analysis. Gastric acid output was expressed as mmol/30 min. Food discussion significantly (p < 0.02, Wilcoxon's rank sum test) increased colonic pressure activity compared with control or basal activity. Smell of food without sight or taste also significantly (p < 0.03) increased the colonic pressure activity compared with control and basal periods. Sham feeding and sight and smell of food without taste significantly (p < 0.02 and p < 0.03) increased colonic pressures compared with control but not basal activity. The increase in colonic activity after sight of food without smell or taste was not significantly different from control or basal activity (p = 0.44 and p = 0.34). Food discussion was the strongest colonic stimulus tested. Food discussion and sham feeding significantly (p<0.02) stimulated gastric acid output above control and basal values. Sight and smell of food without taste significantly (p<0.02) increased acid output above basal. Smell of food without sight or taste and sight of food without smell or taste did not significantly (p=0.06, p=0.34) increase acid output. In contrast with the effect on colonic pressures, sham feeding was the best stimulus of acid output. Increased colonic pressure activity after food discussion correlated significantly (r=0.45, p<0.02) with gastric acid output. There was no correlation (r=-0.1, p>0.5) between colonic pressure activity and gastric acid output in the control study. These data show that there is a cephalic phase of the colonic response to food.

Adult↗
PubMed1999

Human right and left colon differ in epithelial cell apoptosis and in expression of Bak, a pro-apoptotic Bcl-2 homologue.

BACKGROUND: Propensity to colonic neoplasia differs between the right and left colon. AIMS: To examine whether this difference may be related to regional differences in epithelial apoptosis, in expression of a proapoptotic regulatory protein, Bak, and in proliferation. PATIENTS: Individuals with no history of colorectal neoplasia. METHODS: Archival blocks of colorectal tissues were immunostained for proliferating cells (antibody to Ki-67 antigen), and Bak expression (polyclonal antiserum). Cells containing DNA strand breaks, a marker of apoptosis, were identified by terminal deoxyuridine nucleotidyl nick end labelling (TUNEL). RESULTS: There were fewer TUNEL positive epithelial cells in the right colon (mean 1.2 (SE 0.1)% of all epithelial cells) than the left colon (2.2 (0.1)%, p<0.0001) or rectum (2.2 (0.3)%, p<0.05). Bak expression was less common in the right colon (mean 46 (2.3)% of epithelial cells immunoreactive) than the left colon (66 (2.7)%, p<0.0001), or rectum (67 (2.3)%, p<0.001). Bak expression and TUNEL positivity were highly positively correlated (p<0.0001). In contrast to apoptosis, mean whole crypt proliferation labelling index was similar throughout the colorectum (right colon: 15.6 (3.2)%; left colon: 13. 5 (1.2)%; rectum: 13.3 (2.3)%). CONCLUSION: The percentage of proliferating colonic epithelial cells is constant throughout the colon, but fewer epithelial cells undergo Bak mediated apoptosis in the right than in the left colon or rectum. This suggests that colonocytes may be lost by methods other than apoptosis in the right colon.

Apoptosis↗
PubMed2005

Electroacupuncture at ST-36 accelerates colonic motility and transit in freely moving conscious rats.

Acupuncture is useful for functional bowel diseases, such as constipation and diarrhea. However, the mechanisms of beneficial effects of acupuncture on colonic function have scarcely ever been investigated. We tested the hypothesis that electroacupuncture (EA) at ST-36 stimulates colonic motility and transit via a parasympathetic pathway in conscious rats. Hook-shaped needles were inserted at bilateral ST-36 (lower limb) or BL-21 (back) and electrically stimulated at 10 Hz for 20 min. We also studied c-Fos expression in response to EA at ST-36 in Barrington's nucleus of the pons. EA at ST-36, but not BL-21, significantly increased the amplitude of motility at the distal colon. The calculated motility index of the distal colon increased to 132 +/- 9.9% of basal levels (n = 14, P < 0.05). In contrast, EA at ST-36 had no stimulatory effects in the proximal colon. EA at ST-36 significantly accelerated colonic transit [geometric center (GC) = 6.76 +/- 0.42, n = 9, P < 0.001] compared with EA at BL-21 (GC = 5.23 +/- 0.39, n = 7). The stimulatory effect of EA at ST-36 on colonic motility and transit was abolished by pretreatment with atropine. EA-induced acceleration of colonic transit was also abolished by extrinsic nerve denervation of the distal colon (GC = 4.69 +/- 0.33, n = 6). The number of c-Fos-immunopositive cells at Barrington's nucleus significantly increased in response to EA at ST-36 to 8.1 +/- 1.1 cells/section compared with that of controls (2.4 +/- 0.5 cells/section, n = 3, P < 0.01). It is concluded that EA at ST-36 stimulates distal colonic motility and accelerates colonic transit via a sacral parasympathetic efferent pathway (pelvic nerve). Barrington's nucleus plays an important role in mediating EA-induced distal colonic motility in conscious rats.

Acupuncture Points↗
PubMed1997

Colonic smooth muscle cells possess a different subtype of somatostatin receptor from gastric smooth muscle cells.

Somatostatin (SS) alters colonic motility. To investigate whether SS has a direct effect on colonic smooth muscle cells, we prepared isolated muscle cells from the descending guinea pig colon and compared the effects of SS with those on isolated gastric smooth muscle cells. In gastric cells, SS had no effect on carbachol-induced contraction, whereas in colonic cells it caused inhibition. In colonic muscle cells, SS-28 caused >85% inhibition of contraction by cholecystokinin octapeptide (CCK-8), bombesin, 12-O-tetradecanoylphorbol-13-acetate, and ionomycin, whereas it had no effect on contraction by these agents in gastric cells. In gastric cells, SS inhibited relaxation. Three synthetic SS analogs had different relative affinities for causing effects in gastric and colonic cells. Pertussis toxin inhibited the action of SS-28 in each muscle cell type by 50-75%. SS-28 alone had a small contractile effect on cells from the circular layer of the colon. SS-28 inhibited carbachol-induced contraction in colonic cells from both the longitudinal and circular layers. These results demonstrate that the action of SS differs in colonic and gastric smooth muscle cells. SS inhibits contractants in colonic cells and relaxants in gastric cells. In colonic cells, SS has a weak contractile effect due to an effect on circular muscle cells and an inhibitory effect on cells from both longitudinal and circular layers. A different SS receptor subtype mediates the actions of SS in colonic and gastric muscle cells. In both cell types, the actions of SS are mediated by pertussis toxin-sensitive and -insensitive G proteins.

Animals↗
PubMed2001

Cholinergic stimulation enhances colonic motor activity, transit, and sensation in humans.

The cholinesterase inhibitor neostigmine indirectly stimulates muscarinic M(1)/M(2)/M(3) receptors, thereby reducing colonic distension in acute colonic pseudo-obstruction. We investigated the dose-response profile for the colonic sensorimotor effects of neostigmine and bethanechol, a direct muscarinic M(2)/M(3) agonist in humans. A barostat-manometric assembly recorded phasic pressures, tone, and pressure-volume relationships (compliance) in the descending colon and rectum of 30 healthy subjects who received intravenous neostigmine (0.25, 0.75, or 1.5 mg; n = 15) or subcutaneous bethanechol (2.5, 5, or 10 mg; n = 15). Sensation to luminal distension was also assessed. Thereafter, the effects of neostigmine and bethanechol on colonic transit (geometric center) were compared with those of saline by scintigraphy in 21 subjects. Both drugs increased colonic phasic pressure activity, reduced rectal compliance, and enhanced urgency during rectal distension. Neostigmine also reduced colonic and rectal balloon volumes, reflecting increased tone by an average of 12% and 25% for the highest dose, respectively. Only neostigmine reduced colonic compliance, accelerated colonic transit [mean geometric center at 90 min 2.5 vs. 1.0 (placebo)], and increased pain perception during colonic distension. We conclude that neostigmine has more prominent colonic motor and sensory effects than bethanechol. Moreover, neostigmine induces coordinated colonic propulsion, perhaps by stimulating muscarinic M(1) receptors in the myenteric plexus.

Adult↗
PubMed1992

Short-term effect of aldosterone on Na-Cl transport across equine colon.

In ponies fed concentrated (pelleted) meals, postprandial increases of plasma aldosterone have been temporally associated with a decrease in colonic fluid volume that parallels the conclusion of postfeeding fermentation. To determine the significance of short-term increases of plasma aldosterone on the rate of colonic Na absorption, in vitro transport studies were conducted on the mucosae of three morphologically distinct colonic segments (i.e., ventral, dorsal, and small colons) from ponies infused with a high physiological concentration of aldosterone for an 8-h period. In control ponies, basal NaCl absorption across the proximal colon (ventral and dorsal colons) was amiloride-insensitive and electroneutral. In aldosterone-treated ponies, the rate of electroneutral Na absorption was doubled in both segments and a small, amiloride-sensitive current was detected in the dorsal colon. However, consistent with previous observations [Clarke and Argenzio. Am. J. Physiol. 259 (Gastrointest. Liver Physiol. 22): G62-G69, 1990], expression of electroneutral Na absorption in the ventral colon required pretreatment of the tissues with an inhibitor of prostaglandin synthesis, i.e., indomethacin. In the distal (small) colon, basal absorption was entirely electrogenic and amiloride-sensitive, and aldosterone treatment tripled the rate of absorption. The above findings are consistent with the notion that postprandial hyperaldosteronism can significantly increase colonic Na absorption and, thereby, may facilitate colonic fluid absorption during the concluding period of meal-induced fermentation (8-12 h postfeeding). However, in the ventral colon (i.e., the principal site of fermentation), mineralocorticoid action does not dominate control of electroneutral Na transport because accelerated absorption could be abolished by the antiabsorptive effect of local prostanoids.

Aldosterone↗
PubMed1997

Role of colonic motility in guiding therapy in patients with constipation.

Constipation is a common condition defined by less than three bowel movements per week. Often constipation is secondary to altered motility of the colon. Tests that measure colonic motility lead the clinician to appropriate therapy. Colonic transit measured with either radionuclides or radio-opaque markers determine whether the transit through the colon is truly slow, and then identify the potential region of the colon that impedes the movement of intraluminal contents. Patients with normal colonic transit do not require further evaluation of their colonic motor function. Colonic and anorectal manometry differentiate patients in to 3 groups: (1) functional anal outlet obstruction; (2) uncoordinated distal colonic phasic contractions, and (3) colonic inertia. Functional outlet obstruction may be treated successfully by increasing the water content of their stools and biofeedback. Antispasmodics including anticholinergics, nitrates and calcium channel blockers may decrease the functional obstruction caused by phasic colonic contractions. The prokinetics such as cisapride have successfully improved constipation due to colonic inertia, Parkinson's disease or spinal cord injury as well as idiopathic inertia. Occasionally patients with inertia may require colectomy with ileorectal anastomosis to treat severe constipation.

Colon↗
PubMed1994

[Studies on cholinergic nerve function of the aganglionic colon in murin model].

The true role of the extrinsic cholinergic nerve fibers proliferating abundantly in the aganglionic colon of Hirschsprung's disease has not yet been established. Electrophysiological and pharmacological studies using superfusion method were carried out on rectal muscle strips of piebald lethal mice, one of murine models of Hirschsprung's disease and their siblings as a control. The muscle strips were preincubated with [3H] choline in Krebs solution. The contractions and the release of [3H] acetylcholine evoked by electrical transmural stimulation of the muscle strips were measured. In addition, the contractility of muscle strips treated with acetylcholinesterase blocking agents were recorded. In the aganglionic colon, as in the normal colon, the release of [3H] acetylcholine evoked by electrical transmural stimulation was recognized. However, no contractions were evoked in the aganglionic colon. The uptake of [3H] choline in the aganglionic colon was larger than in the normal colon presumably due to the proliferated extrinsic cholinergic nerve fibers. On the other hand, the release of [3H] acetylcholine evoked by electrical transmural stimulation was smaller in the aganglionic colon. In the aganglionic colon, no contractions were evoked by acetylcholinesterase blocking agents, indicating that there is no spontaneous release of acetylcholine. In the presence of low concentration of acetylcholinesterase blocking agents, the form of contractions evoked by electrical transmural stimulation in the aganglionic colon was different from those in the normal colon. These results have indicated that in the murine aganglionic colon, the proliferated extrinsic cholinergic nerve fibers may not directly regulate the smooth muscles through the functional neuro-muscular junction. In conclusion, the proliferated extrinsic cholinergic nerve fibers is not related to the narrowing of the aganglionic colon.

Acetylcholine↗
PubMed1988

[Effect of vasoactive intestinal peptide on the motility of guinea-pig colon in vitro].

The effects of vasoactive intestinal peptide (VIP) on longitudinal and circular muscle strips of guinea-pig proximal and distal colons, and on propulsive activity of guinea-pig distal colon were investigated in vitro. VIP (10(-9)-10(-6) M) produced relaxations of longitudinal and circular muscle strips in proximal colon and of circular muscle strip in distal colon, but produced a contraction of longitudinal muscle strip in distal colon. VIP-induced responses of the muscle strips were not influenced by indomethacin (10(-6) M). Tetrodotoxin (10(-6) M) and atropine (10(-6) M) converted VIP-induced contraction into relaxation in longitudinal muscle strip of distal colon, although these nerve blockers did not influence VIP-induced relaxations of longitudinal and circular muscle strips in proximal colon and of circular muscle strip in distal colon. VIP (10(-6) M) inhibited spontaneous and carbachol (10(-8) M)-stimulated propulsive activities of the isolated segment in distal colon. These results suggest that VIP may directly relax colonic smooth muscle cells and may indirectly contract longitudinal muscle strip of distal colon, mainly via stimulation of cholinergic neurones in the myenteric plexus of the muscle strip. It is also suggested that VIP-induced watery diarrhea in WDHA syndrome may not due to a direct stimulation of colonic motility.

Animals↗
PubMed1986

Investigation of regional differences in water and electrolyte absorption across the human colon by in vivo perfusion method.

Colonic perfusion studies were performed to evaluate regional differences in water and electrolyte absorption across the human colon. In 19 healthy male volunteers, a 5-lumen tube with two balloons was inserted into the colon by the endoscopic retrograde bowel insertion (ERBI) method and a 25 cm segment of either the right or the left colon was perfused with an isotonic electrolyte solution simulating the fasting ileal content at a rate of 5 ml/min. Additionally into 5 subjects of the right colon and 5 subjects of the left colon, PSP solution was injected and mean transit time was calculated by the dilution method. Higher absorption rates of water, Na and Cl were observed in the right than in the left colon. Mean transit time was longer in the left than in the right colon. It was considered that the right colon had greater absorptive capacity than the left. The colonic perfusion study by the use of ERBI method made it possible to determine the absorption of water and electrolytes in the right and left colon directly in man, and would be useful to elucidate the pathophysiology of colonic diarrhea.

Adolescent↗
PubMed1995

Medical malpractice involving radiologic colon examinations: a review of 38 recent cases.

OBJECTIVE: Our purposes were to determine the causes of malpractice claims against radiologists performing contrast examinations of the colon and to design strategies to reduce litigation and diminish patient morbidity. MATERIALS AND METHODS: Reports of malpractice claims were collected from legal journals and databases between 1985 and 1994. For this period, 38 plaintiffs raised 52 allegations of malpractice that involved radiologists performing barium or Hypaque (meglumine diatrizoate; Winthrop Pharmaceuticals, New York, NY) colon examinations. For the 38 cases, 18 plaintiffs for decedents alleged that failure to diagnose colorectal cancer by barium enema examination caused delay in treatment and the patient's death. Eighteen plaintiffs alleged that improper performance of barium (17 cases) or meglumine diatrizoate (one case) colon examinations caused perforation of the colon, resulting in significant morbidity (15 cases) or death (three cases). Miscellaneous causes for malpractice claims were recorded in two cases. RESULTS: In 18 cases of failure to diagnose colorectal cancer, the initial radiographs were interpreted as follows: normal findings in 14 cases, diverticulosis in one case, and spastic bowel in two cases; in the remaining case, colon cancer was missed because of nonopacification of the cecum. In retrospect, 17 of 18 colorectal cancers were visualized. The delay in the diagnosis of colorectal cancer ranged from 5 to 72 months. Missed colorectal cancers occurred in the cecum (two cases), transverse colon (two cases), rectosigmoid area (nine cases), or unspecified area (five cases). In 18 cases of colon perforation, the site was the cecum (one case), transverse colon (one case), extraperitoneal rectum (seven cases), rectosigmoid area (one case), colostomy stoma (two cases), or unspecified area (six cases). One patient experienced anaphylactic shock that required hospitalization. One underwent unnecessary surgery because barium enema films showing colon cancer were mislabeled with her name. CONCLUSION: On the basis of our analyses of malpractice claims, we suggest strategies to prevent medicolegal litigation. Strategies include communicating with the patient about the type and indications of the barium enema examination, performing digital rectal examinations on all patients to detect distal rectal lesions or strictures, recognizing colon perforation, and obtaining immediate surgical consultation if colon perforation occurs. The number of missed colon cancers may be reduced by reading twice or reviewing at a later time all barium enema examinations.

Adult↗
PubMed2000

Mechanisms in the chemoprevention of colon cancer: modulation of protein kinase C, tyrosine protein kinase and diacylglycerol kinase activities by 1,4-phenylenebis-(methylene)selenocyanate and impact of low-fat diet.

Epidemiological and experimental studies suggest an inverse relationship between the intake of dietary selenium and/or low fat-intake and colon cancer risk. Efficacy studies in rodents suggest that the organoselenium compound 1, 4-phenylenebis(methylene)selenocyanate (p-XSC), is a more effective and less toxic chemopreventive agent than other organic or inorganic selenium compounds such as selenomethionine and Na2SeO3. The efficacy of p-XSC against colon cancer is significantly augmented by a low-fat diet. To explore the mechanisms by which this combined inhibiting effect against colon carcinogenesis comes about, we have investigated protein kinase C (PKC), tyrosine protein kinase (TPK), diacylglycerol kinase (DGK) activities and 8-isoprostane levels in colonic mucosa and tumor tissues in an azoxymethane (AOM)-induced rat colon cancer model. Weanling male F344 rats were fed the semipurified AIN-76A diet until seven weeks of age. Then various experimental groups were fed the low- or high-fat diets containing 0 or 20 ppm p-XSC (10 ppm as selenium). At seven weeks of age, groups of rats were injected s.c. with azoxymethane (AOM; 15 mg/kg body wt., once weekly for 2 weeks) and continued on their respective experimental diets until 38 weeks after the second AOM treatment. They were then sacrificed and colonic mucosal and tumor samples were evaluated for PKC, TPK, DGK and 8-isoprostane levels. Administration of p-XSC along with a low-fat diet significantly inhibited Ca+2-dependent and -independent PKC (P<0.05-0.01) activities in colonic mucosa and tumors. Administration of p-XSC either low-fat or high-fat diet significantly suppressed both colonic mucosal and tumor TPK activity (P<0.05-0.01). Suppression of TPK activity was more pronounced in rats maintained on a low-fat diet containing p-XSC. In contrast, rats receiving p-XSC with either low- or high fat diet showed significantly increased DGK activity (P<0.01-0.0001). Rats fed low-fat or high-fat plus p-XSC had lower-levels of 8-isoprostane in the colonic tumors than animals who had been given low- or high-fat diets without the organoselenium compound. Interestingly, 8-isoprostane levels were lower in the colon tumors of the rats fed the low-fat diet than those fed the high-fat diet. Our findings suggest that p-XSC induced down-regulation of PKC and TPK activities and up-regulation of DGK activity. These events may in part be responsible for the chemopreventive activity against colon carcinogenesis. Further, this study implies that p-XSC with a low-fat dietary regimen will augment regulation of PKC, TPK and DGK activities in the colon.

Animals↗
PubMed2000

Chemoprevention of colon cancer by specific cyclooxygenase-2 inhibitor, celecoxib, administered during different stages of carcinogenesis.

Epidemiological observations and laboratory research have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of colon cancer and that the inhibition of colon carcinogenesis by NSAIDs is mediated through the modulation of prostaglandin production by rate-limiting enzymes known as cyclooxygenases (COXs). Because traditional NSAIDs inhibit both COX-1 and COX-2, these drugs induce side effects, such as gastrointestinal ulceration and renal toxicity, through the inhibition of the constitutive COX-1. Overexpression of COX-2 has been observed in colon tumors; therefore, specific inhibitors of COX-2 could serve as chemopreventive agents. Our previous study has shown that celecoxib, an inhibitor of COX-2, while sparing COX-1, inhibited azoxymethane (AOM)-induced colon tumorigenesis when administered during both initiation and postinitiation stages, ie., celecoxib administered continuously before, during, and after carcinogen treatment. This study examined the dose-response effect of celecoxib when administered during the initiation and postinitiation stages. In addition, the chemopreventive effects of high-dose celecoxib administered during the promotion/progression stage of colon carcinogenesis, ie., continuous celecoxib administration beginning 14 weeks after the carcinogen treatment, was determined in male F344 rats. We also measured the steady-state levels of celecoxib in the plasma of animals given this inhibitor. Groups of 5-week-old male F344 rats were fed either a control diet or experimental diets containing 500, 1000, or 1500 ppm celecoxib. At 7 and 8 weeks of age, rats scheduled for carcinogen treatment were injected s.c. with AOM at a dose rate of 15 mg/kg body weight/week. Groups of animals destined for the promotion/ progression study and initially receiving the control diet were switched to a diet containing 1500 ppm celecoxib beginning 14 weeks after the second AOM treatment. All rats remained on their respective dietary regimens until the termination of the study, ie., 52 weeks, and were then sacrificed. Colon tumors were evaluated histopathologically. Administration of 500, 1000, or 1500 ppm celecoxib during the initiation and postinitiation stages significantly inhibited the incidence (P < 0.01 to P < 0.0001) as well as the multiplicity (P < 0.01 to P < 0.0001) of adenocarcinomas of the colon in a dose-dependent manner. Importantly, administration of 1500 ppm celecoxib during the promotion/progression stage also significantly suppressed the incidence and multiplicity of adenocarcinomas of the colon (P < 0.01). Also, administration of celecoxib to the rats during the initiation and postinitiation periods and throughout the promotion/progression stage strongly suppressed colon tumor volume (P < 0.0002 to P < 0.001). The steady-state plasma concentration of celecoxib increases somewhat with the dose. Thus, in this model system, the chemopreventive efficacy of celecoxib is dose-dependent when this COX-2 inhibitor is administered during the initiation and postinitiation periods. This study provides the first evidence that celecoxib is also very effective when it is given during the promotion/progression stage of colon carcinogenesis, indicating that the chemopreventive efficacy is achieved during the later stages of colon tumor development. This suggests that celecoxib may potentially be an effective chemopreventive agent for the secondary prevention of colon cancer in patients with familial adenomatous polyposis and sporadic polyps.

Administration, Oral↗