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At least 487 records · Page 27Linked to original sources
PubMed2001

Assessing the impact of a nurse-led health education intervention for people with peripheral vascular disease who smoke: the use of physiological markers, nicotine dependence and withdrawal.

This study evaluated the impact of a nurse-led health education programme on the behaviour, nicotine dependence and nicotine withdrawal in patients who smoke and suffer from peripheral vascular disease, based in a large teaching hospital in the north of England. Smoking behaviour was measured by self report, end-expired carbon monoxide and urinary cotinine. Nicotine dependence and withdrawal were measured using a nicotine dependence scale and a nicotine withdrawal scale. The findings demonstrated that the programme did have some impact on behaviour. The study raised issues concerning the measurement of physiological markers for smoking as nursing outcomes. Issues about the measurement of nicotine dependence and withdrawal are highlighted.

Aged↗
PubMed1990

Identification of exposure markers in smokers' breath.

Volatile organic compounds present in the exhaled breath of 26 smokers and 43 non-smokers were evaluated in an effort to identify possible biochemical markers resulting from the exposure to cigarette smoke. The total ion current profiles obtained from gas chromatography-mass spectrometry (GC-MS), which contained about 230 GC-MS peaks, were first analyzed by using standard statistical procedures to select a subset of 22 peaks. The importance of the peaks was ranked using factor analysis, which further reduced the dimensionality of the data, and discriminant analysis served to develop classification functions. One peak, 2,5-dimethyl furan, had sufficient discriminatory power in the GC-MS profiles to allow almost complete differentiation (96% correct classification) between the smokers and non-smokers groups. In addition, several other compounds were able to separate the groups with a high level of accuracy.

Biomarkers↗
PubMed2000

Acute hypoxia and reoxygenation impairs exhaled nitric oxide release and pulmonary mechanics.

OBJECTIVE: Changes in exhaled nitric oxide levels often accompany conditions associated with elevated pulmonary vascular resistance and altered lung mechanics. However, it is unclear whether changes in exhaled nitric oxide reflect altered vascular or bronchial nitric oxide production. This study determined the effects of acute hypoxia and reoxygenation on pulmonary mechanics, plasma nitrite levels, and exhaled nitric oxide production. METHODS: Ten piglets underwent 90 minutes of hypoxia (fraction of inspired oxygen = 12%), 1 hour of reoxygenation on cardiopulmonary bypass, and 2 hours of recovery. Five additional animals underwent bypass without hypoxia. Exhaled nitric oxide, plasma nitrite levels, and pulmonary mechanics were measured. RESULTS: Exhaled nitric oxide decreased to 36% of baseline by end hypoxia (34 +/- 14 vs 12 +/- 9 ppb, P =.005) and declined further to 20% of baseline at end recovery (7 +/- 6 ppb). Aortic nitrite levels decreased from baseline during hypoxia (from 102 +/- 13 to 49 +/- 7 micromol/L, P =.05) but returned to baseline during recovery. Pulmonary arterial nitrite also decreased during hypoxia (from 31.4 +/- 7.8 to 22.9 +/- 9.5 micromol/L, P =.04) and returned to baseline at end recovery. Decreased production of exhaled nitric oxide was associated with impaired gas exchange (alveolar-arterial gradient = 32 mm Hg at baseline and 84 mm Hg at end recovery), decreased pulmonary compliance (6.6 +/- 0.9 mL/cm H(2)O at baseline, 5.0 +/- 0.7 mL/cm H(2)O at end hypoxia, and 5.4 +/- 0.7 mL/cm H(2)O at end recovery), and increased inspiratory airway resistance (41 +/- 4 cm H(2)O. L(-1). s(-1) at baseline, 56 +/- 4.9 cm H(2)O. L(-1). s(-1) at end hypoxia, and 50 +/- 5 cm H(2)O. L(-1). s(-1) at end recovery). CONCLUSIONS: A decrease in exhaled nitric oxide persisted after hypoxia, and plasma nitrite levels returned to baseline on reoxygenation, indicating that alterations in exhaled nitric oxide during hypoxia-reoxygenation might be unrelated to plasma nitrite levels. Furthermore, decreased exhaled nitric oxide corresponded with altered pulmonary mechanics and gas exchange. Reduced exhaled nitric oxide after hypoxia-reoxygenation might reflect bronchial epithelial dysfunction associated with acute lung injury.

Acute Disease↗
PubMed2002

Bitumen fumes: review of work on the potential risk to workers and the present knowledge on its origin.

Bitumens fumes contain polycyclic aromatic compounds (PAC). There is a possibility of long-term health effects following chronic exposure by inhalation or skin contamination in asphalt road pavers and highway maintenance workers. Epidemiological and experimental studies on this topic are reviewed and the possible causes of cancer discussed with a primary focus on heterocyclic polyaromatic compounds. In 2001, the results of the IARC epidemiological study confirmed an excess of lung cancer despite a lower cancer mortality. In vitro genotoxicity and mechanistic studies demonstrated a mutagenic effect of bitumen fume condensates (BFC) and some data suggested that the polycyclic aromatic hydrocarbons (PAH) analysed were not the major genotoxic compounds in bitumen fume condensates. Other compounds such as nitrogen-, sulfur- and/or oxygen-containing PAH or their alkyl substituted analogues, mutagenic in the Ames mutation assay, may be involved in the genotoxic effect of BFC. After skin painting with BFC, DNA adducts were found in skin, lung and lymphocytes of all the treated animals. Differences in the adduct patterns were also observed, but a more polar adduct was common to the three tissues and not observed in those from rats treated with coal-tar fume condensates (CTFC). Rat inhalation experiments with bitumen fumes confirmed the presence of a DNA-adduct in the lungs with the same Rf as the previous polar adduct. This adduct therefore merits further investigation as a potential biomarker in lymphocyte DNA to follow exposed workers. All the analytical data and the mechanistic data are complementary and suggest the potential role of thiophenes in the genotoxicity of bitumen fumes. Some thiophenes have lower mutagenic activity than their isosteric PAH, whereas others are very potent carcinogens. Generally, the sulfur analogues of PAH (SPAH) in bitumen fumes have a higher concentration than the PAH of similar molecular weight, whereas the SPAH in coal-tar fumes have a much lower concentration than the corresponding PAH. This may explain why the more polar adducts have been detected only in animals exposed to bitumen fume. In a skin carcinogenicity study of condensed asphalt roofing fumes, it has been demonstrated that the most active fractions were those containing a variety of aromatic SPAH. In conclusion to this review, there is an interest in determining the chemical identity of the major DNA adducts induced by BFC. This would allow experimental studies on the carcinogenic potency of these compounds and their validation as potential biomarkers. These compounds could thus merit further analytical investigation in preference to the PAH included in the list of the US Environmental Protection Agency that are currently being analysed by the industry in field studies.

Administration, Cutaneous↗
PubMed1999

Characterization of equine natural killer and IL-2 stimulated lymphokine activated killer cell populations.

Natural killer (NK) cells are an important component of the innate immune system. Though intensively studied in humans and rodents. NK cells remain less well characterized in other species. Studies are often limited by the lack of specific cell markers; however, the mAb NK-5C6 has been suggested to recognize an evolutionarily conserved molecule on NK cells and reacts with cells from several species. This mAb was used in the current investigation to identify and characterize equine NK cells, and was found to label approximately 10% of peripheral blood lymphocytes (PBL). Two-color flow cytometry analysis identified the NK-5C6+ cell population as being CD3-CD4- and CD8-, but positive for MHC class I and LFA-1 expression. Depletion of CD3+ T cells increased the percent NK-5C6+ cells in PBL; this enriched population demonstrated a specific cytotoxic response against a major histocompatibility complex (MHC) deficient NK target cell line (K-562), but not MHC+ target cells (EqT8888). These results provide evidence for an equine NK cell population, which exhibits endogenous lytic activity and a phenotype similar to that of human and mouse NK cells. Stimulation of peripheral blood mononuclear cells (PBMC) with IL-2 promoted the development of LAK cells. These cells were predominantly CD3+ T cells, demonstrated intracellular perforin expression, and effectively lysed both K-562 and EqT8888 target cells. Hence, equine NK cells can be identified by the NK-5C6 mAb and distinguished from IL-2 stimulated LAK cells by their cytotoxic response to specific target cell lines.

Animals↗
PubMed1997

The kinetics of methanol elimination in alcoholics and the influence of ethanol.

Methanol concentrations were studied during the end phase of ethanol elimination and for about five hours afterwards in 12 alcoholics admitted with alcohol intoxication for acute care. The rate of ethanol elimination (beta 60) ranged from 0.114 g/kg/h to 0.270 g/kg/h (mean 0.178 +/- 0.045 g/kg/h). The methanol concentration was found to remain almost steady as long as ethanol levels were relatively high, and changed only to an extent that could be explained by the combined opposing influences of methanol excretion and endogenous synthesis. There was no significant relationship between the rate of ethanol elimination and the methanol level. The methanol concentration began to decrease when the ethanol concentration had fallen to under 0.2 g/kg. When the ethanol concentration had fallen to base levels, methanol was eliminated at a rate characterized by an elimination constant (kel) of 0.212-0.481 h-1, and a half life of 1.44-3.27 h. There was a positive correlation between the rate of ethanol elimination and the rate of methanol elimination (r = 0.642; p < 0.05).

Adult↗
PubMed2003

Tissue (muscle) oxygen saturation (StO2): a new measure of symptomatic lower-extremity arterial disease.

OBJECTIVES: Near-infrared spectroscopy provides a noninvasive method of measuring tissue oxygen saturation and has been used to monitor extremity compartment syndrome. Tissue O(2) saturation (StO(2)) is potentially useful in assessing patients with peripheral arterial disease (PAD). The purposes of this feasibility study are to (1) explore the diagnostic sensitivity of StO(2) in subjects with PAD and symptoms of intermittent claudication (IC) compared with normal subjects, and (2) correlate the change in StO(2) during and after exercise with the ankle brachial index (ABI) in patients with IC. Material and methods Forty-nine subjects, 35 normal and 14 PAD, from two centers were evaluated in a prospective cross-sectional analysis comparing StO(2) by using the InSpectra tissue spectrometer and ABI at rest (baseline) and after treadmill exercise. Measurements were obtained at baseline and peak exercise (normal subjects) and at baseline, initial claudication distance (ICD) and absolute claudication distance (ACD) in PAD subjects. Endpoint values were the mean of 15 data points. Times to 50% of StO(2) recovery to baseline (T(50)) and complete recovery to baseline (T(100)) were measured. Receiver-operator characteristic curves were constructed to assess the sensitivity/specificity values associated with various StO(2) cut-points. RESULTS: The PAD patients were older (P =.0002) and 57% were male, compared with 37% males in the normal group. The ABI was 0.68 +/- 0.14 in PAD patients versus 1.14 +/- 0.08 in normal subjects (P <.0001). The baseline StO(2) was 65% in both groups. The peak exercise StO(2) was significantly lower and the absolute change in StO(2) and the percent change in StO(2) were significantly greater in PAD patients (P < 0.45). The T(50) and T(100) were longer in the PAD patients compared to normal subjects (P =.0001 and.002, respectively). A T(50) of >70 seconds yielded a sensitivity of 89% and a specificity of 85% for PAD. CONCLUSIONS: StO(2) is a new and potentially useful technique to evaluate patients with PAD. Resting StO(2) was similar in PAD-IC subjects and normals. There was a significantly greater drop in StO(2) and longer recovery times in PAD-IC subjects. Interestingly, StO(2) at the ICD and ACD was similar. StO(2) offers a different and perhaps more appropriate end point for diagnosis and monitoring of the management of patients with PAD, and may offer additional insight into the pathophysiology of exercise-induced muscle ischemia and its recovery.

Adult↗
PubMed2001

Oxygen toxicity: simultaneous measure of pentane and malondialdehyde in humans exposed to hyperoxia.

In order to estimate cell damage caused by free radicals during oxygenotherapy, we investigated the time course of two markers of lipoperoxidation: pentane in breath and malondialdehyde (MDA) in blood during brief normobaric hyperoxia. Nine healthy subjects inhaled hydrocarbon-free air (HCFA) for 30 minutes, hydrocarbon-free 100% O2 (HCFO2) for 125 minutes and then HCFA for 70 minutes. After 15 minutes of washout with HCFA, ambient pentane was eliminated. After HCFO2, at T175 versus T30 (i.e., 145 min from the start of 100% HCFO2), pentane production increased (P< 0.05). MDA rose significantly at T155 min (i.e., 125 min from the start of HCFO2), versus T30 (P< 0.01). These results suggest that acute hyperoxia causes a moderate increase in lipid peroxidation in healthy subjects. The increase of pentane and MDA confirms that acute hyperoxia induces lipid peroxidation in healthy subjects.

Aged↗
PubMed2000

Breath alkanes as a marker of oxidative stress in different clinical conditions.

We assessed oxidative stress in three different clinical conditions: smoking, human immunodeficiency virus (HIV) infection, and inflammatory bowel disease, using breath alkane output and other lipid peroxidation parameters such as plasma lipid peroxides (LPO) and malondialdehyde (MDA). Antioxidant micronutrients such as selenium, vitamin E, C, beta-carotene and carotenoids were also measured. Lipid peroxidation was significantly higher and antioxidant vitamins significantly lower in smokers compared to nonsmokers. Beta-carotene or vitamin E supplementation significantly reduced lipid peroxidation in that population. However, vitamin C supplementation had no effect. In HIV-infected subjects, lipid peroxidation parameters were also elevated and antioxidant vitamins reduced compared to seronegative controls. Vitamin E and C supplementation resulted in a significant decrease in lipid peroxidation with a trend toward a reduction in viral load. In patients with inflammatory bowel disease, breath alkane output was also significantly elevated when compared to healthy controls. A trial with vitamin E and C is underway. In conclusion, breath alkane output, plasma LPO and MDA are elevated in certain clinical conditions such as smoking, HIV infection, and inflammatory bowel disease. This is associated with lower levels of antioxidant micronutrients. Supplementation with antioxidant vitamins significantly reduced these lipid peroxidation parameters. The results suggest that these measures are good markers for lipid peroxidation.

Alkanes↗
PubMed1999

Clinical application of breath biomarkers of oxidative stress status.

Isolation and quantification of volatile breath biomarkers indicative of relevant alterations in clinical status has required development of new techniques and applications of existing analytical chemical methods. The most significant obstacles to successful application of this type of sample have been reduction in required sample volume permitting replicate analysis (an absolute requirement for all clinical studies), separation of the analyte(s) of interest from background molecules, water vapor and other molecules with similar physical properties, introduction of automation in analysis and the use of selective detection systems (electron impact mass spectrometry, flame photometric, thermionic detectors), and automated sample collection from the human subject. Advances in adsorption technology and trace gas analysis have permitted rapid progress in this area of clinical chemistry.

Animals↗
PubMed2000

Methods for measuring ethane and pentane in expired air from rats and humans.

Numerous studies in animals and humans provide evidence that ethane and pentane in expired air are useful markers of in vivo lipid peroxidation. The measurement of breath hydrocarbons, being noninvasive, is well suited for routine use in research and clinical settings. However, the lack of standardized methods for collecting, processing, and analyzing expired air has resulted in the use of a wide variety of different methods that have yielded highly disparate results among investigators. This review outlines the methods that we have developed and validated for measuring ethane and pentane in expired air from rats and humans. We describe the advantages of these methods, their performance, as well as potential errors that can be introduced during sample collection, concentration, and analysis. A main source of error involves contamination with ambient-air ethane and pentane, the concentrations of which are usually much greater and more variable than those in expired air. Thus, it appears that the effective removal of ambient-air hydrocarbons from the subject's lungs before collection is an important step in standardizing the collection procedure. Also discussed is whether ethane or pentane is a better marker of in vivo lipid peroxidation.

Animals↗
PubMed1998

[Exhale nitric oxide (NO) and respiratory function measured with body plethysmography in children].

BACKGROUND: Exhaled nitric oxide (NO) may be a marker of airway inflammation. Previous studies in adults have shown that the level of NO in exhaled air is influenced by several factors (breath holding, exercise, etc), or by several disease (asthma, congestive heart failure, diseases of the upper respiratory tract, cystic fibrosis, etc). However, few studies have been performed in children less than 3 years of age. The aim of this study was to determine endogenous NO levels in children with various diseases during lung volume measurements. PATIENTS AND METHODS: Fifty-two children aged 18.3 +/- 9.5 months were studied. The population was divided in two groups, according to the underlying disease: a group of 39 children with cystic fibrosis (n = 7), bronchopulmonary dysplasia (n = 17), asthma (n = 7) or recurrent respiratory tract infections (n = 8) and a second group of 13 children without respiratory disease. Lung function was measured by whole body plethysmography and several respiratory parameters were calculated (functional residual capacity [FRC], compliance and resistances of the respiratory system, trapped volume). NO production was measured on a chemiluminescence analyzer from mixed exhaled air collected into a bag, over a period of 5 minutes. RESULTS: NO production was related to disease: exhaled NO levels were three times higher in bronchopulmonary dysplasia and cystic fibrosis, compared to NO levels in children without respiratory disease. They were higher in asthma. They were not altered in recurrent respiratory tract infections. No correlation was found between respiratory parameters and NO production. However, exhaled NO levels were correlated to trapped volume, which defined dynamic part of pulmonary hyperinflation. CONCLUSION: Levels of endogenous NO in infants were similar to those measured in adults with and without inflammatory respiratory disease. Lung distention influenced exhaled NO production.

Biomarkers↗
PubMed2003

Exhaled breath condensate acidification in acute lung injury.

Lung injury in ventilated lungs may occur due to local or systemic disease and is usually caused by or accompanied by inflammatory processes. Recently, acidification of exhaled breath condensate pH (EBC-pH) has been suggested as marker of inflammation in airway disease. We investigated pH, ammonia, Lactate, pCO2, HCO3-, IL-6 and IL-8 in EBC of 35 ventilated patients (AECC-classification: ARDS: 15, ALI: 12, no lung injury: 8). EBC-pH was decreased in ventilated patients compared to volunteers (5.85 +/- 0.32 vs. 7.46 +/- 0.48; P < 0.0001). NH4+, lactate, HCO3-, pCO2, IL-6 and IL-8 were analyzed in EBC and correlated with EBC-pH. We observed correlations of EBC-pH with markers of local (EBC IL-6: r = -0.71, P < 0.0001, EBC IL-8: r = -0.68, P < 0.0001) but not of systemic inflammation (serum IL-6, serum IL-8) and with indices of severity of lung injury (Murray's Lung Injury Severity Score; r = -0.73, P < 0.0001, paO2/FiO2; r = 0.54, P < 0.001). Among factors potentially contributing to pH of EBC, EBC-lactate and EBC-NH4+ were found to correlate with EBC-pH. Inflammation-induced disturbances of regulatory mechanisms, such as glutaminase systems may result in EBC acidification. EBC-pH is suggested to represent a marker of acute lung injury caused by or accompanied by pulmonary inflammation.

Acute Disease↗
PubMed1998

Exhaled nitric oxide; relationship to clinicophysiological markers of asthma severity.

Bronchial asthma is an airway disorder associated with bronchial hyperresponsiveness, variable airflow obstruction and elevated levels of nitric oxide (NO) in exhaled air. The variables all reflect, in part, the underlying airway inflammation in this disease. To understand their interrelationships we have investigated the relationship between exhaled NO levels and clinicophysiological markers of asthma severity. Twenty-six steroid naive atopic asthmatics participated in the analysis. All were given diary cards and were asked to record their peak expiratory flow (PEF) rates twice daily together with their asthma symptom scores and beta-agonist use. Diary cards were collected 2 weeks later and measurements of exhaled NO levels, FEV1 and histamine bronchial hyperreactivity (PC20 histamine) were undertaken. Exhaled NO levels were significantly higher in our study population than in normal control subjects and correlated negatively with PC20 histamine (r = -0.51; P = 0.008) and positively with PEF diurnal variability (r = 0.58; P = 0.002), but not with symptom scores, beta-agonist use of FEV1 (%). We conclude that a significant relationship exists between exhaled NO levels and the two characteristic features and markers of asthma severity, namely bronchial hyperreactivity and PEF diurnal variability. The lack of correlation between symptom score and beta-agonist use, of FEV1 (%) predicted and exhaled NO suggests that these measures are reflective of differing aspects of asthma.

Adolescent↗