Small intestinal bacterial overgrowth and warfarin dose requirement variability.

The dose of warfarin needed to obtain a therapeutic anticoagulation level varies widely among patients and can undergo abrupt changes for unknown reasons. Drug interactions and genetic factors may partially explain these differences. Intestinal flora produces vitamin K2 (VK2) and patients with small intestinal bacterial overgrowth (SIBO) rarely present reduced INR values due to insufficient dietary vitamin K. The present study was undertaken to investigate whether SIBO occurrence may affect warfarin dose requirements in anticoagulated patients. Based on their mean weekly dose of warfarin while on stable anticoagulation, 3 groups of 10 patients each were defined: low dose (LD, or=70 mg/wk). Each patient underwent a lactulose breath test to diagnose SIBO. Plasma levels of warfarin and vitamin K-analogues were also assessed. Patients with an altered breath test were 50% in the VHD group, 10% in the HD group, and none in the LD group (P=0.01). Predisposing factors to SIBO were more frequent in the VHD group, while warfarin interfering variables were not. VHD patients were younger and had a higher plasma vitamin K1 (VK1) concentration (P>0.05). On the contrary, the plasma VK2 levels tended to be lower. This pilot study suggests that SIBO may increase a patient's warfarin dose requirement by increasing dietary VK1 absorption through the potentially damaged intestinal mucosa rather than increasing intestinal VK2 biosynthesis. Larger studies are needed to confirm these preliminary data and to evaluate the effects of SIBO decontamination on warfarin dosage.

A simplified method for anal ultrasonography: preliminary report.

BACKGROUND: Anal endosonography (AES) is able to reliably visualize and identify anal sphincter abnormalities. However, dedicated probes are quite expensive. AIM: We describe a simple and less costly method to perform AES in a unit that already has echoendoscopes available by inserting the endoscope through a disposable anoscope filled with standard ultrasound gel. PATIENTS: Subjects without anal abnormalities and patients with anal disease (abscesses, fistulas) were evaluated. RESULTS: Good-quality images were obtained in both controls and patients, with optimal visualization of the anatomic structures and pathologic features. The latter (abscesses, fistulas) were always confirmed by magnetic resonance imaging. CONCLUSIONS: This simple and less costly method allows to perform good-quality AES in units having echoendoscopes availability, without the need of a more expensive dedicated probe.

Antroduodenojejunal motor activity in untreated and treated celiac disease patients.

BACKGROUND AND AIM: Patients with celiac disease may present with abnormal upper gut motor activity. However, it is not known if these abnormalities persist after the introduction of a gluten-free diet. The present study aimed to compare antroduodenojejunal motor variables recorded in untreated celiac patients with those of celiac patients given a gluten-free diet and healthy volunteers. METHODS: Eleven untreated celiac disease patients, 12 age- and sex-matched celiac patients on a gluten-free diet (at least 12 months), and 33 controls entered the study. Antroduodenojejunal motility was recorded for 6 h during fasting and for 3 h after a standard meal by means of a perfused, multiple lumen catheter. RESULTS: More than 80% of untreated celiac patients had discrete motor abnormalities of the upper gut, in both fasting and fed recordings, compared to the other subjects. Patients on a gluten-free diet also showed motor abnormalities, albeit to a lesser extent. In these patients histological evaluation showed the persistence of mild mucosal abnormalities. CONCLUSIONS: Upper gut motor abnormalities are frequent in patients with celiac disease, even in those on a gluten-free diet. In the latter group, these abnormalities may suggest an incomplete adherence to the dietary regimen.

Ski/SnoN expression in the sequence metaplasia-dysplasia-adenocarcinoma of Barrett's esophagus.

Barrett's esophagus (BE) is a precancerous condition. However, the mechanisms underlying the transformation from metaplastic to dysplastic to adenocarcinomatous epithelium are still poorly understood. As loss of transforming growth factor-beta growth inhibition is considered a hallmark of several human neoplasms, we evaluated the expression of Ski and SnoN (proteins that antagonize transforming growth factor-beta signaling through physical interaction with Smad complex and by recruiting histone deacetylases), as markers of the transforming growth factor-beta signaling pathway, in BE with and without dysplasia. Biopsy samples from 37 patients (26 men, aged 60 +/- 8 years) with histologically proven BE were evaluated; 10 patients had concomitant low-grade dysplasia, 7 high-grade dysplasia (HGD), and 6 HGD associated with adenocarcinoma. Ski and SnoN expression was assessed immunohistochemically. Neither Ski nor SnoN was expressed in normal esophageal epithelium, but both were strongly expressed in BE tissue, with intense cytoplasmic positivity. Expression of these proteins decreased markedly in dysplastic areas in patients with low-grade dysplasia and was absent in those with HGD or HGD/adenocarcinoma. Ski and SnoN proteins are overexpressed in BE and may be involved in abnormal signaling elicited by transforming growth factor-beta in this epithelium, enhancing the tumorigenesis process. These observations might help to elucidate the molecular mechanisms involved in the BE tumorigenesis process.

TAFI deficiency in liver cirrhosis: relation with plasma fibrinolysis and survival.

INTRODUCTION: TAFI (thrombin-activatable fibrinolysis inhibitor) is a potent anti-fibrinolytic and anti-inflammatory factor of liver origin. It is markedly reduced in liver cirrhosis but its effect on fibrinolysis remains controversial and no data are available on its prognostic value. We evaluated the relationship of TAFI level with plasma fibrinolysis and survival in cirrhotic patients. PATIENTS AND METHODS: Sixty-five patients with liver cirrhosis were studied. TAFI antigen, plasma fibrinolysis and other laboratory variables were assayed at study entry and their association with mortality was assessed during a 3-year follow-up. RESULTS: TAFI level and fibrinolysis time were markedly reduced in liver cirrhosis as compared to healthy subjects (p<0.0001) and TAFI deficiency was strongly correlated with fibrinolysis time (p=0.0002). TAFI level at entry, but not fibrinolysis time, was significantly lower in non-survivors (n=25) than in survivors (n=40, p=0.0001). By Cox regression analysis, after adjustment for possible confounding factors, TAFI, but not fibrinolysis time, was identified as an independent predictor of mortality. TAFI assay, moreover, showed a clinically relevant accuracy in assessing patients' survival (ROC curve analysis, p<0.0001) achieving a sensitivity of 92%, a specificity of 55%, and a negative predictive value of 91.7%. CONCLUSIONS: Our data indicate that TAFI deficiency in liver cirrhosis is associated with enhanced plasma fibrinolysis. Moreover, they suggest that TAFI, but not fibrinolysis time, is a strong predictor of survival and thus TAFI assay might prove useful to select candidates for liver transplantation.

The prevalence of hyper- and hypothyroidism in patients with ulcerative colitis.

BACKGROUND: The association between ulcerative colitis and thyroid disorders has been previously reported. However, most reports consist of single case description, and a systematic assessment of this relationship has only sporadically been investigated. AIMS: To study a cohort of patients with ulcerative colitis to establish the prevalence of hyper- and hypothyroidism. MATERIAL AND METHODS: During a four-year period, we studied thyroid function in 162 ulcerative colitis patients (62 men, 100 women, age range 18-78 years). RESULTS: Thyroid dysfunction was present in 4 patients (2.5%) of the overall population and was represented by both hypo- (3 patients) and hyperthyroidism (1 patient). The incidence of this kind of thyroid dysfunction was significantly (p=0.03) lower than that found in a large (more than 5000 subjects) control group. CONCLUSIONS: We conclude that the prevalence of hyper-/hypothyroidism is relatively low in patients with ulcerative colitis, at least in our country, and does not justify a systematic investigation of the thyroid function, except in selected cases, probably those with scarce or no response to standard therapeutic measures.

Psicanálise, políticas públicas e caso único / Psychoanalysis, public politics and unique case

A partir de dois fragmentos de casos atendidos em um programa destinado a acompanhar jovens em conflito com a lei na cidade de Belo Horizonte, discute-se a pertinência da psicanálise nas políticas públicas e a importância do 'analista-cidadão', sacando do coletivo o singular de cada um(AU)

Psicanálise, políticas públicas e caso único / Psychoanalysis, public politics and unique case

A partir de dois fragmentos de casos atendidos em um programa destinado a acompanhar jovens em conflito com a lei na cidade de Belo Horizonte, discute-se a pertinência da psicanálise nas políticas públicas e a importância do analista-cidadão, sacando do coletivo o singular de cada um.

Pasta naturally enriched with isoflavone aglycons from soy germ reduces serum lipids and improves markers of cardiovascular risk.

Most studies of soy and cholesterol have tested foods made from purified soy proteins containing mainly isoflavone glycosides. Fermented soy foods have mainly isoflavone aglycons and account for a high proportion of the soy protein source in Asia, where there is an inverse relationship between soy intake and serum cholesterol. The aim of this study was to compare a novel soy germ pasta, naturally enriched in isoflavone aglycons as a result of the manufacturing process, with conventional pasta for effects on serum lipids and other cardiovascular risk markers. In this randomized, controlled, parallel study design of 62 adults with hypercholesterolemia who consumed a Step II diet that included one 80-g serving/d of pasta, we measured serum lipids, high sensitivity C-reactive protein (hsCRP), urinary isoprostanes, and brachial artery flow-mediated vasodilatation at baseline and after 4 and 8 wk. The pasta delivered 33 mg of isoflavones and negligible soy protein and led to a serum isoflavone concentration of 222 +/- 21 nmol/L; 69% of subjects were equol producers. Soy germ pasta reduced serum total and LDL cholesterol by 0.47 +/- 0.13 mmol/L (P = 0.001) and 0.36 +/- 0.10 mmol/L (P = 0.002) more than conventional pasta, representing reductions from baseline of 7.3% (P = 0.001) and 8.6% (P = 0.002), respectively. Arterial stiffness (P = 0.003) and hsCRP (P = 0.03) decreased and improvements in all the above risk markers were greatest in equol producers. All measures returned to baseline when patients were switched to conventional pasta. In conclusion, pasta naturally enriched with isoflavone aglycons and lacking soy protein had a significant hypocholesterolemic effect beyond a Step II diet and improved other cardiovascular risk markers.

Enteric glial cells: new players in gastrointestinal motility?

The enteric glial cells, in addition to being support structures for the enteric nervous system, have many other additional roles, such as modulators for the homeostasis of enteric neurons, cells involved in enteric neurotransmission and antigen-presenting cells. Moreover, in the last years, data have been accumulating that demonstrate a possible active role of these cells in the pathophysiology of gastrointestinal motor activity. Thus, as also shown by recent evidence in both experimental animal models, and in some human diseases, alterations of enteric glial cells might have some role in the development of intestinal motor abnormalities.

CD1-restricted recognition of exogenous and self-lipid antigens by duodenal gammadelta+ T lymphocytes.

Gammadelta T cells are present in the mucosal intestinal epithelia and secrete factors necessary to maintain tissue integrity. Ags recognized by these cells are poorly defined, although in mice non-classical MHC class I molecules have been implicated. Since MHC class I-like CD1 receptors are widely expressed at the surface of epithelial and dendritic intestinal cells and have the capacity to present lipid Ags to T cells, we hypothesized that these molecules might present autologous and/or exogenous phospholipids to intestinal gammadelta T lymphocytes. Intraepithelial T lymphocytes from normal human duodenal mucosal biopsies were cloned and exposed to natural and synthetic phospholipids using CD1a-, CD1b-, CD1c- or CD1d-transfected C1R lymphoblastoid or HeLa cell lines as APCs. Their cytolytic properties and regulatory cytokine secretion were also examined. Most clones obtained from duodenal mucosa (up to 70%) were TCRalphabeta+, and either CD4+ or CD8+, whereas 20% were CD4-CD8- (6 clones) or TCRgammadelta+ (12 clones). A relevant percentage (up to 66%) of TCRgammadelta+ but few (<5%) TCRalphabeta+ T cell clones responded to synthetic and/or natural phospholipids presented by CD1 molecules, as measured by both [(3)H]thymidine incorporation and IL-4 release assays. A Th1-like cytolytic and functional activity along with the ability to secrete regulatory cytokines was observed in most phospholipid-specific gammadelta T cell clones. Thus, a substantial percentage of TCRgammadelta+ but few TCRalphabeta+ from human duodenal mucosa recognize exogenous phospholipids in a CD1-restricted fashion. This adaptive response could contribute to mucosal homeostasis, but could also favor the emergence of inflammatory or allergic intestinal diseases.

Colonic neuropathological aspects in patients with intractable constipation due to obstructed defecation.

One of the most frequent subtypes of constipation is represented by obstructed defecation, and it has recently been reported that these patients may have colonic motor abnormalities in addition to alterations of the anorectal area. However, it is unknown whether these patients display abnormalities of the enteric nervous system, as reported in other groups of constipated subjects. For this reason, we evaluated the neuropathologic aspects of the enteric nervous system in a homogeneous group of patients with obstructed defecation. Colonic specimens from 11 patients (nine women, age range 39-66 years) undergoing surgery for symptoms refractory to any therapeutic measure, including biofeedback training, were obtained and examined by means of conventional histological methods and immunohistochemistry (NSE, S100, c-Kit, formamide-mAb, Bcl-2, CD34, alfa-actin). Analysis of the specimens showed that the enteric neurons were significantly decreased only in the submucosal plexus of patients (P<0.0001 vs controls), whereas the enteric glial cells of constipated patients were reduced in both the myenteric (P=0.018 vs controls) and the submucosal plexus (P=0.004 vs controls). No difference between patients and controls were found concerning c-Kit and CD34 expression, and the number of apoptotic neurons. These findings support the concept that at least a subgroup of patients with obstructed defecation and severe, intractable symptoms display abnormalities of the enteric nervous system, mostly related to the enteric glial cells. These findings might explain some of the pathophysiological abnormalities, and help to better understand this condition.

The enteric nervous system in chagasic and idiopathic megacolon.

Chagas disease frequently causes megacolon. We investigated the enteric nervous systems in patients with chagasic megacolon compared to idiopathic megacolon and controls. Surgical specimens were obtained from 12 patients with chagasic megacolon (1 woman, 11 men, age range 41 to 72 y) and 9 patients with idiopathic megacolon (3 women, 6 men, age range 39 to 68 y), undergoing surgery for intractable constipation. A control group of 10 patients (9 women, 1 man, age range 43 to 75 y) undergoing left hemicolectomy for nonobstructing colorectal cancer was also studied. Colonic sections were investigated by conventional and immunohistochemical methods, also taking into consideration the presence of lymphocytes. Compared to controls, the 2 megacolon groups showed a decrease of enteric neurons (not due to increased apoptosis) and of enteric glial cells (all more important in chagasic patients). The interstitial cells of Cajal subtypes were decreased but not absent in megacolons, although an increase of the intramuscular subtype was found, suggesting a possible compensative mechanism. An increased amount of fibrosis was found in the smooth muscle and the myenteric plexus of chagasic patients compared to the idiopathic megacolon and the control group. A mild lymphocytic infiltration of the enteric plexuses (more evident in Chagas disease) was also found in megacolons but not in controls. Patients with chagasic megacolon display important abnormalities of several components of the enteric nervous system. Similar alterations, although of lesser severity, may be found in patients with idiopathic megacolon.

Audit of constipation in a gastroenterology referral center.

This study was designed to assess the various subtypes of functional constipation in a referral gastrointestinal center of a Latino-American country. All patients referred for evaluation of constipation during a 10-year period were audited, and those with functional constipation according to Rome I criteria classified by physiologic tests of colonic transit, as well as tests of anorectal and pelvic floor function. More than 70% of patients with functional constipation had evidence of pelvic floor dysfunction, whereas those with slow transit and constipation-predominant irritable bowel syndrome subtypes were less frequently represented. Even in a setting different from those most frequently reported in the literature, pelvic floor dysfunction represents the most common cause of functional constipation. Simple, physiologic testing is needed and useful for the diagnosis. This fact has therapeutic implications, especially because many such patients may benefit from biofeedback.

Comparison of three methods to assess enteric neuronal apoptosis in patients with slow transit constipation.

BACKGROUND: The pathophysiological basis of slow transit constipation are scarcely understood. Some recent evidence suggests that increased apoptotic phenomena in the colonic enteric neurons may play a role. However, the best method to assess these phenomena has not been evaluated. AIMS: To compare three different methods to detect enteric neuronal apoptosis in these patients. METHODS: Serial colonic tissue sections obtained in 10 patients with intractable slow transit constipation were evaluated with immunohistochemical methods aimed at evaluating apoptotic phenomena: the formamide-MAb method, the TUNEL, and the caspase-3. RESULTS: The highest yield of apoptotic neurons was obtained by means of the formamide-MAb method, compared to the other two, whereas the lowest yield was observed with the caspase-3. CONCLUSIONS: The formamide-MAb method, which is able to distinguish apoptosis from necrosis and is not influenced by DNA breaks, may prove useful to assess neuronal apoptotic phenomena in the human enteric nervous system. This represents a relevant method to detect enteric neuronal apoptosis.

Enteric neuropathology of the terminal ileum in patients with intractable slow-transit constipation.

Slow-transit constipation is usually considered a colonic motor disorder. However, there is some evidence that abnormalities may be present in locations other than the colon. In particular, several studies have reported abnormal motor activity of the small bowel in these patients. We evaluated the neuropathological aspects of the terminal ileum in patients with slow-transit constipation to see whether abnormalities are present that may explain an abnormal motility of the small intestine. Specimens of the terminal ileum were obtained from 16 female patients (age range, 42-76 years) with slow-transit constipation undergoing surgery for intractable symptoms. Fifteen age- and sex-matched controls were used for comparison. Histologic and immunohistochemical evaluation of the myenteric plexus and the smooth muscle of the proximal ileal resection margin was carried out by means of hematoxylin and eosin, trichrome and periodic acid-Schiff stain, neuron-specific enolase, S-100, CD117, CD34, anti-alpha-actin, desmin, and vimentin antibodies. The patient group displayed a significantly reduced number of glial cells, compared with controls, in both the submucosal and the myenteric plexus. Only 1 of the 3 populations of interstitial cells of Cajal (that associated with the deep muscular plexus) was decreased in patients. No differences were found between patients and controls concerning ganglia neurons, fibroblast-like cells, enteric neurons, apoptotic phenomena, and smooth muscle. Patients with slow-transit constipation display neuropathological abnormalities of the terminal ileum to a lesser extent than those we previously found in the colon, which might explain the abnormal motor aspects sometimes found in these patients.

Colonic propulsive and postprandial motor activity in patients with ulcerative colitis in remission.

BACKGROUND: Although it is known that colon motility is abnormal in ulcerative colitis, data are still scarce with regard to the underlying mechanisms. Recent evidence suggests that the propulsive activity is highly increased during the active phase of the disease, probably contributing to the diarrhoea. However, data are even scarcer in the quiescent phase of the disease. AIMS: To assess the colonic high-amplitude and low-amplitude propulsive activity and the colonic motor response to eating in patients with ulcerative colitis in remission. PATIENTS AND METHODS: Fourteen patients were recruited, all with the disease in remission as documented by clinical and endoscopic criteria. Twenty-four hour manometric recordings were obtained in these patients, and compared to those of 16 healthy controls. RESULTS: The high-amplitude propagated contractions were similar in both groups (5.8+/-2.6 events in ulcerative colitis patients and 5.5+/-0.8 in controls (P=0.13)), whereas patients tended to display a higher number of low-amplitude propagated events (134.4+/-34 vs. 60.9+/-16 in controls (P=0.058)). No differences were found in the colonic motor response to eating between patients and controls. CONCLUSIONS: Colonic propulsive activity in ulcerative colitis in remission is almost normal, even though the low-amplitude propagated activity tends to be similar to that observed in patients with the irritable bowel syndrome, thus possibly contributing to the persistence of abdominal symptoms in a subgroup of patients.

Biofeedback is superior to laxatives for normal transit constipation due to pelvic floor dyssynergia.

BACKGROUND & AIMS: Uncontrolled trials suggest biofeedback is an effective treatment for pelvic floor dyssynergia (PFD), a type of constipation defined by paradoxical contraction, or inability to relax, pelvic floor muscles during defecation. The aim was to compare biofeedback to laxatives plus education. METHODS: Patients with chronic, severe PFD were first treated with 20 g/day fiber plus enemas or suppositories up to twice weekly. Nonresponders were randomized to either 5 weekly biofeedback sessions (n = 54) or polyethylene glycol 14.6-29.2 g/day plus 5 weekly counseling sessions in preventing constipation (n = 55). Satisfaction with treatment, symptoms of constipation, and pelvic floor physiology were assessed 6 and 12 months later. The biofeedback group was also assessed at 24 months. Laxative-treated patients were instructed to increase the dose of polyethylene glycol from 14.6 to 29.2 g/day after 6 months. RESULTS: At 6 months, major improvement was reported by 43 of 54 (80%) biofeedback patients vs 12 of 55 (22%) laxative-treated patients (P < .001). Biofeedback's benefits were sustained at 12 and 24 months. Biofeedback also produced greater reductions in straining, sensations of incomplete evacuation and anorectal blockage, use of enemas and suppositories, and abdominal pain (all P < .01). Stool frequency increased in both groups. All biofeedback-treated patients reporting major improvement were able to relax the pelvic floor and defecate a 50-mL balloon at 6 and 12 months. CONCLUSIONS: Five biofeedback sessions are more effective than continuous polyethylene glycol for treating PFD, and benefits last at least 2 years. Biofeedback should become the treatment of choice for this common and easily diagnosed type of constipation.

3alpha-6alpha-Dihydroxy-7alpha-fluoro-5beta-cholanoate (UPF-680), physicochemical and physiological properties of a new fluorinated bile acid that prevents 17alpha-ethynyl-estradiol-induced cholestasis in rats.

3alpha-6alpha-Dihydroxy-7alpha-fluoro-5beta-cholanoate (UPF-680), the 7alpha-fluorine analog of hyodeoxycholic acid (HDCA), was synthesized to improve bioavailability and stability of ursodeoxycholic acid (UDCA). Acute rat biliary fistula and chronic cholestasis induced by 17alpha-ethynyl-estradiol (17EE) models were used to study and compare the effects of UPF-680 (dose range 0.6-6.0 micromol/kg min) with UDCA on bile flow, biliary bicarbonate (HCO(3)(-)), lipid output, biliary bile acid composition, hepatic enzymes and organic anion pumps. In acute infusion, UPF-680 increased bile flow in a dose-related manner, by up to 40.9%. Biliary HCO(3)(-) output was similarly increased. Changes were observed in phospholipid secretion only at the highest doses. Treatment with UDCA and UPF-680 reversed chronic cholestasis induced by 17EE; in this model, UDCA had no effect on bile flow in contrast to UPF-680, which significantly increased bile flow. With acute administration of UPF-680, the biliary bile acid pool became enriched with unconjugated and conjugated UPF-680 (71.7%) at the expense of endogenous cholic acid and muricholic isomers. With chronic administration of UPF-680 or UDCA, the main biliary bile acids were tauro conjugates, but modification of biliary bile acid pool was greater with UPF-680. UPF-680 increased the mRNA for cytochrome P450 7A1 (CYP7A1) and cytochrome P450 8B (CYP8B). Both UDCA and UPF-680 increased the mRNA for Na(+) taurocholate co-transporting polypeptide (NCTP). In conclusion, UPF-680 prevented 17EE-induced cholestasis and enriched the biliary bile acid pool with less detergent and cytotoxic bile acids. This novel fluorinated bile acid may have potential in the treatment of cholestatic liver disease.

Evidence that hydrogen sulfide exerts antinociceptive effects in the gastrointestinal tract by activating KATP channels.

Hydrogen sulfide (H(2)S) functions as a neuromodulator, but whether it modulates visceral perception and pain is unknown. Cystathionine beta-synthase (CBS) and cystathionine-gamma-lyase (CSE) mediate enzymatic generation of H(2)S in mammalian cells. Here we have investigated the role of H(2)S in modulating nociception to colorectal distension, a model that mimics some features of the irritable bowel syndrome. Four graded (0.4-1.6 ml of water) colorectal distensions (CRDs) were produced in conscious rats (healthy and postcolitic), and rectal nociception was assessed by measuring the behavioral response during CRD. Healthy rats were administered with sodium hydrogen sulfide (NaHS) (as a source of H(2)S), L-cysteine, or vehicle. In a second model, we investigated nociception to CRD in rats recovering from a chemically induced acute colitis. We found that CBS and CSE are expressed in the colon and spinal cord. Treating rats with NaHS resulted in a dose-dependent attenuation of CRD-induced nociception with the maximal effect at 60 micromol/kg (p < 0.05). Administration of L-cysteine, a CSE/CBS substrate, reduced rectal sensitivity to CRD (p < 0.05). NaHS-induced antinociception was reversed by glibenclamide, a ATP-sensitive K(+) (K(ATP)) channel inhibitor, and N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME), a nitric-oxide (NO) synthase inhibitor. The antinociceptive effect of NaHS was maintained during the resolution of colon inflammation induced by intrarectal administration of a chemical irritant. In summary, these data show that H(2)S inhibits nociception induced by CRD in both healthy and postcolitic rats. This effect is mediated by K(ATP) channels and NO. H(2)S-releasing drugs might be beneficial in treating painful intestinal disorders.