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Each of 28 Vibrio strains and 3 Campylobacter strains was immobilized in distilled water (pH 6.9), but retained full motility in Trypticase soy broth. This phenomenon was not seen with any of 243 non-Vibrio, non-Campylobacter isolates representing 44 taxa of gram-negative bacteria.
Phenol (87.3 mg/l), p-cresol (58.6 mg/l), o-cresol (76.9 mg/l), and 2,5-xylenol (36.7 mg/l) were detected in the urine of workers employed in the distillation of the high temperature phenolic fraction of tar (carbolic oil). The concentrations of these compounds in the urine of non-exposed male workers was 11.7 mg/l, 25.7 mg/l, 68.1 micrograms/l, and 69 micrograms/l respectively. The excretion rates were 4.20 mg/h for phenol, 2.4 mg/h for p-cresol, 3.3 mg/h for o-cresol; and 1.5 mg/h for 2,5-xylenol. The highest concentrations of the mentioned compounds were detected in urine collected between eight and 10 hours from the beginning of exposure. The kinetics of excretion are considered.
BACKGROUND: Inhibitors of angiotensin converting enzyme (ACE) cause a non-productive cough. The insertion/deletion polymorphism of ACE was used as a genetic marker to investigate the relationship between ACE genotype and cough sensitivity. METHODS: A double blind cough challenge was performed in 66 normotensive subjects (34 men) of mean age 34.8 years (range 18-80) using aerosols of distilled water. The number of coughs during the one minute exposure to water was recorded. DNA samples from venous blood were amplified by the polymerase chain reaction and resolved on a 1% agarose gel. They were analysed for the presence of a polymorphism in intron 16 of the ACE gene consisting of an insertion (I) or deletion (D) of an Alu repetitive sequence 287 base pairs long. RESULTS: The distribution of genotypes was 20 II, 26 ID, and 20 DD. The cough response was significantly (p < 0.01) related to the ACE genotype, the mean number of coughs being 15.8, 11.3, and 9.6, respectively, in subjects with the II, ID, and DD genotypes. CONCLUSIONS: The observation that cough challenge is dependent on ACE genotype in normal subjects is evidence of a link between ACE activity and the cough reflex.
Directly measured blood flow pumped through a mixer circuit was compared to estimates of flow from indicator dilution curves derived from bolus injections of indocyanine green dye prepared in 0.9% saline (saline dye) and in triple-distilled water (3 D dye). At flows whose mean appearance time was 1.6 s, the mean error of estimate +/-SD of 2.3 +/- 5.1% using 3 D dye was significantly different (P less than 0.05) from that of 5.6 +/- 7.0% using saline dye. Essentially, there was no difference in estimates of blood flow with each dye solution when mean appearance time was increased to 3.8 s. Thus, the error, which was perhaps due to electrolyte in the concentrated indocyanine green dye (saline dye) and subsequent slowed rate of optical stabilization after dilution in plasma, is small and does not explain the overestimation by indocyanine dilution curves of blood flow in intact dogs.
Refractoriness for bronchial provocation frequently occurs after different challenge tests used to assess bronchial hyperresponsiveness in asthmatic patients. We investigated whether histamine inhalation could cause refractoriness for bronchoconstriction induced by ultrasonically nebulized distilled water (UNDW) and whether histamine causes tachyphylaxis for a subsequent histamine challenge in nine stable asthmatic patients. Preinhalation of histamine induced a significant diminished bronchoconstrictor response to UNDW cumulative dose of inhaled UNDW causing a 20% fall in forced expired volume in 1 s. The mean increased from 3.5 +/- 0.8 to 11.8 +/- 2.6 (SE) ml after histamine challenge (P less than 0.01). However, repeated inhalation of histamine did not change the bronchoconstrictor response to histamine within 1 h after rechallenge (P greater than 0.5). The magnitude of refractoriness for UNDW inhalation after preinhalation of histamine was correlated to the bronchoconstrictor response to histamine (r = 0.73, P less than 0.05). We conclude that inhaled histamine can induce refractoriness for UNDW, which seems to be related to the degree of bronchial hyperresponsiveness.
We evaluated the mechanism of the anti-asthmatic effect of inhaled indomethacin (Indo) by using an animal model (guinea pigs) of airway inflammation. After being exposed to either ozone or room air at identical flow rates (5 l/min) for 2 h, guinea pigs were anesthetized, tracheostomized, and lung resistance (RL) was subsequently measured. Guinea pigs inhaled either saline or Indo (1.5 mg/ml) for 1 min before undergoing an ultrasonically nebulized distilled water (UNDW) inhalation test. RL increased significantly after 10 min of UNDW inhalation in the room air and ozone groups but more so in the ozone group. This increase in RL was significantly suppressed by pretreatment with Indo. In the morphometric assessment of airway mucosa, a significant swelling of the epithelial cells after UNDW inhalation was observed in both the room air and ozone groups but especially so in the ozone group. This increase was also suppressed with Indo pretreatment. These results suggest that the increase in RL and the swelling of airway epithelial cells induced by inhaled UNDW in ozone-exposed guinea pigs was suppressed by pretreatment of inhaled Indo and that this suppression may be one of the reasons for the anti-asthmatic effect of inhaled Indo.
BACKGROUND: Bronchial asthma is a chronic inflammatory disease characterized by airway inflammation and hyperresponsiveness due to the release of multiple mediators, such as cysteinyl-leukotrienes (cys-LTs). OBJECTIVE: Our study was designed to investigate whether oral pretreatment with zafirlukast (a cys-LTs receptor antagonist) reduces bronchoconstriction against methacholine (MC) and ultrasonically nebulized distilled water (UNDW) challenge in patients with mild asthma. METHODS: Fourteen non-atopic patients (8 males, 20-42 years, forced expiratory volume in 1 s (FEV(1)) 97% SD +/- 0.4) with mild, intermittent bronchial asthma performed a sequential weekly pulmonary function test following challenge with MC or UNDW 2 h after zafirlukast or placebo administration, according to a single-blind method. RESULTS: We found that pretreatment with zafirlukast significantly decreased bronchoconstriction MC (maximum FEV(1) drop -10.75% SD +/- 1.89, p < 0.001) and UNDW induced (maximum FEV(1) drop -12% SD +/- 0.15, p < 0.001), while pretreatment with placebo did not protect patients against FEV(1) drop following MC (maximum FEV(1) drop -33.22% SD +/- 1.42, p < 0.001) and UNDW challenge (maximum FEV(1) drop -30.02% SD +/- 0.4, p < 0.001). CONCLUSIONS: Pretreatment with zafirlukast significantly reduced bronchoconstriction against MC and UNDW challenge in individuals with mild intermittent asthma, indicating that cys-LTs receptor antagonists might be useful as preventive therapy in these patients population.
Lever-pressing rates plotted as a function of number of hours of food deprivation produces an inverted U curve, the activation performance curve. Since delta 9-tetrahydrocannabinol depresses the response rate on variable interval (VI) performance, it may be that the response depression reflects changes in this curve. Rats were tested VI performance at five levels of food deprivation and were treated with a vehicle control, marijuana extract distillate (MED) at 7.5 and 11.25 mg/kg, cannabidiol (CBD), at 15 mg/kg or combinations: 7.5 mg/kg MED + 15 mg/kg CBD and 11.25 mg/kg MED + 15 mg/kg CBD. MED produced a depression of VI performance which was greatest at low levels of deprivation. CBD did not depress performance. When CBD was conbined with MED, potentiation of depression occurred. The potentiation depression was not additive, but occurred at high levels of deprivation. It appears that MED depresses performance most at low levels of deprivation and that CBD potentiates the depression produced by MED at high levels of deprivation.
We studied the bronchial response to exercise and ultrasonically nebulized distilled water (UNDW) challenge in 19 normal controls (3 females and 16 males; age 6-13 years) and in 44 asthmatic children (12 females and 32 males; age 6-13 years) in order (1) to determine the sensitivity and specificity of the two challenges and (2) to evaluate the relationship between bronchial responses and clinical and functional characteristics. A 20% fall in FEV1 was regarded as a significant bronchial response. The specificity of both challenges was high (100%), whereas the sensitivity of exercise (77.3%) was twice that of UNDW (38.6%). The combination of the two challenges increased the sensitivity to 81.8%. There was no correlation between the magnitude of bronchial response to exercise and UNDW (rs = -0.03; p greater than 0.05). Exercise responders were not different from nonresponders in regard to gender, age, resting lung function, length of asthmatic history and treatment requirement to control symptoms. However, the UNDW responders were different from nonresponders in regard to age (p less than 0.05) and length of asthmatic history (p less than 0.001). Children younger than 9 years old are unlikely to show a bronchial response to UNDW inhalation, since only 9.5% of them developed a significant bronchoconstriction. We suggest that the two stimuli recognize some different pathways or subjects have basic biological differences.
To ascertain whether inhaled aminophylline was effective in preventing the bronchial response induced by inhalating of an ultrasonic mist of distilled water (UMDW), we examined 8 asthmatic patients who had previously been shown to be reactive to this agent. Patients were given either 30 mg aminophylline or saline placebo aerosols followed by inhalation of 60 liters of UMDW; measurements of specific airway conductance (sGaw) were made before and after aminophylline or saline administration and after UMDW challenge. UMDW consistently induced a significant decrease in sGaw in all patients; however, in our subjects as a group, the degree of UMDW-induced bronchoconstriction was significantly less after premedication with aminophylline aerosol than after saline (p less than 0.01). Our results suggest that aminophylline is effective in preventing UMDW-induced bronchoconstriction; the possible relationships between bronchial response to UMDW and its modulation by inhaled aminophylline are discussed.
In an attempt to evaluate the influence of inspiratory flow rate on the sensitivity of the bronchial challenge with ultrasonic mist of distilled water (UMDW), we studied 8 symptom-free asthmatic patients who inhaled 60 liters of UMDW at a flow rate of either 0.35 or 1.2 1/s on two separate occasions. Tidal volume and the total duration of the respiratory cycle were kept constant during all inhalation tests. The bronchial response was assessed in terms of percent changes of baseline airway conductance. The results demonstrate that the mean bronchial response after 0.35 1/s UMDW inhalation was significantly greater than after 1.2 1/s inhalation of comparable doses of UMDW. Furthermore, 3 patients who developed a significant bronchoconstriction after 0.35 1/s UMDW inhalation showed only a mild, not significant bronchial response when the mist was inhaled at 1.2 1/s. We conclude that the sensitivity of the UMDW challenge is increased if the agent is inhaled during slow, tidal breathing.
In 20 guinea pigs 4 test areas were treated with a standard surfactant vehicle twice weekly for 3 weeks. In another 20 animals the same treatment was carried out with the addition of 1% cadmium sulfide on one area, of 10% coal tar distillate on another, 2% ichthyol sodium on the 3rd and 1% Omadine MDS on the 4th. At the end of the test in both animal collectives the number of mitoses in the basal cells of the epidermis (Colcemid method) and the thickness of the epidermis (microscopically) were determined in each of the 4 test areals. All 4 agents lead to a significant inhibition of mitoses compared with the surfactant vehicle. Coal rat also produces an acanthosis. The mitosis inhibition supports the opinion that these agents are suitable for the treatment of dandruff.
We evaluated the effect of inhaled indomethacin, a nonsteroidal antiinflammatory drug (NSAID), against bronchoconstriction induced by ultrasonically nebulized distilled water (UNDW) in children with asthma. Ten children with asthma (eight males and two females, with a mean +/- SEM age of 10.7 +/- 0.7 yr), who had a decrease in FEV1 of at least 20% after UNDW inhalation, were enrolled in this study. These subjects were pretreated with inhaled indomethacin (3 mg/m2 body-surface area) or placebo (0.9% saline) according to a single-blind, randomized, crossover design, and underwent a UNDW challenge test 15 min after the pretreatment. Furthermore, to study the possibility that indomethacin has a direct effect on airway smooth muscle, bronchial provocation with histamine was performed in seven subjects on two further days after pretreatment with indomethacin or placebo. Inhaled indomethacin had no effect on baseline pulmonary function, but did prevent the UNDW-induced decline in FEV1 (p < 0.01). Inhaled indomethacin did not modify the bronchoconstrictor response to histamine, indicating that a direct effect of this agent on airway smooth muscle is unlikely. The inhibition of local prostaglandin synthesis in the airways may be involved in the effect of indomethacin.
Although bronchial hyperresponsiveness in asthma is associated with inflammation within the airways, it is not known whether the degree and type of inflammation influence the response to different stimuli and whether pathologic changes of airway structure influence the bronchoconstrictive responses. Therefore, number of inflammatory cells in the epithelium and the lamina propria and the basement membrane thickness were estimated from bronchial biopsies taken in 27 asthmatic subjects (range percent predicted FEV1: 75.6 to 132.1, range of daily PEF variability: 1.9% to 20%) and related to the degree of bronchial responsiveness to ultrasonically nebulized distilled water (UNDW) and methacholine (M). PD20UNDW (provocative dose) was measurable in 15 of 27 patients and ranged between 1.01 and 20.4 ml. PC20M (provocative concentration) ranged between 0.15 and 31.7 mg/ml. In the 15 responders to UNDW, total inflammatory cells (p<0.04) and eosinophils (p<0.015) within the epithelium were higher than in 12 nonresponders to UNDW (PD20 > 34.8 ml). There was no correlation between PD20UNDW and any cell counts whereas negative correlations were found between PC20M and both total inflammatory cells (rs = -0.57; p<0.005) and eosinophils (rs = -0.63; p< 0.0015) within the epithelium. The degree of thickening of subepithelial layer ranged between 7 and 16 micrometers+ (n=26). Thickness correlates both with total inflammatory cells (rs = 0.49; p<0.025) and eosinophils (rs = 0.61; p< 0.003) within the epithelium. Moreover, it was correlated with baseline FEV1 (rs = -0.57; p<0.003) and daily peak expiratory flow (PEF) variability (rs = 0.51; p<0.01). A weak but significant correlation was also found between subepithelial layer thickness and PC20M (rs = -0.42; p<0.04). The results of this study demonstrate that eosinophilic inflammation of bronchial epithelium plays a role in determining UNDW and M responsiveness in asthma. Moreover, they suggest that remodeling of the airways such as thickening of subepithelial layer correlates with indices of asthma severity and could contribute to the degree of M but not to UNDW responsiveness.
Acute denervation of the lungs occurs after heart-lung transplantation (HLT), affecting both afferent and efferent nerves below the tracheal anastomosis. After surgery, the carina and main bronchi are perfused by mediastinal collaterals derived from the coronary arteries, and the intrapulmonary airways by retrograde blood flow from pulmonary artery collaterals. During acute rejection, the lungs are subjected to inflammation, particularly perivascular lymphocytic infiltrates. Rejection can be diagnosed by transbronchial biopsy (TBB). We report the bronchial responses to inhaled methacholine and ultrasonically nebulized distilled water (USNDW) in 16 HLT patients 2 wk to 43 months after surgery, relating them to the lung histopathology from concurrent TBB. Methacholine bronchial hyperresponsiveness was common, but it was not associated with airway epithelial or submucosal inflammation or perivascular lymphocytic infiltration. Six patients had a modest response to USNDW (fall in FEV1 greater than 10%). The responsiveness to USNDW was not associated with enhanced methacholine responsiveness or epithelial and mucosal inflammation. However, it was more commonly seen in patients with lung rejection and perivascular infiltrates. Methacholine hyperresponsiveness in HLT patients could therefore reflect denervation hypersensitivity of airway smooth muscle muscarinic receptors. The modest response to USNDW in some patients cannot be a result of a vagal reflex but could reflect a pathologic vascular response associated with lung rejection. These observations offer insight into the possible mechanisms of bronchial hyperresponsiveness in disease.
Inhaled furosemide has been shown to prevent bronchoconstriction induced by inhalation of ultrasonic nebulization of distilled water (UNDW) in bronchial asthma. To evaluate whether inhaled furosemide also prevents the increase in serum neutrophil chemotactic activity (NCA) observed during UNDW bronchoconstriction, we measured NCA during UNDW challenge without (control) and immediately after inhalation of furosemide (40 mg) or placebo (saline) in 10 asthmatics responsive to UNDW, in a randomized, double-blind study. NCA was assessed by measuring the maximal distance reached by neutrophils in a filter when challenged with the subject serum in a Boyden chamber ("leading front"). UNDW inhalation produced a significant increase in NCA in each subject. Gel filtration chromatography on S400 column indicated that the NCA released were 600 to 700 kD. Saline had no effect on bronchoconstriction nor on NCA increase induced by UNDW in nine patients. Furosemide did not change baseline FEV1, but it prevented bronchoconstriction and NCA increase in nine patients. In the whole group the maximal decrease in FEV1 after UNDW was -31.1%, SEM 4.7 after saline and -7.5%, SEM 5.2 after furosemide, p less than 0.001, the maximal increase in NCA after UNDW was +52.9%, SEM 9.2 after saline and +3.8%, SEM 3.1 after furosemide, p = 0.001. These results indicate that inhaled furosemide prevents both the bronchoconstriction and the NCA increase induced by UNDW inhalation in most asthmatic patients. This finding adds support to the suggestion that furosemide acts on mast cells.
Atrial natriuretic peptide (ANP) is secreted by cardiac atria and lung tissue; it has a bronchodilator action in normal subjects and patients with asthma and has been shown to protect against histamine-induced bronchoconstriction in patients with asthma. Bronchoconstriction caused by inhalation of ultrasonically nebulized distilled water (fog), in contrast to histamine-induced bronchoconstriction, has features in common with exercise-induced asthma but can be given more easily in a dose-response fashion. The present study aimed to determine the effect of elevated plasma ANP concentrations on the bronchoconstrictor response to inhalation of fog. Eight patients with atopic asthma were studied, mean baseline FEV1 3.00 1, equivalent to 89% (range 76-103%) predicted. The provocation dose of fog producing a 25% fall in FEV1 (PD25) was determined for each subject. On 4 study days, subjects received an intravenous infusion of placebo or ANP at a rate of 1.25, 3.0, or 10.0 pmol/kg/min in randomized, double-blind manner for 30 min to allow steady-state plasma concentrations to be achieved; the PD25 fog was then administered and FEV1 recorded over 30 min. Mean (SEM) baseline plasma ANP concentration was 19.3 (4.1) pg/ml and increased to 39.4 (6.6), 106.4 (11.1), and 445.9 (105.4) with the three rates of ANP infusion. The highest rate of infusion increased prechallenge FEV1 by 8.7 (2.4)% (p less than 0.01), but the lower rates of infusion had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)
To evaluate a possible seasonal change in bronchial responsiveness and the relation of such change to atopy, we administered 2,537 bronchial challenge tests in winter and spring to a dynamic population cohort of children 7 to 10 yr of age. The bronchial challenge test consisted of 10 min of tidal inhalation of an aerosol of ultrasonically nebulized distilled water; the resulting percentage decrease in FEV1 (dFEV1%) was recorded. Atopy was determined on the basis of skin-test positivity (any wheal with a diameter greater than that obtained with a positive control) to seven allergens (cat dander, dog dander, house-dust mite, birch, raygrass, orchard grass, and Alternaria). Greater bronchial responsiveness in winter was independently and significantly predicted by a physician's diagnosis of asthma (difference in dFEV1%, 5.6; 95% confidence intervals [95% CI], 2.8 to 8.5; p = 0.0001) and by shortness of breath (difference in dFEV1%, 4.2; 95% CI, 2.1 to 6.3; p = 0.0001). These factors were also predictive of greater responsiveness in the spring, as was atopy (difference in dFEV1%, 3.2; 95% CI, 1.8 to 4.6; p = 0.0001). Analysis of specific allergens further revealed that reactivity to perennial allergens (house-dust mite, cat dander) was predictive of bronchial responsiveness in both winter and spring. However, the change in responsiveness between seasons was most significantly predicted by allergy to seasonal grass pollen, i.e., ragweed or orchard grass (change in dFEV1%, 2.6; 95% CI, 0.6 to 4.5; p = 0.01). In summary, our study demonstrates increased bronchial responsiveness in spring among children allergic to grass pollen.(ABSTRACT TRUNCATED AT 250 WORDS)