Pharmacokinetics of tramadol and metabolites O-desmethyltramadol and N-desmethyltramadol in adult horses.

Objective: To determine the pharmacokinetics of tramadol and its metabolites O-desmethyltramadol (ODT) and N-desmethyltramadol (NDT) in adult horses.

Animals: 12 mixed-breed horses.

Procedures: Horses received tramadol IV (5 mg/kg, over 3 minutes) and orally (10 mg/kg) with a 6-day washout period in a randomized crossover design.

Association between fecal hydrogen sulfide production and pouchitis.

Purpose: The beneficial effect of antibiotics in pouchitis suggests that an unidentified fecal bacterial product causes this condition. A candidate compound is hydrogen sulfide, a highly toxic gas produced by certain fecal bacteria, which causes tissue injury in experimental models. We investigated hydrogen sulfide release and sulfate-reducing bacterial counts in pouch contents to determine whether hydrogen sulfide production correlates with pouchitis.

Effectiveness of devices purported to reduce flatus odor.

Objective: A variety of charcoal-containing devices are purported to minimize problems with odoriferous rectal gas; however, the evidence supporting the efficacy of these products is virtually all anecdotal. We objectively evaluated the ability of these devices to adsorb two malodorous, sulfide gases (hydrogen sulfide and methylmercaptan) instilled at the anus.

Methods: Via a tube, 100 ml of nitrogen containing 40 ppm of sulfide gases and 0.

The effect of antibiotics and bismuth on fecal hydrogen sulfide and sulfate-reducing bacteria in the rat.

Colonic bacteria produce the highly toxic thiol, hydrogen sulfide. Despite speculation that this compound induces colonic mucosal injury, there is little information concerning manipulations that might reduce its production. We studied the effect of antibiotics and bismuth on the production of hydrogen sulfide in rats.

Simplification of the end-alveolar carbon monoxide technique to assess erythrocyte survival.

We have described a simple, rapid method for determining red blood cell (RBC) life span based on measurement of alveolar carbon monoxide (CO) concentration corrected for atmospheric CO as determined with a device that simulates the body's equilibration with CO. This study was designed to determine whether direct measurements of ambient CO can be substituted for sampling with the equilibrator device. Atmospheric samplings obtained in our medical center over a period of weeks indicated that CO concentration was sufficiently constant that a single ambient CO measurement at the time of breath collection adequately corrected for atmospheric CO.

Physiology of sulfide in the rat colon: use of bismuth to assess colonic sulfide production.

Colonic bacteria produce hydrogen sulfide, a toxic compound postulated to play a pathogenetic role in ulcerative colitis. Colonic sulfide exposure has previously been assessed via measurements of fecal sulfide concentration. However, we found that <1% of fecal sulfide of rats was free, the remainder being bound in soluble and insoluble complexes.

Comparison of volatile sulfur compound concentrations measured with a sulfide detector vs. gas chromatography.

The accuracy of the Halimeter, an inexpensive, simple instrument that measures total breath volatile sulfur compounds (VSCs), has not been adequately tested. We compared Halimeter measurements with those obtained with a specific and sensitive gas chromatographic (GC) technique. The Halimeter gave different, biexponential responses to a constant concentration of different VSCs: The relative response rate and sensitivity were hydrogen sulfide > methyl mercaptan > dimethylsulfide.

Spontaneous fluctuations in the concentrations of oral sulfur-containing gases.

Breath hydrogen sulfide (H2S) and methyl-mercaptan (CH3SH) concentrations are used as quantitative indicators of halitosis. However, measurements of these gases in duplicate oral samplings often show poor reproducibility. To determine if this poor reproducibility is an artifact of the collection/analytical procedure or a true biological phenomenon, we used a standardized technique to collect from 20 to 30 oral gas samples at two-minute intervals from 11 healthy subjects.

Oxidation of hydrogen sulfide and methanethiol to thiosulfate by rat tissues: a specialized function of the colonic mucosa.

Colonic bacteria release large quantities of the highly toxic thiols hydrogen sulfide (H(2)S) and methanethiol (CH(3)SH). These gases rapidly permeate the colonic mucosa, and tissue damage would be expected if the mucosa could not detoxify these compounds rapidly. We previously showed that rat cecal mucosa metabolizes these thiols via conversion to thiosulfate.

Measurement of fecal sulfide using gas chromatography and a sulfur chemiluminescence detector.

We describe a simple technique to measure sulfide in fecal homogenates (or any other liquid milieu), which involves acidification followed by the G.C. measurement of H2S in a gas space equilibrated with a small quantity of homogenate.

Morning breath odor: influence of treatments on sulfur gases.

We assessed the effects of several treatments on the concentrations of oral sulfur-containing gases, compounds thought to be responsible for morning breath. Upon awakening in the morning, healthy volunteers collected oral gas samples before and for eight hours after the following treatments: no treatment, brushing the teeth with toothpaste, brushing the tongue, rinsing with 5 mL of 3% hydrogen peroxide, breakfast ingestion, or swallowing two BreathAsure capsules. The gas samples were analyzed for sulfur-containing volatiles via gas chromatography.

Binding of hydrogen sulfide by bismuth does not prevent dextran sulfate-induced colitis in rats.

Several lines of evidence suggest that ulcerative colitis could be caused by excessive bacterial production of H2S in the colon. A rodent model of colitis involves the feeding of nonabsorbable, carbohydrate-bound sulfate in the form of dextran sulfate or carrageenan. The observation that metronidazole blocks the development of this colitis suggested that the injurious agent could be a sulfur-containing compound (such as H2S) that is released during the bacterial metabolism of the nonabsorbed sulfate.

Detoxification of hydrogen sulfide and methanethiol in the cecal mucosa.

Colonic bacteria liberate large quantities of the highly toxic gases hydrogen sulfide (H(2)S) and methanethiol (CH(3)SH). The colonic mucosa presumably has an efficient means of detoxifying these compounds, which is thought to occur through methylation of H(2)S to CH(3)SH and CH(3)SH to dimethylsulfide (CH(3)SCH(3)). We investigated this detoxification pathway by incubating rat cecal mucosal homogenates with gas containing H(2)S, CH(3)SH, or CH(3)SCH(3).

Differentiation of mouth versus gut as site of origin of odoriferous breath gases after garlic ingestion.

Utilizing the sulfur-containing gases of garlic as probes, we investigated the gut versus mouth origin of odoriferous breath gases. Five individuals ingested 6 g of garlic, and sulfur gases in mouth, alveolar air, and urine samples were measured. The mouth normally contained low concentrations of hydrogen sulfide, methanethiol, and dimethyl sulfide.

Failure of activated charcoal to reduce the release of gases produced by the colonic flora.

Objective: Activated charcoal is used to treat excessive volume or malodor of intestinal gas. Our previous studies demonstrated that activated charcoal failed to bind appreciable quantities of the volumetrically important gut gases. However, the odor of feces and flatus derives primarily from trace quantities of sulfur-containing gases, primarily H2S and methanethiol, which should avidly bind to activated charcoal.

Gas production in human ingesting a soybean flour derived from beans naturally low in oligosaccharides.

Background: Ingestion of soy products may cause excessive intestinal gas. This gas results from colonic bacterial fermentation of the indigestible oligosaccharides raffinose and stachyose, which are present in high concentrations in legumes.

Objective: The objective of the study was to compare gas production and gaseous symptoms in healthy volunteers after ingestion of 34 and 80 g soy flour made from either conventional soybeans or soybeans naturally low in indigestible oligosaccharides.

Identification of gases responsible for the odour of human flatus and evaluation of a device purported to reduce this odour.

Background/aims: While the social significance of flatus derives mainly from its odour, previous studies have focused on the non-odoriferous components of rectal gas. The aims of the present study were to determine the role of sulphur-containing gases in flatus odour and test the efficacy of a device purported to reduce this odour.

Methods: Flatus was quantitatively collected via rectal tube from 16 healthy subjects who ingested pinto beans and lactulose to enhance flatus output.

Bismuth subsalicylate markedly decreases hydrogen sulfide release in the human colon.

Background & Aims: Hydrogen sulfide is one of the main malodorous compounds in human flatus. This toxic gas also has been implicated in the pathogenesis of ulcerative colitis. Therefore, a treatment that reduces colonic H2S levels could be clinically useful in the treatment of flatus odor and of ulcerative colitis.

Production and elimination of sulfur-containing gases in the rat colon.

Highly toxic sulfur-containing gases have been pathogenetically implicated in ulcerative colitis. Utilizing a rat model, we studied the production and elimination of sulfur-containing gases within the unperturbed colon. The major sulfur-containing gases were hydrogen sulfide (H2S), methanethiol, and dimethyl sulfide with cecal accumulation rates of 2.

Fecal hydrogen sulfide production in ulcerative colitis.

Objective: Sulfide, a product of sulfate-reducing bacteria, has been proposed to play an etiologic role in ulcerative colitis. Ulcerative colitis feces have increased numbers and activity of sulfate-reducing bacteria, but only modestly increased sulfide. However, fecal sulfide exists largely in the volatile, highly toxic H2S form that moves rapidly from feces to surrounding gas.

Insights into human colonic physiology obtained from the study of flatus composition.

To better understand the physiology of colonic gas production, each flatus passage of 16 subjects over a 4-h period was analyzed by gas chromatography for N2, O2, H2, CO2, CH4, and for odoriferous sulfur-containing gases. Appreciable intraindividual and enormous interindividual variability was observed, indicating that each gas passage reflected the interaction of highly variable liberation and/or removal mechanisms. The predominant flatus gas was CO2, H2, and N2 in seven, six, and three subjects, respectively.

Carbon monoxide generation from hydrocarbons at ambient and physiological temperature: a sensitive indicator of oxidant damage?

This paper shows that a variety of carbon-containing materials (wool, cotton, wood, paper, latex, Tygon) release CO during incubation at ambient temperature. This CO production was enhanced by aerobic versus anaerobic incubation, increasing temperature, and exposure to fluorescent light. CO production from glucose solutions was enhanced by alkaline pH or prior boiling or autoclaving and reduced by the presence of superoxide dismutase or catalase.

Pitfalls in the use of breath pentane measurements to assess lipid peroxidation.

Literature values for breath pentane, an indicator of lipid peroxidation, vary by 1,000-fold in healthy subjects. This report describes multiple technical artifacts that may explain this disparity. First, we found that a major component of human breath (probably isoprene) co-eluted with pentane on columns used by some investigators, resulting in erroneously high determinations.

First-pass gastric mucosal metabolism of ethanol is negligible in the rat.

Ethanol metabolism by gastric alcohol dehydrogenase (ADH) is thought to be an important determinant of peripheral ethanol time-concentration curves (AUCs) in rats and humans. We quantitated this metabolism in rats by measuring the gastric absorption of oral ethanol (0.25 g/kg) and the gastric venous-arterial (V-A) difference of ethanol versus ethanol metabolites (acetate, acetaldehyde, and bicarbonate).