首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 31 毫秒
1.
1. The aim of the present study was to determine whether the steady state NOx concentration reflects NOx formation in vivo. 2. A NO3- load study was performed after achieving NOx steady state. Chronological changes in NOx concentrations in plasma and whole blood samples from nine healthy subjects were determined by the HPLC-Griess system and NOx concentrations in erythrocytes were estimated as a possible NOx compartment influential in regulating plasma NOx concentrations. 3. Analysis was performed using the first-order one-compartment open model and the NOx formation rate was subsequently calculated. 4. The mean (+/-SEM) steady state NOx concentration of plasma (15.5 +/- 1.6 micromol/L), whole blood (12.8 +/- 1.2 micromol/L) and erythrocytes (11.9 +/- 0.7 micromol/L) did not correlate with the NOx formation rate in the compartments (0.50 +/- 0.05, 0.61 +/- 0.04 and 0.91 +/- 0.17 micromol/kg per h, respectively), whereas a significant correlation was found between the steady state NOx concentration and NOx elimination rate (Kel) in plasma (r=-0.69; P=0.04) and whole blood (r=-0.79; P=0.01). 5. Although there was no direct correlation between steady state NOx concentrations and serum creatinine levels, the correlation between half-life and serum creatinine levels was significant (plasma: r=0.60, P=0.02; whole blood: r=0.49, P=0.04). 6. Plasma NOx concentrations correlated significantly with erythrocyte NOx concentrations (r=0.92, P <0.01; erythrocyte NOx=0.66 x plasma NOx). 7. The results of the present study indicate that NOx does not accumulate excessively into erythrocytes at steady state and during a NO3- load and that the steady state NOx concentration in whole blood and plasma preferentially implies NOx elimination (mainly depending on renal function) rather than NOx formation.  相似文献   

2.
Blood flow and plasma fibrinolytic factors were measured on five occasions in both forearms of eight otherwise healthy male smokers during unilateral brachial artery infusion of the endothelium-dependent vasodilator, substance P (2 to 8 pmol/min), and the endothelium-independent vasodilator, sodium nitroprusside (2 to 8 microg/min). On the first occasion, intra-arterial vitamin C was co-infused at 25 mg/min. On subsequent occasions, subjects attended after 28 and 35 days treatment with oral vitamin C (1 g daily) or placebo in a double-blind randomized crossover design still smoking but with and without acute smoke inhalation (3 cigarettes over 30 minutes). Basal plasma ascorbate concentrations increased from 37 +/- 6 micromol/L to 105 +/- 11 micromol/L following oral vitamin C supplementation (P = 0.002). Substance P caused dose-dependent increases in forearm blood flow (P < 0.001, ANOVA) and t-PA release (P < 0.05, ANOVA) that was unaffected by acute recent smoke inhalation, intra-arterial vitamin C, or oral vitamin C administration (p = ns). Likewise there were no effects on sodium nitroprusside-induced vasodilatation (p = ns). Neither acute local intra-arterial nor prolonged oral vitamin C supplementation reverses smoking-related endothelial dysfunction and impaired endogenous t-PA release. We conclude that the adverse vascular actions of smoking are not principally mediated through oxidative stress.  相似文献   

3.
The extent of smoke exposure via mother's milk and passive smoking was investigated in a prospective, longitudinal matched-pair study by comparison between children, whose mothers smoked substantially throughout pregnancy and nursing period and children whose mothers did not smoke. Our preliminary results show that not only infants of smoking mothers but also those of smoking fathers show reduction of birth weight. Smoking mothers weaned their babies earlier than non-smokers. Cotinine concentrations in breast milk depended on the number of cigarettes smoked. The highest urinary excretion of cotinine (as expressed by ng cotinine/mg creatinine ratios) were observed in infants fully breast-fed by smoking mothers. After weaning the values were in the same range as those of formula-fed infants of smoking mothers (exposed to passive smoking only). In the group of non-smokers only small or undetectable amounts of cotinine were found. Thus it is demonstrated that both nursing and--to a lower degree--passive smoking contribute to the exposure of infants to nicotine and its metabolite cotinine.  相似文献   

4.
Determination of plasma cotinine concentration is the predominant assay employed to quantify smoking and exposure to environmental tobacco smoke in epidemiological studies. However, cotinine is biotransformed into secondary metabolites. This pilot study determined plasma concentrations of cotinine, cotinine glucuronide, 3-hydroxycotinine, and 3-hydroxycotinine glucuronide. Total cotinine concentration was determined by summation of all four metabolites. The goals of this study were (1) to explore the stability and validity of total cotinine concentration as a measure of tobacco smoking and as a measure of exposure to environmental tobacco smoke in nonsmokers, (2) to explore the stability of plasma concentrations of each of the four nicotine metabolites in smokers by performing a.m. and p.m. measures, and (3) to explore the stability of indices of glucuronidation as measures of possible markers for enzymatic activity. The subject sample included 76 white volunteers (32% smokers and 68% nonsmokers). Plasma total cotinine concentration appeared to be very stable, suggesting that total cotinine concentration may be a good measure for epidemiological studies employing a single plasma sample. Moreover, plasma total cotinine concentration also reflected exposure to environmental tobacco smoke more accurately than did plasma cotinine concentration, which would have not identified 27% of passive smokers. 3-Hydroxycotinine glucuronide and 3-hydroxycotinine plasma concentrations were almost as stable as cotinine concentrations. However, cotinine glucuronide and its indices of glucuronidation were unstable, suggesting that cotinine glucuronide undergoes deconjugation. New studies of total cotinine in plasma using more than two blood collections during the day are needed to definitively establish that it is a stable biomarker for epidemiological studies.  相似文献   

5.
Relationships between machine smoking nicotine yield and different smoke exposure indicators were investigated in a cross-sectional study. For each of the four yield classes H (1.0-1.2 mg), M (0.7-0.9 mg), L (0.4-0.6 mg) and U (0.1-0.3 mg) 18 male and 18 female subjects were recruited. The experimental design (2 x 2) included smoking with lip contact or with a flowmeter holder, natural smoking of one cigarette or forced smoking (30 puffs). The analysis of presmoking measures revealed for plasma nicotine H greater than L, U; M greater than U, for plasma cotinine H, M greater than U, and no differences for respiratory CO. Pre- to postsmoking boosts of CO and nicotine increased with yield, but the differences were smaller than those in yield. This partial compensation can be attributed to puffing behavior as revealed by the differences between yield classes with respect to flowmeter measures (puff volume, flow parameters, number of puffs). Contact condition hardly influenced the results. Forced puffing revealed down regulation mechanisms in smoke absorption and, less pronounced, in puffing behavior. Cardiovascular and subjective effects were widely independent of yield. Plasma cotinine appeared as the best smoke exposure indicator, due both to its high retest reliability and its relationship to nicotine yield.  相似文献   

6.
Relationships of population characteristics, smoking history, and cigarette yield with smoke exposure as measured by peripheral blood concentrations of thiocyanate, carboxyhemoglobin, nicotine and cotinine were sought in 170 male smokers. This population of smokers had significant elevations of serum thiocyanate, blood carboxyhemoglobin and plasma nicotine and cotinine concentrations as compared with an equal number of age- and sex-matched nonsmokers and these concentrations correlated significantly with past 24-hour cigarette consumption. Although the nicotine yield of the cigarette correlated significantly with plasma cotinine and marginally with plasma nicotine, the reduction in plasma nicotine and cotinine was not proportionate to the reduced yield of the cigarettes, suggesting that smokers partially compensate for the lower yields of their cigarettes. Blood levels of carboxyhemoglobin, nicotine and cotinine were also significantly associated with the weight of the subjects, presumably due to the relationship between weight and the volume of distribution. Univariate and multiple regression analyses provided evidence that coffee and alcohol consumption and years smoked also may be important determinants of smoke exposure.  相似文献   

7.
Meconium samples collected from 115 neonates were analysed for nicotine, cotinine and trans -3-hydroxycotinine (OH-cotinine) by means of high-performance liquid chromatography (HPLC) to identify prenatal smoke exposure. The self-reported maternal smoking status during pregnancy was determined by means of a questionnaire and verified by measurements in urine prior to childbirth. The total sum of nicotine and its metabolites (Sum(tot)) of the first passed meconium samples was 1560 +/- 1024 pmol/g in newborns of smoking mothers. Smoking of less than five cigarettes was clearly detected. Sum(tot) remained constant in all meconium samples passed by a neonate in succession. However, the proportion of nicotine decreased with the time of passage after birth and the OH-cotinine proportion increased, whereas cotinine hardly changed. Nicotine or its metabolites were not detectable in meconium (detection limit < 20 pmol/g), when the mothers were only exposed to environmental tobacco smoke (ETS) using the HPLC method. The hypothesis that the content of nicotine metabolites in meconium reflects long-term smoke exposure could not be confirmed in newborns whose mothers had quit smoking during the latter half of pregnancy. Determining Sum(tot) enables the intensity of continuous smoking during pregnancy to be estimated in all meconium samples passed by a newborn.  相似文献   

8.
SUMMARY: Smoking in pregnancy is associated with a well-characterized increase in perinatal risks. Despite their wish to discontinue smoking, some pregnant women cannot stop. To characterize nicotine and cotinine levels in women who could not quit smoking after the first trimester, the authors recruited 19 white women (age 17-41 years) between 14-23 weeks of gestation who could not quit smoking. They started smoking at ages 11-22 years (mean 14.5) and smoked for 17 +/- 6 years. They had their first cigarettes 5-60 minutes after waking up (mean 12). Nicotine levels were compared with those expected in white patients in the general population, and the cotinine levels per cigarette smoked were compared with the population-based values. Sixteen of the 19 women had nicotine levels substantially lower than those expected. The mean level of serum cotinine produced by one cigarette per day was 19.1 +/- 15.8 ng/mL (range 6.1-67). The expected levels in white patients in the general population are 13 +/- 7.7 ng/mL. The data suggest that pregnant women who cannot quit heavy smoking in the second trimester form a selective group with pharmacokinetic predisposition to a high rate of nicotine metabolism.  相似文献   

9.
OBJECTIVES: The purpose of the present study was to assess the levels of nicotine and cotinine in biological fluids (plasma, saliva, and urine) following hubble-bubble (HB) smoking. METHODS: Fourteen healthy male volunteers, aged 28 +/- 8 years, body weight of 82.7 +/- 13.53 kg, participated in the study. All volunteers were habitual HB smokers for 3.29 +/- 1.90 years who smoked at least 3 runs per week with an average of 20 g Mua'sel per run. Volunteers were requested to avoid smoking, at least 84 hours prior to the time of the study. After baseline samples were taken, volunteers started smoking 20 g of Mua'sel for a period of 45 minutes. Heparinized blood samples (5 or 10 ml each) were drawn for nicotine and cotinine analysis before, during and after the smoking period. Saliva samples were collected just before smoking (time 0) and at the end of smoking (45 min). Urine also was collected at time 0 and 24-hour urine collection was also taken to measure nicotine and cotinine excretion. Nicotine and cotinine were extracted from samples and assayed by gas chromatography. All data are presented as mean +/- SEM throughout the text, Tables and Figures unless indicated otherwise. RESULTS: Plasma nicotine levels rose from 1.11 +/- 0.62 ng/ml at baseline to a maximum of 60.31 +/- 7.58 ng/ml (p < 0.001) at the end of smoking (45 min). Plasma cotinine levels increased from 0.79 +/- 0.79 ng/ml at baseline to its highest concentration of 51.95 +/- 13.58 ng/ml (p < 0.001) 3 hours following the end of smoking. Saliva nicotine levels significantly rose from 1.05 +/- 0.72 to 624.74 +/- 149.3 ng/ml and also saliva cotinine levels significantly increased from 0.79 +/- 0.79 ng/ml to 283.49 +/- 75.04 ng/ml. Mean amounts of nicotine and cotinine excreted in urine during the 24-hour urine collection following smoking were equal to 73.59 +/- 18.28 and 249 +/- 54.78 microg, respectively. CONCLUSION: Following a single run of HB smoking, plasma, saliva and urinary nicotine and cotinine concentration increased to high values. This observation suggests that HB may not be an innocent habit, as people believe.  相似文献   

10.
A method is described for the analysis of cotinine in plasma, saliva and urine using packed-column gas-liquid chromatography, which is sufficiently sensitive and reproducible for quantitative study of the low levels resulting from exposure of non-smokers to other people's smoke. The lower limit of detection of cotinine in these fluids was 100 pg ml-1. The coefficient of variation over the range 0.25 to 2.0 ng ml-1 averaged 7.7%. In a sample of 85 non-smokers the concentrations of cotinine in plasma correlated 0.82 with those in urine and saliva, while the correlation between the saliva and urine concentrations was 0.91. Saliva cotinine concentrations were quantitatively related to passive exposure to parental smoking in a population study of 569 non-smoking schoolchildren.  相似文献   

11.
Smoking by pregnant and parturient women is generally suspected to increase nicotine levels in fetal and infant blood. Supportive data of nicotine levels in infants is, however, inadequate. We investigated blood and muscle nicotine and cotinine levels in 14 autopsy cases of newborn babies and infants using gas chromatography. Among the 14 cases investigated, nicotine or cotinine was detected in six cases (42.9%). In each of these six cases, the mother was a smoker. Route of exposure to nicotine originating from smoking was transplacental in three cases, via breast milk in one case and secondhand smoke in two cases. Nicotine and cotinine levels in blood from the two cases with placental exposure were 10.6-84.4 ng/ml and 20.3-183 ng/ml, and levels in muscle from one case were 43.9 ng/g and 308 ng/g, respectively. Nicotine and cotinine levels in blood from exposure via breast milk were 19.1 ng/ml and 87.1 ng/ml, and from secondhand smoke were 0 ng/ml and 14.6-20.1 ng/ml. Mean concentrations of blood nicotine and cotinine in 68 autopsy cases of adult habitual smokers were 30.0 ng/ml and 247 ng/ml. Our data for nicotine and cotinine levels in infant blood seem to indicate that some infants who are born and develop under exposure to smoking by family members, particularly the mother, may show high nicotine levels in blood and experience possible health risks.  相似文献   

12.
Exposure to toxic metals during pregnancy may have detrimental effects on foetal development. We assessed the role of sociodemographic characteristics and active and passive smoking on blood concentrations of metals (As, Cd, Pb, Hg, Sb, U, Mn and Mo). Venous blood drawn from 50 pregnant women, randomly selected from the mother-child birth cohort 'Rhea'. Extensive questionnaire data on active and passive smoking were collected. Urinary cotinine was measured to validate self-reported exposure and non-smoking status. Smokers had higher concentrations of Cd (1.0 μg/L) as compared with non-smokers (0.29 μg/L, P?相似文献   

13.
Six volunteer female habitual smokers were exposed during a 2-wk experimental period to cigarette smoke, both actively and passively, in an exposure chamber (volume 10 m3, average air exchange rate 6.8 times/h), where the ambient carbon monoxide, particle, and aldehyde concentrations were monitored. Three of the six subjects were smoking at the time, 2 cigarettes (filtered, self-burning low tar brand) per person per hour, 30 cigarettes altogether during each of the 5-h experimental days in the chamber. Samples of blood and urine were taken from each subject after 3 nonsmoking days and after each day of active or passive smoking. Among the parameters tested, blood carboxyhemoglobin, plasma cotinine, and urinary mutagenicity were higher in samples taken after active smoking than after nonsmoking periods. Although the exposure conditions were similar for all subjects, the parameters measured showed quite high interindividual variation. Thioethers and thiocyanates were not significantly elevated in the active smoking samples; neither were there any differences during this short experimental period in the sister chromatid exchange frequencies. The only parameters showing an increasing trend after passive exposure, as compared with nonsmoking samples, were urinary mutagenicity and plasma cotinine, the main metabolite of nicotine.  相似文献   

14.
Environmental tobacco smoke (ETS) is a significant component of indoor air pollution yet the acute upper respiratory response has not been well studied. The goal of this study was to determine the response of healthy subjects to moderate levels of sidestream tobacco smoke (SS). Twenty-three subjects were challenged on 2 separate days to clean air or SS (2 h, 15 ppm carbon monoxide, at rest) . Subjects completed symptom questionnaires, posterior rhinomanometry, and body plethysmography. Average total and differential cell counts and albumin concentration were determined on nasal lavage samples. The urinary cotinine : creatinine ratio was used as a biomarker of exposure. Following SS exposure, irritant and rhinitis symptoms increased, nasal resistance rose from 4.9 +/- 0.4 to 6.3 +/- 0.6 cm H2 O/L/s and specific airway conductance decreased from 0.14 +/- 0.01 to 0.13 +/- 0.01 cm H2 O-1 s-1. Total cell counts, neutrophils, and albumin were unchanged. An increased nasal congestive response did not correlate with an increased cotinine : creatinine ratio. A history of ETS rhinitis did not predict an increased group response to smoke, but individuals with the largest physiologic and inflammatory response were historically ETS sensitive. In summary, healthy normal subjects demonstrate nasal congestion with exposure to moderate levels of SS without evidence of increased nasal vascular permeability.  相似文献   

15.
Exposure to tobacco smoke, both from active smoking and from passive exposure to environmental tobacco smoke, can be monitored by measuring cotinine, a metabolite of nicotine, in a variety of biological sources including blood, urine, and saliva. Previously, a sensitive atmospheric-pressure ionization, tandem mass spectrometric (LC-API-MS-MS) method for cotinine measurements in serum was developed in support of a large, recurrent national epidemiologic investigation. The current study examined the application of this LC-API-MS-MS method to both serum and saliva cotinine measurements in a group of 200 healthy adults, including both smokers and nonsmokers. The primary objective of this study was to evaluate the relationship between serum and saliva cotinine concentrations to facilitate the linking of results from epidemiologic studies using salivary cotinine measurements to existing national data based on serum cotinine analyses. The results indicate that a simple, linear relationship can be developed to describe serum and saliva cotinine concentrations in an individual, and the expression describing this relationship can be used to estimate with reasonable accuracy (approximately +/- 10%) the serum cotinine concentration in an individual given his or her salivary cotinine result. It was further confirmed that saliva cotinine samples are generally quite stable during storage after collection, even at ambient temperatures, and this sample matrix appears to be well-suited to the requirements of many epidemiologic investigations.  相似文献   

16.
In the present study, we examined the effects of acute treatment with paroxetine on the consumption of cigarette smoking and caffeine in 65 patients who met the DSM-IV criteria for major depressive disorder (M/F: 28/37, age: 48 +/- 15 years). Plasma levels of cotinine or caffeine were analysed using high-performance liquid chromatography (HPLC). The amount of cigarette smoking and plasma levels of cotinine, but not caffeine, decreased 4 weeks after paroxetine treatment. There was no difference between smokers and nonsmokers with respect to their response to paroxetine treatment. In addition, plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) levels in responders to paroxetine treatment was higher than those in nonresponders, and there was a negative correlation between the changes in plasma MHPG levels and the changes in Hamilton rating scale for depression (Ham-D) scores before and 4 weeks after paroxetine administration. These results suggest that paroxetine has the potential to reduce the amount of cigarette smoking in depressed smokers, and we reconfirmed our previous results that depressed patients with higher plasma MHPG levels had better response to paroxetine treatment than those with lower plasma MHPG levels using larger depressed samples.  相似文献   

17.
OBJECTIVES: Cigarette smoking causes cardiovascular (CV) disease, but the relative roles of nicotine and other components of tobacco smoke remain unclear. We investigated the effect of stopping smoking by using nicotine replacement therapy (NRT) on hemorheology parameters, on the cotinine and thiocyanate plasma concentrations and the exhaled carbon monoxide (CO). DESIGN: Open, parallel-group trial (intervention group and control smokers). SUBJECTS: 197 males, aged 25-45 years, smoking > 20 cigarettes per day (cpd). INTERVENTIONS: 164 subjects were instructed to stop smoking and received NRT for 12 weeks and 33 acted as controls. After 12 weeks, NRT was discontinued and all subjects were followed-up at 26 weeks. Beginning with week 4, the treated subjects were divided into abstainers (self-reported, verified by exhaled CO < 10 ppm) and nonabstainers, not able to stay abstinent since baseline. The group of the nonabstainers was stratified in 2 subgroups, the reducers (smoked < 50% of baseline number of cpd) and relapsers (smoked 50-100% of baseline cpd). MAIN OUTCOME MEASURES: Plasma viscosity, erythrocyte deformability, fibrinogen, transcutaneous partial oxygen tension (tcpO2), hematocrit, white blood cells, cotinine and thiocyanate plasma concentrations and exhaled CO, all assessed at 4, 8, 12 and 26 weeks. RESULTS: After 6 months, plasma fibrinogen (228.2 vs. 275.4 mg/dl at baseline, p < 0.001), tcpO2 (50.4 vs. 34.9 mm mercury at baseline, p < 0.0001) were significantly improved in abstainers, but changes in plasma viscosity and erythrocyte deformability were inconclusive. Cotinine and thiocyanate (abstainers: 6.2 ng/ml at week 26 vs. 10.4 ng/ml at baseline, p < 0.0001) and expired CO (abstainers: 30.4 vs. 4.2 ppm, control vs. week 26, p < 0.0001) accurately followed the changes in smoking and/or NRT use in all of the groups. Other CV risk factors such as hematocrit and white blood cell count decreased to a greater extent in abstainers than in reducers and relapsers. Not only abstainers but also reducers did benefit of the temporarily stop smoking. CONCLUSIONS: Smoking cessation improved CV parameters despite the measured cotinine and thiocyanate plasma levels, and use of nicotine medications did not negate these improvements. A smoking cessation for a short time and smoking of reduced cpd also improved these parameters temporarily.  相似文献   

18.
On switching to cigarettes with lower tar and nicotine yields, most individuals smoke more intensively, but it is not clear if this effect persists over a long period. Smoking behaviour was monitored in 10 male and 18 female volunteers at five monthly visits, smoking commercially available cigarettes (tar yield>10 mg), then for six more visits at 6-week intervals after switching (mean reduction of 5.9 mg tar and 0.45 mg nicotine). Puffing behaviour was monitored with a flow sensing holder, and measurements were made before and after smoking of plasma cotinine, carboxyhaemglobin and alveolar carbon monoxide. After switching, cotinine levels only fell 40% of that predicted from the fall in nicotine yields, and there were no systematic trends for the rest of the study. Puff volumes rose (reflecting perhaps the reduced draw resistance of the lower yield cigarettes), and remained higher thereafter. The number of puffs per cigarette appeared to rise on switching, but then decreased again. In conclusion, most effects of switching to lower yield cigarettes appeared to persist for at least 36 weeks, suggesting that the strategy of reducing exposure to cigarette smoke by lowering tar and nicotine yields may be of limited value.  相似文献   

19.
BackgroundThe significance of the free radicals is emphasized in the pathophysiology of diabetes and the progression of chronic diabetic complications. Smoking cigarettes increases the risk of developing type II diabetes and intensifies pathophysiological processes during the development of type I diabetes. Tobacco smoke is also additional source of free radicals. Moreover, smoking causes variety of adverse effects on organs, that have no direct contact with the tobacco smoke itself. The objective of the study was to examine the effects of tobacco smoke on the serum concentrations of relevant oxidative stress markers such as total protein (TP), reduced glutathione (GSH), glutathione S-transferase (GST) and thiobarbituric acid reactive substances (TBARS), as well as renal (creatinine, urea) and liver function (alkaline phosphatase, ALP; alanine aminotransferase, ALT; aspartate aminotransferase, AST) among animals with induced diabetes after administration of a single dose of streptozotocin (65 mg/kg, ip).MethodsThe markers of oxidative stress and biochemical parameters were determined using spectrophotometric methods. As a biomarker of exposure to tobacco smoke, cotinine was determined using high-performance liquid chromatography with diode array detection (HPLC-DAD).ResultsTobacco smoke exposure of diabetic rats was manifested by significantly elevated liver enzymes activity - ALT (p < 0.05) and ALP (p < 0.01), higher creatinine and urea concentration (p < 0.01), lower GSH amount (p < 0.05), and higher GST activity (p < 0.05).ConclusionsTobacco smoking induce liver and renal damage through the mechanisms including increased oxidative stress.  相似文献   

20.
Exposure to phosgene has been shown to cause severe and life-threatening pulmonary edema. There is evidence that successful treatment of phosgene-induced acute lung injury may be related to increased antioxidant activity. Acetylenic acids such as 5,8,11, 14-eicosatetraynoic acid (ETYA) have been shown to be effective in preventing pulmonary edema formation (PEF). In phosgene-exposed guinea pigs, we examined the effects of ETYA on PEF. Lipid peroxidation (thiobarbituric acid-reactive substance, TBARS) and total glutathione (GSH) were measured in lung tissue from isolated, buffer-perfused guinea pig lungs at 180 min after start of exposure. Guinea pigs were challenged with 175 mg/m(3) (44 ppm) phosgene for 10 min (1750 mg( small middle dot)min/m(3)). Five minutes after removal from the exposure chamber, guinea pigs were treated, ip, with 200 microl of 100 microM ETYA in ethanol (ETOH). Two hundred microliters of 50 microM ETYA in ETOH was added to the 200 ml perfusate every 40 min beginning at 60 min after start of exposure (t = 0). There were four groups in this study: air-exposed, phosgene-exposed, phosgene + ETYA-posttreated, and air + ETYA-posttreated. Posttreatment with ETYA prevented GSH depletion, 2. 7 +/- 0.5 micromol/mg protein versus 1 +/- 0.2 micromol/mg protein, for the untreated phosgene-exposed lungs (p < or =.05). ETYA posttreatment also significantly decreased PEF (p 相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号