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. Our aim was to quantify the fecal release of H₂S and other volatiles (CO₂, H₂, CH₂, methanethiol, and dimethylsulfide).
Methods: Fecal samples from 25 subjects with ulcerative colitis and 17 controls were incubated in 4-L containers, and gas release was assessed at intervals over 24 h.
Results: H₂S release by ulcerative colitis feces was elevated 3–4-fold at every measurement point compared with normal feces (   p < 0.003  at 24 h). The only other significant difference was increased CO₂ release by ulcerative colitis feces at 1 h. Supplementation of fecal homogenates with sulfur-containing substrates showed that organic compounds (mucin, cysteine, taurocholate) provided more readily utilizable substrate for H₂S production than did sulfate.
Conclusions: Increased H₂S release is a relatively localized metabolic aberration of ulcerative colitis feces. This increased H₂S may reflect abnormalities of the fecal bacteria and/or substrate availability.     

Fermentation of the Carbohydrate of Banana (Paradisiaca sapientum) in the Human Large Intestine.

Fermentation of dietary fiber and resistant starch is one of the major physiological functions of the human large intestine. The major substrate for fermentation is probably starch. This study assessed the effect of bananas—a carbohydrate with a highly resistant starch content—on breath hydrogen and methane production in methane and nonmethane-producing subjects. The results showed that both groups produced significant quantities of hydrogen after a banana meal, compared with a sucrose control test meal, measured as area under the curve (28 ± 5.6 vs. 8.1 ± 1.4 10³ pm/min, p = 0.008 in methane producers and 39 ± 15.2 vs. 10.5 ± 4.1 10³ ppm/min, p = 0.01 in methane nonproducers). The rise in breath hydrogen started a half hour after the banana meal and peaked at 31/2 h in methane nonproducers, whereas in methane producers, the rise began after 2 h and peaked at 5 h. Methane production was not significantly stimulated by the test meals. This study shows that bananas stimulate fermentation mainly through the production of hydrogen, with minimal effect on methane production. The possible mechanisms for this process are discussed.     

Evaluation of an extremely flatulent patient

We recently encountered a patient with severe flatulence who previously had been subjected to innumerable diagnostic tests and ineffective therapies based on the belief that his rectal gas was produced in the colon. Analysis of three flatus samples demonstrated that nitrogen (N₂) was the predominant flatus gas whereas the three gases produced in the gut (CO₂, H₂ [hydrogen], and CH₄ [methane]) comprised  <16%  of rectal gas. This result plus a series of other diagnostic tests clearly indicated that the patient's flatus was derived almost entirely from swallowed air. Based on this case, the present report summarizes available data on excessive flatulence and suggests a rational approach to the patient complaining of this problem. Particular emphasis is placed upon a sequential strategy consisting of: 1) a count of flatus passages to determine if the subject truly is abnormal (normal:  <20 passages/day  ); 2) an analysis of flatus to determine if the flatus originates from swallowed air (predominantly nitrogen) or intraluminal production (predominantly CO₂, H₂, and CH₄); and 3) treatment based upon the origin of the rectal gas.     

Melatonin reduces H2O2-induced lipid peroxidation in homogenates of different rat brain regions

Abstract: The ability of melatonin to modify H₂O₂-induced lipid peroxidation in brain homogenates was determined. The concentrations of brain malonaldehyde (MDA) and 4-hydroxyalkenals (4-HDA) were assayed as an index of induced membrane oxidative damage. Homogenates from five different regions of the brain (cerebral cortex, cerebellum, hippocampus, hypothalamus, and corpus striatum) derived from two different strains of rats, Sprague-Dawley and Wistar, were incubated with either H₂O₂ (5 mM) alone or H₂O₂ together with melatonin at increasing concentrations ranging from 0.1 to 4 mM. The basal level of lipid peroxidation was strain-dependent and about 100% higher in homogenates from the brain of Wistar rats than those measured in Sprague-Dawley rats. MDA + 4-HDA levels increased after H₂O₂ treatment in homogenates obtained from each region of the brain in both rat strains but the sensitivity of the homogenates from Sprague-Dawley rats was greater than that for the homogenates from Wistar rats (increases after H₂O₂from 45 to 165% compared 20 to 40% for Sprague-Dawley and Wistar rats, respectively). Melatonin co-treatment reduced H₂0₂-induced lipid peroxidation in brain homogenates in a concentration-dependent manner; the degree of protection against lipid peroxidation was similar in all brain regions.     

Leucine and Glucose Turnover in Chronic Alcoholics During Early Abstinence and After an Ethanol Load

We studied leucine turnover using a primed infusion of [1-¹⁴C]- l -leucine and glucose turnover using a primed infusion of [6-³H]- d -glucose in five alcoholic patients without liver damage and five age-matched controls. Infusions were maintained for 6 hr, and at the end of the 3rd hour, a 0.8 g/kg iv ethanol load was administered in 20 min. Leucine flux, nonoxidative disposal and oxidation rates, and glucose rate of appearance were calculated during the 3rd and 6th hours of infusion. Ethanol disappearance rate and the percentage completely metabolized to CO₂ and H₂O in 3 hr were also calculated. Compared with controls, alcoholics had significantly higher basal leucine flux (55.6 ± 12 vs. 37.3 ± 9.3 μ m /m²/min) and nonoxidative disposal (48.7 ± 8.7 vs. 31.1 ± 7.5 μ m /m²/min). No differences were observed in basal glucose appearance rates in alcoholics and controls (397.6 ± 115.2 vs. 349.4 ± 120.6 μ m /m²/min). Compared with controls, alcoholics had a higher alcohol disappearance rate (2.72 ± 0.59 vs. 1.84 ± 0.43 m m /kg/min) and percentage of ethanol metabolized to CO₂ and H₂O in 3 hr (40.6 ± 10.2 vs. 22.9 ± 6.9%). After the ethanol load, both leucine turnover and glucose rate of appearance decreased significantly only in alcoholics. There was a positive correlation between the change in leucine flux and ethanol disappearance rate and percentage metabolized to CO₂ and H₂O in alcoholics.     

Effect of Guar, Pectin, Psyllium, Soy Polysaccharide, and Cellulose on Breath Hydrogen and Methane in Healthy Subjects

Different types of dietary fiber are fermented to various extents in vitro, but little is known about the effects of fiber on breath hydrogen and methane levels in vivo. Therefore, we studied the effects on breath hydrogen and methane of 15 g of guar, pectin, psyllium, soy polysaccharide, or cellulose in eight healthy subjects over a 12-h period. None of the fibers had a significant effect on breath hydrogen or methane concentrations, compared with the control (fasting). The four methane producers had lower breath hydrogen levels than the nonproducers 1 h after 15 g of lactulose (3 +/- 1 vs. 42 +/- 9, p less than 0.005) and 5-12 h after the different fibers (3.3 vs. 4.8 ppm; pooled SEM = 0.8; p less than 0.025). When the methane responses of the methane producers were expressed as increments relative to the control, there were small differences between treatments, with guar producing a larger response, 8.2 +/- 3.3 ppm, than cellulose, -2.9 +/- 2.3 ppm (p less than 0.05). The incremental methane responses of the different fibers in vivo were related to the previously reported production of propionic acid (r = 0.94, n = 5, p less than 0.02) and methane (r = 0.93, n = 4, NS) from in vitro fermentation of the same fibers. We conclude that methane producers have lower breath hydrogen levels than nonproducers. Purified fermentable and nonfermentable dietary fibers have no effect on breath hydrogen levels over 12 h in subjects previously consuming a normal diet. However, fermentable fibers may produce small increases in breath methane in methane-producing subjects.     

Mixing of the intestinal content and variations of fermentation capacity do not affect the results of hydrogen breath test

OBJECTIVE: Although the hydrogen (H(2)) breath test has been in use for many years for diagnosis of sugar malabsorption, research is still underway to improve its diagnostic accuracy. In this study, we investigated whether possible confusing factors caused by the ingestion of the test solution itself (such as the delivery to the colon of other fermentable substrates pre-existing in the small bowel lumen, the release of preformed H(2) trapped in the feces, or differences in the fermenting capacity of the colonic bacteria) may interfere with the increase of breath H(2) concentration, an expression of malabsorption of the test substrate. METHODS: In 25 patients with untreated celiac disease and 23 sex- and age-matched healthy volunteers, breath H(2) excretion was measured after ingestion of a 250-ml solution containing sorbitol, a poorly absorbed alcohol sugar. On 2 other separate days, 12 randomly selected subjects in each group underwent breath H(2) excretion measurement after ingestion of 250 ml of a sugar free, nonabsorbable electrolyte solution and 250 ml of a solution containing lactulose, a nonabsorbable disaccharide. RESULTS: After sorbitol ingestion, celiac disease patients showed a significantly higher breath H(2) excretion than did healthy volunteers. Otherwise, breath H(2) responses to electrolyte solution and lactulose showed no difference between the two groups of subjects. CONCLUSIONS: In a group of patients with sugar malabsorption, increased breath H(2) excretion does reflect malabsorption. The washout or the mixing of the intestinal content or intergroup difference of fermenting activity of the colonic bacteria do not represent interfering factors and do not modify the accuracy of the H(2) breath test in day-to-day clinical practice.     

Impedance Planimetry: An Integrated Approach for Assessing Sensory, Active, and Passive Biomechanical Properties of the Human Esophagus

Objectives : Our objective was to study the biomechanical properties and their relationships to the sensory and motor function of the esophagus, which has seldom been examined in humans. Methods : We used impedance planimetry, to study these properties. This system measures cross-sectional area (CSA) and intraluminal pressure simultaneously and facilitates calculation of some of the biomechanical properties of the esophageal wall. We performed 15 studies in 12 healthy volunteers. In three subjects, the studies were repeated to test reproducibility. Results : Stepwisc increments in balloon pressure from 5 to 40 cm H₂O induced an increase in CSA (mean ± SD), 91 ± 27 to 469 ± 63 mm², the wall tension 27 ± 4 to 484 ± 32 mm ± cm H₂O, and the strain 0.2 ± 0.1 to 1.3 ± 0.3. The tension/strain relationship increased exponentially. The compliance did not change. The threshold for first sensation was 30 ± 11 cm H₂O (mean ± SD). In three subjects, when the balloon was distended > 40 cm H₂O, chest pain was induced at a threshold of 62 ± 3 cm H₂O. and the compliance decreased. Balloon distension induced tertiary contractions and secondary peristalsis at thresholds of 15 ± 4 cm H₂O, and 19 ± 5 cm H₂O. Repeat studies showed good correlation ( r = 0.9). Conclusion : Graded balloon distension increases esophageal CSA, wall tension, and strain. When a threshold is reached, tertiary contractions and secondary peristalsis develop at pressures less than 50% of sensory threshold. At higher pressures, chest pain is induced. Impedance planimetry promises to be a simple, objective, reproducible, and comprehensive technique for evaluating the sensory, motor, and viscoelastic properties of the esophagus.     

Inflammatory markers in exhaled breath condensate from patients with asthma

Background and objective:   Evaluation of airway inflammation is important for the diagnosis and treatment of asthma. Exhaled breath condensate (EBC) is a minimally invasive method for assessing inflammation and may be useful for monitoring airway inflammation in asthma. The aims of this study were to establish an EBC collection method, to assess biomarkers reflecting asthmatic airway inflammation, and to determine the relationship of these biomarkers with asthma severity and lung function.
Methods:   Fifty-eight non-smoking healthy subjects, seven asymptomatic smokers, nine subjects with common cold and 55 asthmatics with disease severity ranging from mild intermittent to severe persistent were studied. The efficacy of a pipette method was compared with that of a commercial collecting device. pH, CRP, albumin, hydrogen peroxide (H₂O₂) and nitrite/nitrate levels were measured in EBC.
Results:   Except for the quantity of EBC collected and albumin levels, there were no differences between the commercial method and the pipette method in levels of biomarkers measured. Levels of CRP, H₂O₂ and nitrite/nitrate were significantly higher in the asthma group than that in the control group. In terms of asthma severity, pH and levels of CRP, H₂O₂ and nitrate were significantly higher in the mild persistent group than that in the other groups. In addition, H₂O₂ levels in EBC correlated significantly with the level of nitrite/nitrate. FEV₁ and PEF showed significant negative correlations with H₂O₂ and nitrite/nitrate levels.
Conclusion:   Measurement of EBC biomarkers is a non-invasive and useful way to evaluate airway inflammation in patients with asthma.     

Alpha1-Adrenergic Receptor Modulation of Repolarization in Canine Purkinje Fibers

Alpha-Agonists and Repolarization. Introduction: Alpha-adrenergic receptor stimulation increases contractility and prolongs repolarization. These effects are modulated by α₁-adrenergic receptor-mediated inhibition of transsarcolemmal potassium currents.
Methods and Results: We used standard microelectrode techniques to study the actions of 4-aminopyridine (4-AP), which blocks the transient outward current, I_to, and WAY-123,398, which blocks the delayed rectifier, I_k, on canine Purkinje fiber action potential prolongation induced by phenylephrine. At a basic cycle length of 1 second, phenylephrine (0.1 to 10 μ) dose-dependently prolonged action potential duration at 90% repolarization (APD₉₀) from 331 ± 10 msec to 400 ± 12 msec (P < 0.05) at phenylephrine, 10 μ. Phenylephrine did not change phase 1 or plateau height. 4-AP (0.1 mM) decreased phase 1 magnitude, shifted plateau height to more positive potentials (from 0.1 ± 1.8 mV to 14.3 ± 1.1 mV [P < 0.05]), and shortened APD₉₀ from 318 ± 9 msec to 294 ± 8 msec (P < 0.05). 4-AP did not block phenylephrine effects on APD₉₀, which increased, at 10 μ phenylephrine, from 294 ± 8 msec to 342 ± 6 msec (P < 0.05). In contrast, WAY-123,398 (0.1 μ) prolonged APD₉₀ from 360 ± 6 msec to 452 ± 6 msec (P < 0.05), and had no effect on plateau height. In the presence of WAY-123,398, phenylephrine no longer increased APD_9o.
Conclusion: (1) Agents that block I_to shorten APD in Purkinje fibers; and (2) the α-agonist mediated increase of APD in canine Purkinje fibers can be explained by inhibition of I_k.     

Reproducibility and Simplification of 13C-Octanoic Acid Breath Test for Gastric Emptying of Solids

Objective: The accuracy of the ¹³C-octanoic acid breath test is enhanced by breath sampling over 6 h rather than 4 h, but this increases the cost of the test. Our aim was to validate a less costly but accurate sequence of breath sampling for measuring gastric emptying of solids.
Methods: We performed the ¹³C-octanoic acid breath test and tested its reproducibility relative to simultaneous scintigraphy in 30 healthy volunteers.
Results: There was a significant but weak correlation between t _1/2 measured by the two tests (   r _s= 0.54  ,   p < 0.005  ), but not between the duration of the lag phase. The differences in the t _1/2 measurements between the tests were different between subjects but were highly reproducible within subjects. Within- and between-subject variations of measurements of gastric emptying with the ¹³C-octanoic acid breath test were not significantly different from the variations observed with scintigraphy. A subset of 11 breath samples collected over 6 h (24 samples) predicted (   r ² > 0.95  ) the variables characterizing the cumulative appearance of ¹³CO₂ in breath; these samples were at 35, 50, 95, 110, 140, 155, 215, 245, 260, 290, and 335 min. The accuracy of this subset of sampling times was confirmed in a separate set of breath test samples over 6 h from the same 30 subjects.
Conclusions: The ¹³C-octanoic acid breath test for gastric emptying of solids is as reproducible as scintigraphy. A subset of 11 sampling times provides sufficient information to characterize the whole breath-test curve, but the sampling period should be extended to 6 h after dosing.     

Protection against cell death and sustained tyrosine hydroxylase phosphorylation in hydrogen peroxide- and MPP+-treated human neuroblastoma cells with melatonin

Abstract:  Neuroprotective effects of melatonin against oxidative stress-induced neuronal cell degeneration in human SH-SY5Y neuroblastoma cells were investigated in this report. The results demonstrate that exogenous administration of H₂O₂ and 1-methyl, 4-phenyl, pyridinium ion (MPP⁺) significantly decreased cell viability in SH-SY5Y cultured cells. Desipramine, a monoamine uptake blocker was able to abolish the toxic effects of MPP⁺ but not H₂O₂ in reduction of cell viability. Conversely, melatonin reversed the toxic effects of H₂O₂ and MPP⁺ on cell viability. In addition, the reduction of phosphorylation of tyrosine hydroxylase, the rate limiting enzyme in dopamine synthesis, and phosphorylation of cyclic AMP responsive element-binding protein by H₂O₂ and MPP⁺ was also diminished by melatonin. These results demonstrate some effective roles of melatonin on neuroprotection and its action on the modulation of tyrosine hydroxylase phosphorylation.     

Adriamycin stimulates proliferation of human lymphoblastic leukaemic cells via a mechanism of hydrogen peroxide (H2O2) production

It is becoming clear that adriamycin cytotoxicity may be mediated by semiquinone-free radicals derived from the drug itself and reactive oxygen species (ROS). Recent evidence supports the concept that low concentrations of ROS are able to stimulate cell proliferation, and, based on the observation that subtoxic concentrations of adriamycin can also induce cell proliferation, we hypothesize that low concentrations of adriamycin stimulate cell proliferation by a ROS generation mechanism. We have employed spin-trapping and electron spin resonance (ESR) spectroscopy to investigate the nature of the adriamycin-generated ROS. The spin trap 3,5-dibromo-4-nitrosobenzenesulphonate (DBNBS), which is oxidized in the presence of H₂O₂ and peroxidase enzymes, was used to produce a characteristic three-line spectrum, and it was found that an identical spectrum was produced by human lymphoblastic leukaemic cells (CCRF-CEM cells) after exposure to adriamycin. We tested our hypothesis further by exposing CCRF-CEM cells to subtoxic concentrations of adriamycin (10⁻⁸, 10⁻⁹ and 10⁻¹⁰  M ) and low concentrations of H₂O₂ (10⁻⁸, 10⁻⁹ and 10⁻¹⁰  M ) and subsequently monitored cell proliferation. We found that low concentrations of both adriamycin and H₂O₂ significantly stimulate CCRF-CEM cell proliferation. We therefore conclude that subtoxic concentrations of adriamycin are likely to induce cell proliferation via an H₂O₂ mediated mechanism.     

Fermentation in ileostomy bags: Control of excessive gas with diet, pH and antibiotics

The composition of early morning gas from the bags of 10 ileostomates was determined using gas chromatography. Seven of the 10 had a predominance of gases attributable to bacterial fermentation (H₂ and CO₂, 70 ± 12%). The remaining three contained mainly atmospheric gases, N₂ and O₂, with only small amounts of fermentation gases (7 ± 3%).
When a controlled low fibre (0.7 g) dinner was substituted for a high fibre (13.5 g) evening meal, there was a corresponding decrease in the volume of fermentation gas in the ileostomy bag the next morning ( P < 0.05).
Gas production from ileostomy effluent was inhibited in vitro by 10 < pH < 5 and by antimicrobial agents. The most effective were metronidazole, chloramphenicol, tetracycline, erythromycin and chlorhexidine. These reduced fermentation gas by more than 95%.
It was concluded that the majority of the gas produced by ileostomates is formed by bacterial fermentation of the faecal waste in their ileostomy bag and that this may be controlled by careful manipulation of their diet.     

H2O2 Release from Filtration Leukapheresis-Procured Leukocytes

Abstract. Filtration leukapheresis-procured leukocytes (FL-leukocytes), which were collected by the elution of filtration columns with vigorous tapping, released a certain amount of H₂O₂, even in the absence of any phagocytic stimuli. Furthermore, FL-leukocytes, eluted with either gentle or vigorous tapping, exhibited a marked release of H₂O₂ during phagocytosis. The myeloperoxidase (MPO) activity of FL-leukocytes was lower than that of leukocytes collected by the dextran sedimentation method (DS-leukocytes). The data suggest that the release of both H₂O₂ and MPO from FL-leukocytes may be related to adverse transfusion reactions and abnormal post-transfusion kinetics of FL-leukocytes due to their toxic effects on living cells.     

Breath hydrogen response to lactulose in healthy subjects: relationship to methane producing status.

In order to assess the relationship between methane (CH4) producing status and the breath excretion of hydrogen (H2) in healthy subjects, breath CH4 and H2 were simultaneously measured for 14 hours after oral ingestion of 10 g lactulose in 65 young volunteers. Forty were breath CH4 producers and 25 were not. Statistically significant differences were observed between both groups, with lower values for CH4 producers recorded for the following parameters: fasting basal value of breath H2 (8.1 (4.9) v 5.2 (3.7) ppm, p less than 0.05), mouth-to-caecum transit time (68 (24) v 111 (52) min, p less than 0.005), and breath H2 production measured as area under the curve 13.1 (6.9) v 8.8 (3.8) 10(3) ppm/min, p less than 0.02). There was no significant correlation between individual production of breath H2 and CH4. These results indicate that the response to lactulose depends on breath CH4 producing status. In clinical practice, defining normal values of mouth-to-caecum transit time without knowledge of breath CH4 producing status may lead to misinterpretation of the H2 breath test.     

Melatonin-induced estrogen receptor α-mediated calbindin-D9k expression plays a role in H2O2-mediated cell death in rat pituitary GH3 cells

Abstract:  Calbindin-D9k (CaBP-9k) is a 9-kDa polypeptide possessing two calcium-binding sites that is expressed in the mammalian intestine, uterus, and pituitary gland. The factors regulating the expression of the estrogen receptor (ER) and CaBP-9k in the pituitary gland are currently unknown. In this study, we investigated whether the ER and CaBP-9k expression are regulated by melatonin during H₂O₂-induced cell death in rat pituitary GH3 cells. Cell survival increased by approximately 27–36% in H₂O₂ plus melatonin compared to H₂O₂ alone, and CaBP-9k expression was augmented by treatment with H₂O₂ plus melatonin. These results suggest that the increase in cell survival and the melatonin-induced CaBP-9k expression may play a role in protecting cells against H₂O₂-mediated cell death. This result is also consistent with the increase in CaBP-9k expression leading to rises in p-ERK and p-Bad (S112). Over-expression of CaBP-9k caused an increase in p-ERK. ERα expression was higher in H₂O₂ plus melatonin-treated cells compared to those treated with H₂O₂ alone, while ERβ expression was not. Also, ERα in the nuclear fraction increased in the presence of melatonin and decreased in the presence of ICI 182 780 or ICI 182 780 plus melatonin. The relative binding affinity of ERα for melatonin was higher than that of ERβ, suggesting that melatonin has the potential to preferentially bind ERα. In conclusion, these results indicate that melatonin may increase CaBP-9k expression through ERα.     

Enzyme replacement for lactose malabsorption using a beta-D-galactosidase

We evaluated 10 healthy symptomatic lactose malabsorbers for effect of an oral beta-D-galactosidase derived from Aspergillus oryzae (Lactrase, Kremers Urban Company, Milwaukee, WI, U.S.A.) on symptom and breath hydrogen response to challenge with 50 g lactose. Basally and at 30-min intervals for 8 h after lactose challenge, end-alveolar breath samples were collected and analyzed for hydrogen using gas chromatography. Symptoms were scored at 30 min and hourly for 8 h, rating bloating, cramps, nausea, pain, diarrhea, and flatulence. Four challenges were performed on 4 separate days with at least 3 days between challenges. The first two challenges served as baselines. Just before ingestion of 50 g powdered lactose dissolved in 200 ml water, beta-D-galactosidase capsules were given orally as a 250-mg dose for the third challenge and a 500-mg dose for challenge 4. Hydrogen excretion, quantified by using a trapezoidal method for computing area under the discontinuous curve of breath hydrogen concentration, was decreased in subjects receiving beta-D-galactosidase (base-line I, 346.0 ppm/h; baseline II, 367.2 ppm/h; 250-mg galactosidase 208.2 ppm/h; 500-mg galactosidase, 178.0 ppm/h; p less than or equal to 0.05). Other analyzed parameters of H2 excretion were also decreased. Analysis of symptom response scores showed a dose-related decrease for bloating and flatus (p less than or equal to 0.05) and no statistical difference in the other assessed symptoms. We conclude that beta-D-galactosidase from Aspergillus oryzae, when given just before ingestion of lactose by lactose malabsorbers, can produce a dose-dependent reduction (statistically significant for the 500-mg dose) in breath hydrogen excretion, bloating, and flatus.     

Demonstration of an Excitable Gap in the Common Form of Atrioventricular Nodal Reentrant Tachycardia

Premature ventricular depolarizations were introduced during sustained atrioventricular nodal reentrant tachycardia ("slow-fast" type) in a single patient during electrophysiological study. Preexcitation of the atrium with retrograde His bundle capture occurred over an 85 msec range of coupling intervals between the last antegmde His bundle depolarization and the first retrograde His bundle depolarimtion associated luith the premature beat (H₁ - H₂ interval). The interval between the retrograde His bundle depolarization (H₂) and the retrograde atrial depolarization (A₂) remained constant over this 85 msec excitable gap as the H₁-H₂ interval decreased. This indicates the presence of fully excitable tissue luithin the retrograde fast pathway of the reentrant circuit during the tachycardia and demonstrates the utility of this technique for defining the extent and conduction properties of the excitable gap in reentrant arrhythmias     

Prolonged Effect of Omeprazole on the 14C-Urea Breath Test

Objectives : We investigated omeprazole's effect on ¹⁴C-urea breath testing. We also determined the duration of omeprazole's effect on the breath test. Finally, we studied whether effects on breath testing were dose dependent. Methods : Fifty-seven employees and outpatients were screened for Helicobacter infection. Those positive for serology, CLO, or histology were asked to undergo baseline breath testing. Those with a positive breath test took omeprazole 20 mg/day for 14 days followed by repeat breath testing 1, 3, and 5 days after therapy. Subjects with persistently positive breath tests despite omeprazole 20 mg/day were asked to take omeprazole 20 mg b.i.d. for 14 days. Repeat breath tests were performed as above. Results : Thirteen of 57 had HP infection. Ten of 13 underwent a baseline breath test. Eight of 10 with baseline breath tests experienced a significant decrease in expired ¹⁴CO₂ after omeprazole 20 mg/day. Five of 13 with active HP infection developed a negative breath test after omeprazole. All subjects had a positive breath test within 5 days of stopping omeprazole 20 mg/day. Five of eight with persistently positive breath tests despite omeprazole 20 mg/day took omeprazole 40 mg/day. Four of five developed a significant decrease in ¹⁴CO₂ excretion after omeprazole. All subjects had a positive breath test within 5 days of stopping omeprazole 40 mg/day. Conclusions : Recent treatment with omeprazole 20 mg/day led to false-negative breath tests in 38.5%. This effect appeared to be dose dependent and lasted up to 5 days after cessation of omeprazole.