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PubMed2000

Some aromatic nitrate esters: synthesis, structural aspects, thermal and explosive properties.

1-(2-Nitroxyethylnitramino)-2,4,6-trinitrobenzene (I-A), 1, 3-bis(2-nitroxyethylnitramino)-2,4,6-trinitrobenzene (II-A) and 1,3, 5-tris(2-nitroxyethylnitramino)-2,4,6-trinitrobenzene (III-A) have been prepared by condensing picryl chloride, styphnyl chloride and 1, 3,5-trichloro-2,4,6-trinitrobenzene with ethanol amine, respectively, followed by nitration. These compounds have been characterized by infrared spectrum (IR), the elemental analysis and 1H NMR. Further, these compounds have been studied for their thermal and explosive properties. The activation energy of thermal decomposition of these compounds has also been determined using the Ozawa and the Kissinger methods. The data on explosive properties indicate that the impact, friction and velocity of detonation (VOD) increase with an increase in the number of nitrate ester groups.

Esters↗
PubMedDate not supplied

Differing effects of two nitric oxide synthase inhibitors on experimental colitis.

BACKGROUND/AIMS: The aim of this study was to investigate the effects of two inhibitors of nitric oxide synthase on a rat model of colitis. METHODOLOGY: Colitis was induced by administration of an enema containing trinitrobenzene sulfonic acid. This colitis was treated everyday for one week with NG-nitro-L-arginine (10 mg/kg, i.v.), which is a non-selective inhibitor of both constitutive nitric oxide synthase and inducible nitric oxide synthase, or aminoguanidine (10 mg/kg, i.v.) which is an inhibitor of inducible nitric oxide synthase. Exposure to the trinitrobenzene sulfonic acid enema inhibited the increase in body weight of rats, and markedly increased the colonic damage scores, wet weight, thiobarbituric acid-reactive substances and myeloperoxidase activity. RESULTS: The inhibition of weight increase caused by trinitrobenzene sulfonic acid was significantly reduced by aminoguanidine treatment, whereas weight loss tended to be aggravated by NG-nitro-L-arginine treatment. The increases in the colonic damage scores, wet weight, thiobarbituric acid-reactive substances and myeloperoxidase activity in trinitrobenzene sulfonic acid-colitis were significantly inhibited by aminoguanidine treatment, although they tended to be aggravated by NG-nitro-L-arginine treatment. CONCLUSIONS: These results suggest that an inhibitor of inducible nitric oxide synthase, but not of constitutive nitric oxide synthase, was effective in treating experimental colitis in rats.

Animals↗
PubMed2004

Thermodynamics of nitroaromatic compound adsorption from water by smectite clay.

Nitroaromatic compounds enter the environment through their use as explosives, pesticides, solvents, and synthetic intermediates in the manufacturing of dyes, perfumes, and drugs. Recent studies have found that many nitroaromatic compounds are strongly retained by smectites, especially K+-saturated smectites. Sorption occurs when nitroaromatic compounds replace water associated with the clay and form complexes between K+ and -NO2 groups. This study seeks to further understand nitroaromatic-clay interactions from the viewpoint of energetics. Adsorption isotherms of 1,3-dinitrobenzene, 1,4-dinitrobenzene, and 1,3,5-trinitrobenzene from aqueous solution by K+- and Ca2+-saturated smectite (SWy-2) were measured at several temperatures between 4 degrees C and 37 degrees C to determine the molar differential adsorption enthalpies. Adsorption was found to be an exothermic process on both homoionic K+- and Ca2+-smectite. The smaller adsorption enthalpy on Ca-SWy-2 was consistent with its much smaller adsorption capacity for nitroaromatics compared to K-SWy-2. Our best estimate forthe enthalpy of 1,3,5-trinitrobenzene interactions with K-SWy-2 is -124 kJ/mol, which is referenced to gas-phase 1,3,5-trinitrobenzene, corrected forthe displacement of interlayer water, and can be directly compared with quantum chemical enthalpies from the literature. Our comparable estimates for 1,3- and 1,4-dinitrobenzene interaction enthalpies are near -90 kJ/mol. We conclude that our adsorption enthalpy results are consistent with the hypothesis that nitroaromatic compounds are sorbed strongly by K-smectites because they form inner- and/or outer-sphere complexes with K+ cations in clay interlayers. Indeed, the basal spacings of rewetted clay films in the presence of nitroaromatic compounds imply that water molecules cannot effectively compete with the adsorbed nitrobenzenes for reactive sites on K-SWy-2.

Adsorption↗
PubMed1992

Exacerbation of experimental colitis by nonsteroidal anti-inflammatory drugs is not related to elevated leukotriene B4 synthesis.

The ability of nonsteroidal anti-inflammatory drugs to exacerbate experimental colitis, and the possible contributions of the "shunting" of arachidonate via the 5-lipoxygenase pathway, were investigated using a rat model in which colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid in a vehicle of 50% ethanol. Twice daily treatment with indomethacin (0.1-1 mg/kg SC) during the first week after trinitrobenzene sulfonic acid/ethanol administration resulted in dose-dependent increases in the severity of colitis and in the incidence of mortality. Mortality was not observed in vehicle-treated colitic rats or in normal rats treated with indomethacin. Similar exacerbation of colitis was observed in rats treated with naproxen (5 mg/kg). Whereas treatment with a 5-lipoxygenase inhibitor, PF-5901 (100 mg/kg PO), resulted in a significant reduction of the severity of colitis, concomitant administration of PF-5901 and indomethacin (0.5 mg/kg SC) did not inhibit the exacerbative effects of the indomethacin in this model. In separate studies, administration of indomethacin was found to significantly increase colonic myeloperoxidase activity (a measure of tissue granulocyte numbers) and suppress colonic prostaglandin E2 synthesis, while not significantly affecting colonic leukotriene B4 synthesis. The effect on myeloperoxidase activity was seen during the period 21-24 hours after trinitrobenzene sulfonic acid ethanol administration, but not during the period 45-48 hours after induction of colitis. In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis, inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis. These results suggest that inhibitors of colonic prostaglandin synthesis can markedly exacerbate colitis, and that this effect is unrelated to alterations in colonic leukotriene B4 synthesis. Endogenous prostaglandins may exert anti-inflammatory effects during the acute stages of colitis.

Animals↗
PubMed1975

[Charge-transfer complexes of indolalkylamine and ergoline derivatives].

Charge-transfer complexes of 1,3,5-trinitrobenzene and pyromellitic dianhydride with indolalkylamines (5-hydroxytryptamine, dimethyltryptamine, etryptamine) and with ergoline derivatives having antiserotonin activity (methysergide, methylergometrine, metergoline, nicotergoline) were studied. The value of the association constant of indole derivatives with trinitrobenzene is influenced by variations on the chain; on the contrary, with pyromellitic dianhydride - only etryptamine and dimethyltryptamine form CT-complexes - the different behaviour can not be correlated with any particular structural characteristics. The association constant values of ergoline derivatives with trinitrobenzene are of the same order of magnitude as that of serotonin; with pyromellitic dianhydride only metergoline and nicotergoline form CT-complexes.

Metergoline↗
PubMed2000

The effect of berberine chloride on experimental colitis in rats in vivo and in vitro.

Berberine is an isoquinoline alkaloid with multiple pharmacological actions, including anti-inflammatory activity. The aims of this study were to examine the effect of berberine on the mucosal healing process and to investigate whether berberine can inhibit the increased production of interleukin-8 in trinitrobenzene sulfonic acid-induced colitis in rats. Berberine was administered orally for 3 days or 1 week at a dosage of 7.5 or 15 mg/kg/day. Tissue damage scores, body weight, colon wet weight, and colon wall thickness were measured, and myeloperoxidase activity in colon tissue was also examined. Histological lesions, morphological damage, and myeloperoxidase activity were reduced after 1 week of treatment with berberine at a dosage of 15 mg/kg/day. Furthermore, 1 week after trinitrobenzene sulfonic acid treatment, the production of interleukin-8 by cultured rectal mucosa or cardiac blood mononuclear cells with or without stimulation of lipopolysaccharide for 24 h was also analyzed by enzyme-linked immunosorbent assay. Cardiac blood mononuclear cells and rectal mucosa of normal rats produced substantial amounts of interleukin-8, which increased strikingly with the stimulation of lipopolysaccharide. Cardiac blood mononuclear cells and rectal mucosa of trinitrobenzene sulfonic acid-treated rats secreted more interleukin-8 than those of normal rats. The addition of berberine with a concentration of 10(-5) M to the culture media resulted in an inhibition of interleukin-8 production of rectal mucosa.

Animals↗
PubMed1987

The heparin binding site of human antithrombin III. Selective chemical modification at Lys114, Lys125, and Lys287 impairs its heparin cofactor activity.

Heparin binds to human antithrombin III and accelerates its inhibitory activity in the blood coagulation system. Previous reports (Rosenberg, R. D., and Damus, P. S. (1973) J. Biol. Chem. 248, 6490-6505; Pecon, J. M., and Blackburn, M. N. (1984) J. Biol. Chem. 259, 935-938) have shown that selective chemical modification of a limited number of lysine residues in antithrombin III causes drastic loss of its heparin cofactor activity. We have performed chemical modification of antithrombin III with trinitrobenzene sulfonic acid in order to determine the location of these lysine residues. When antithrombin III was treated with 100 M excess of trinitrobenzene sulfonic acid for 10 min, about 3.2 mol of amino group per mol of antithrombin III were modified. The heparin cofactor activity dropped to about 25%, whereas the progressive inhibitory activity (in the absence of heparin) remained essentially intact (about 95%). The modified amino groups were identified to be Lys114 (75%), Lys125 (94%), and Lys287 (96%). These results were obtained by comparing and analyzing the cyanogen bromide fragments derived from native antithrombin III and the 10-min modified antithrombin III. When antithrombin III was pretreated with heparin, followed by trinitrobenzene sulfonic acid modification, the extent of modification at Lys114 and Lys125 decreased from 75% and 94% to 20% and 40%, respectively, whereas the modification at Lys287 remained nearly quantitative (greater than 95%). Based on these results, we conclude that Lys114 and Lys125 are essential for the heparin cofactor activity of human antithrombin III.

Amino Acids↗
PubMed1995

Transforming growth factor-beta gene therapy ameliorates experimental colitis in rats.

OBJECTIVE: To modulate experimental colitis by the direct intramuscular injection of cDNA expression vector encoding transforming growth factor-beta 1. METHODS: Colitis was induced in rats by the intracolonic administration of 0.25 ml 50% ethanol containing 30 mg trinitrobenzene sulfonic acid. Three and 10 days later the rats were injected intramuscularly with 200 micrograms transforming growth factor-beta 1 cDNA subcloned to the pRSV expression vector (pRSVTGF-beta 1). Control rats were injected with pRSVP2. The rats were sacrificed 2 weeks after trinitrobenzene sulfonic acid treatment and a 10 cm long distal colonic segment was resected, weighted, the lesion area measured, sections obtained for histology and the mucosa extracted for determination of myeloperoxidase activity and leukotriene generation. RESULTS: In pRSVP2-treated rats (n = 17) the colon was inflamed and ulcerated with many adhesions to adjacent structures; the pRSVTGF-beta 1-treated rats (n = 21) had minimal swelling and inflammation in the colon. On histological examination 50% of the pRSVTGF-beta 1-treated rats had minimal or no ulceration, whereas 83% of the pRSVP2-treated rats had a maximal damage score. In pRSVTG-beta 1-treated rats the lesion area and wet weight were 21 and 52.5%, respectively, of the values for pRSVP2-treated rats (P < 0.05). The amelioration of tissue injury was accompanied by a significant decrease in mucosal leukotriene C4 generation. CONCLUSIONS: Direct intramuscular transforming growth factor-beta 1 gene delivery effectively ameliorates trinitrobenzene sulfonic acid-induced colitis, suggesting that gene therapy with immunosuppressive cytokines may be a novel approach for the treatment of inflammatory bowel disease.

Animals↗
PubMed1979

Insertion and turnover of macrophage plasma membrane proteins.

The composition, insertion, and turnover of externally disposed proteins on the macrophage plasma membrane were analyzed. Cells labeled with [35S]methionine were incubated with the nonpermeant reagent trinitrobenzene sulfonic acid to introduce the trinitrophenyl moiety on free amino groups of externally oriented membrane proteins. The cells were then incubated with rabbit anti-dinitrophenyl IgG and the immune complexes formed with the trinitrophenyl-proteins were isolated from detergent lysates of the cells by using fixed Staphylococcus aureus as the immunoadsorbent. Proteins isolated by this method were analyzed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis. The interval between the release of newly synthesized proteins from ribosomes and their appearance at the cell surface, where they became accessible to trinitrobenzene sulfonic acid, was studied in pulse-chase experiments. The "transit" time of four major membrane glycoproteins (48,000--310,000 Mr) ranged from 36 to 55 min and their appearance on the cell surface occurred in a relatively synchronous fashion. The turnover of most proteins of molecular weight above 50,000 was very slow (t1/2 greater than 80 hr) and was rather synchronous. Two exceptions were the 310,000 Mr protein, which was lost with a t1/2 = 21 hr, and a major glycoprotein (Mr 48,000), which exhibited more complex kinetics. Although the overall turnover of surface proteins was biphasic in nature, the rapid phase of protein loss was largely due to low molecular weight species.

Immunologic Techniques↗
PubMed1978

Covalent probe investigations with isolated central nerve myelin preparations.

The interaction of the covalently reacting probes dansyl chloride, fluorodinitrobenzene and trinitrobenzene sulphonic acid with isolated central nerve myelin sheath preparations has been studied. The three probes interact preferentially with accessible amino groups on lipid and protein in the membrane. With isolated myelin some 13% of the total phosphatidyl ethanolamine is labelled with dansyl chloride while the figure is 66% with fluorodinitro benzene and 47% with trinitrobenzene sulphonic acid. Lower levels of phosphatidyl serine are labelled. Phosphatidyl ethanolamine seems to be more accessible to probes in the myelin sheath than is phosphatidyl serine perhaps because the ethanolamine-containing lipid class is localised partially at the external apposition surfaces of the membrane which are most accessible to the probes. The serine phospholipids may not react so well because they are preferentially distributed at the cytoplasmic surface of the system. Analysis of protein labelling patterns after reaction of intact myelin with dansyl chloride indicates that the high molecular weight proteins and the proteolipid protein is accessible to the probe while the basic protein is not, even though this latter component is readily labelled with dansyl choride in purified form. It is suggested that the inability of the basic protein to react with myelin is perhaps due to the fact that it is occluded from interaction with the probe at the cytoplasmic apposition surfaces of the lamellae.

Animals↗
PubMed1995

Role of histamine in a rat model of colitis.

We examined the possible involvement of mast cells in a rat model of colitis, by monitoring levels of histamine at various times after inducing inflammation with intrarectal trinitrobenzene sulfonic acid in 50% ethanol. The ability of a histamine H1 antagonist, diphenhydramine, to modify colitis was also assessed. As expected, trinitrobenzene sulfonic acid in 50% ethanol induced a sustained colitis. Myeloperoxidase levels in macroscopically damaged tissue peaked at one week, and declined thereafter. In contrast, tissue histamine levels were normal at one week, then increased in damaged tissue to approximately four times normal levels at four weeks. Indices of inflammation were markedly suppressed at one week by diphenhydramine, while tissue histamine levels were unaffected. Chronic colitis in rats is thus apparently accompanied by a local mast cell hyperplasia or influx. Moreover, antagonism of a major mast cell mediator, histamine, significantly reduces the severity of inflammation in this model.

Animals↗
PubMed2001

Development of marine toxicity data for ordnance compounds.

A toxicity database for ordnance compounds was generated using eight compounds of concern and marine toxicity tests with five species from different phyla. Toxicity tests and endpoints included fertilization success and embryological development with the sea urchin Arbacia punctulata; zoospore germination, germling length, and cell number with the green macroalga Ulva fasciata; survival and reproductive success of the polychaete Dinophilus gyrociliatus; larvae hatching and survival with the redfish Sciaenops ocellatus; and survival of juveniles of the opossum shrimp Americamysis bahia (formerly Mysidopsis bahia). The studied ordnance compounds were 2,4- and 2,6-dinitrotoluene, 2,4,6-trinitrotoluene, 1,3-dinitrobenzene, 1,3,5-trinitrobenzene, 2,4,6-trinitrophenylmethylnitramine (tetryl), 2,4,6-trinitrophenol (picric acid), and hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX). The most sensitive toxicity test endpoints overall were the macroalga zoospore germination and the polychaete reproduction tests. The most toxic ordnance compounds overall were tetryl and 1,3,5-trinitrobenzene. These were also the most degradable compounds, often being reduced to very low or below-detection levels at the end of the test exposure. Among the dinitro- and trinitrotoluenes and benzenes, toxicity tended to increase with the level of nitrogenation. Picric acid and RDX were the least toxic chemicals tested overall.

Animals↗
PubMed1999

Does microcirculation play a role in the pathogenesis of inflammatory bowel diseases? Answers from intravital microscopic studies in animal models.

The potential role of intestinal microcirculation for the development of inflammatory bowel diseases (IBD) has not been systematically investigated, mainly because of methodological problems. Using a well-established rodent model of IBD and intravital microscopy, the present study investigated whether (and when) gut microcirculation is disturbed in IBD, and whether microcirculatory disorders contribute to histological and functional alterations in the development of IBD. Colitis was induced by rectal injection of trinitrobenzene sulfonic acid. After 1, 3, and 15 days rats were laparotomized for intravital microscopic determination of mucosal colonic blood flow. In a second series it was examined whether enhancing colonic capillary blood flow by hemodilution therapy stabilizes colonic wall resistance and other electrophysiological parameters of gut permeability. Additional measurements involved hemodynamic monitoring and histological examinations. Colonic capillary blood flow was significantly decreased 3 days after colitis induction (1.8 +/- 0.05 vs. 2.6 +/- 0.04 nl/min in healthy control animals) when histology revealed signs of acute inflammation, and normal values after 15 days (2.4 +/- 0.06 nl/min) when chronic histological changes were evident. Hemodilution therapy enhanced colonic capillary blood flow in the initial stage (2.1 +/- 0.02 vs. 1.6 +/- 0.02 nl/min in saline-treated animals with trinitrobenzene sulfonic acid colitis) and improved gut resistance and electronic chloride secretion (73 +/- 15 vs. 33 +/- 8 microA cm2). Histological alterations were not significantly attenuated. Impaired colonic capillary blood flow in the initial stage of experimental colitis and improved mucosal microcirculation with stabilized gut permeability suggests that the early microcirculatory disturbances precede chronic histological changes and influence functional alterations in the course of the disease. Research should be continued in this field because important mechanisms in the pathogenesis of IBD and potentially therapeutic (vasoactive) substances may otherwise be overlooked.

Animals↗
PubMed1975

Experimental alteration of phospholipid-protein interactions within the human erythrocyte membrane. Dependence on glycolytic metabolism.

Phosphatidylethanolamine in freshly drawn human erythrocytes is trinitrophenylated by 2,4,6-trinitrobenzene sulfonic acid only slowly and to a maximum of 32%. After different preincubation procedures at 37 degrees C in saline media in the absence of glucose (24 h without additive, 1-5 h with 8 mM hexanol or 1-4 h with the SH reagent, 5 mM tetrathionate) the rate of subsequent trinitrophenylation of phosphatidylethanolamine, in the absence of the additives, is greatly enhanced and the amount of phospholipid reacting increased. Glucose or inosine prevent these effects, inhibitors of glycosis abolish this protection. The results indicate that in fresh as well as in glycolysing incubated erythrocytes phosphatidylethanolamine in the outer layer of the membrane lipid is shielded by a protein. Conformational changes of this protein induced by metabolic starvation and perturbing agents expose the phospholipid head group to 2, 4, 6-trinitrobenzene sulfonic acid. In addition, a "flip-flop" of phosphatidylethanolamine from the inner to the outer layer may also contribute to the effects observed.

Blood Proteins↗
PubMed1986

Effect of neuraminidase treatment on the topological distribution of phospholipids in chick brain microsomes.

The desialylation of chick brain microsomal membranes affects the transbilayer distribution of phospholipids. When intact microsomes were treated with neuraminidase, less phosphatidylcholine and sphingomyelin could be hydrolysed with phospholipase C under experimental conditions which allowed the hydrolysis of the phospholipids of the external leaflet only. In contrast, the accessibility of phosphatidylethanolamine and phosphatidylserine to the external probes (trinitrobenzene sulfonic acid or phospholipase C) was not affected. After neuraminidase treatment of a microsomal fraction, less phosphatidylcholine, newly synthesized through the cytidine pathway, could be hydrolysed by phospholipase C, whereas the reaction of newly synthesized phosphatidylethanolamine molecules with trinitrobenzene sulfonic acid was not affected. The results suggest that in biological membranes some choline phospholipid molecules may interact with the sialyl residue of sialocompounds. This interaction may contribute to the maintenance of phospholipid asymmetry in brain membranes.

Animals↗
PubMed1990

Participation of thromboxane and other eicosanoid synthesis in the course of experimental inflammatory colitis.

Eicosanoids, as modulators of inflammation, may be involved in the pathogenesis of inflammatory bowel disease. We investigated their potential role in a rat model of chronic granulomatous colonic inflammation induced by trinitrobenzene sulphonic acid. Luminal eicosanoid release was quantified in vivo using a dialysis bag placed into the distal colon. We tested the effect of drugs known to modify inflammatory activity or arachidonic acid metabolism. Three days after intracolonic injection of trinitrobenzene sulphonic acid at different dose levels, the dialysates showed a highly significant increase of prostaglandin E2, 6-keto-prostaglandin F1 alpha, thromboxane B2 (TXB2), and leukotriene B4, compared with levels in controls not subjected to the toxic agent. Remarkably, the release of TXB2 continued to increase during the stage of chronic inflammation (up to day 21), whereas the levels of the remainder eicosanoids declined. Treatment with prednisone or 5-aminosalicylic acid reduced TXB2 levels in the chronic stage of the inflammatory disease and improved the morphological damage as assessed macroscopically and histologically. Moreover, two selective thromboxane synthetase inhibitors, OKY 1581 and R70416, significantly reduced the development of chronic inflammatory lesions in the colon while inhibiting the release of TXB2. Our results indicate that (1) luminal release of thromboxane increases in the chronic stage of colonic inflammation, (2) anti-inflammatory treatment reduces tissue damage and thromboxane release, and (3) selective thromboxane synthetase inhibition improves the course of the disease in our experimental model.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

On the specificity of altered muscle function in experimental colitis in rats.

BACKGROUND: Studies on muscle contraction in colitis yield conflicting data that may reflect differences in the manner in which colitis is induced. Therefore, we compared distal colonic longitudinal muscle contraction in four models of colitis in the rat. METHODS: Distal colitis was induced by intrarectal administration of trinitrobenzene sulfonic, acetic acid, or Trichinella spiralis larvae, or by intraperitoneal injection of mitomycin C. Colonic myeloperoxidase activity was used to monitor acute inflammation. RESULTS: Myeloperoxidase activity increased in each model of colitis. In trinitrobenzene-treated rats, contractile responses to carbachol, substance P, and KCl decreased by 64%, 76%, and 58%, respectively. In acetic acid treated rats, responses induced by carbachol, substance P, or KCl were each significantly decreased by 73%, 68%, and 55% and were similarly reduced by 42%, 77%, and 46%, respectively, in rats with T. spiralis colitis. In mitomycin-induced colitis, these respective responses also decreased significantly by 71%, 55%, and 54%. CONCLUSION: Decreased contractility of longitudinal muscle in acute colitis in rats is independent of the manner in which the colitis is induced and is mediated at a receptor-independent locus on the muscle cell.

Acetates↗
PubMed1995

Experimental colitis alters myenteric nerve function at inflamed and noninflamed sites in the rat.

BACKGROUND & AIMS: Studies in inflammatory bowel disease have shown extensive structural abnormalities in the enteric nervous system of inflamed and noninflamed gut; however, functional correlates are lacking. The aim of this study was to determine the effect of colitis on myenteric nerve function at inflamed and noninflamed sites in rat intestine. METHODS: Tritiated noradrenaline release was measured from longitudinal muscle myenteric plexus preparations from the distal and transverse colon and terminal ileum of rats with colitis induced by trinitrobenzene sulfonic acid or Trichinella spiralis larvae. RESULTS: As characterized by myeloperoxidase activity and histology, both models induced inflammation restricted to the distal colon. In distal colon in trinitrobenzene sulfonic acid colitis, KCl- or electrical field stimulation-evoked 3H release was suppressed by 56% and 60%, respectively; in T. spiralis-infected rats, the KCl-evoked release was suppressed by 58%. 3H release was also suppressed by similar magnitudes in noninflamed transverse colon and terminal ileum of each model. CONCLUSIONS: Experimental distal colitis alters myenteric nerve function in inflamed distal colon and noninflamed gut regions. These changes are independent of the manner in which colitis is induced and provide a basis for the extensive disruption of physiological function observed in inflammatory bowel disease.

Adrenergic Fibers↗