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PubMed2006

Comparative metabolism and disposition of trichloroethylene in Cyp2e1-/-and wild-type mice.

Trichloroethylene (TCE)1 is an important environmental contaminant, a well established rodent carcinogen, and a "probable human carcinogen". Metabolism of TCE occurs primarily via cytochrome P450 (P450)-dependent oxidation. In vitro studies suggested that CYP2E1 is the principal high-affinity enzyme responsible for TCE metabolism. The objective of the present work is to more directly assess the role of CYP2E1 in the metabolism and disposition of 1,2-14C-TCE administered at 250 or 1000 mg/kg (gavage) using Cyp2e1-/-[knockout (KO)] versus wild-type (WT) mice. After dosing, animals were individually placed in glass metabolism cages that allowed the collection of expired air, urine, and feces. Exhalation of TCE-derived 14CO2 increased in a dose-dependent manner in mice of both genotypes and was significantly higher in WT versus KO mice. A significantly greater percentage of the dose was exhaled in KO versus WT mice as organic volatiles (mainly as TCE). Urinary excretion was the major route of TCE metabolism in WT mice, and the percentage of dose eliminated in urine was significantly higher at the 250 versus 1000 mg/kg dose. Furthermore, urinary excretion and CO2 exhalation significantly decreased in KO versus WT mice. Pretreatment with 1-aminobenzotriazole clearly inhibited TCE metabolism as evident from increased exhalation of parent TCE, and decreased urinary excretion and CO2 exhalation in mice of both genotypes. In conclusion, these data showed that whereas CYP2E1 plays an important role in TCE metabolism and disposition, other P450s also play a significant role and may explain earlier results showing that TCE causes lung damage in KO and WT mice.

Animals↗
PubMed1993

Dynamic pulmonary CT: findings in healthy adult men.

The authors examined 10 healthy male subjects with dynamic computed tomography to determine normal dynamic and expiratory findings. In both the supine and prone positions, the average increase in lung attenuation during exhalation was found to be significantly greater in dependent lung regions than in nondependent lung regions. In each of the lung zones studied, there was a significant correlation between the decrease in cross-sectional lung area during exhalation and the increase in lung attenuation. At the lung bases, a greater increase in lung attenuation was noted during exhalation for a given change in cross-sectional lung area than in the upper lungs. All 10 subjects showed a distinct lobar attenuation gradient in the supine position. In general, lung attenuation increased homogeneously during exhalation, but four of the 10 subjects showed regions of inhomogeneity in lung attenuation during rapid exhalation indicative of air trapping, despite normal results on pulmonary function tests.

Adult↗
PubMed1995

Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs.

Nitric oxide generation and hypoxic vasoconstriction in buffer-perfused rabbit lungs. J. Appl. Physiol. 78(4): 1509-1515, 1995.--We investigated the role of nitric oxide (NO) generation in hypoxic pulmonary vasoconstriction in buffer-perfused rabbit lungs. Exhaled NO was detected by chemiluminescence, and intravascular NO release was quantified as perfusate accumulation of nitrite, peroxynitrite, and nitrate (NOx). Under baseline conditions, exhaled NO was 45.3 +/- 4.1 parts per billion (1.8 +/- 0.2 nmol/min), and lung NOx release into the perfusate was 4.1 +/- 0.4 nmol/min. Alveolar hypoxia (alveolar PO2 of approximately 23 Torr) induced readily reproducible pressor responses preceded by a sharp drop in exhaled NO concentration. In contrast, perfusate NOx accumulation was not affected. Vasoconstrictor responses to U-46619 and angiotensin II were not accompanied by a decrease in NO exhalation. NG-monomethyl-L-arginine dose-dependently suppressed NO exhalation and amplified pressor responses to hypoxia > U-46619 and angiotensin II. In conclusion, portions of baseline NO generation originating from sites with ready access to the gaseous space sharply decrease in response to alveolar hypoxia, whereas the intravascular release of NO is unchanged. Such differential regulation of lung NO synthesis in response to hypoxia may suggest a complex role in the regulation or modulation of hypoxic pulmonary vasoconstriction.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2004

Modeling pulmonary nitric oxide exchange.

Nitric oxide (NO) was first detected in the exhaled breath more than a decade ago and has since been investigated as a noninvasive means of assessing lung inflammation. Exhaled NO arises from the airway and alveolar compartments, and new analytical methods have been developed to characterize these sources. A simple two-compartment model can adequately represent many of the observed experimental observations of exhaled concentration, including the marked dependence on exhalation flow rate. The model characterizes NO exchange by using three flow-independent exchange parameters. Two of the parameters describe the airway compartment (airway NO diffusing capacity and either the maximum airway wall NO flux or the airway wall NO concentration), and the third parameter describes the alveolar region (steady-state alveolar NO concentration). A potential advantage of the two-compartment model is the ability to partition exhaled NO into an airway and alveolar source and thus improve the specificity of detecting altered NO exchange dynamics that differentially impact these regions of the lungs. Several analytical techniques have been developed to estimate the flow-independent parameters in both health and disease. Future studies will focus on improving our fundamental understanding of NO exchange dynamics, the analytical techniques used to characterize NO exchange dynamics, as well as the physiological interpretation and the clinical relevance of the flow-independent parameters.

Animals↗
PubMed2006

Airway nitric oxide release is reduced after PBS inhalation in asthma.

Exhaled nitric oxide (NO) is elevated in asthma, but the underlying mechanisms remain poorly understood. Recent results in subjects with asthma have reported a decrease in exhaled breath pH and ammonia, as well as altered expression and activity of glutaminase in both alveolar and airway epithelial cells. This suggests that pH-dependent nitrite conversion to NO may be a source of exhaled NO in the asthmatic airway epithelium. However, the anatomic location (i.e., airway or alveolar region) of this pH-dependent NO release has not been investigated and could impact potential therapeutic strategies. We quantified airway (proximal) and alveolar (peripheral) contributions to exhaled NO at baseline and then after PBS inhalation in stable (mild-intermittent to severe) asthmatic subjects (20-44 yr old; n = 9) and healthy controls (22-41 yr old; n = 6). The mean (SD) maximum airway wall flux (pl/s) and alveolar concentration (ppb) at baseline in asthma subjects and healthy controls was 2,530 (2,572) and 5.42 (7.31) and 1,703 (1,567) and 1.88 (1.29), respectively. Compared with baseline, there is a significant decrease in the airway wall flux of NO in asthma as early as 15 min and continuing for up to 60 min (maximum -28% at 45 min) after PBS inhalation without alteration of alveolar concentration. Healthy control subjects did not display any changes in exhaled NO. We conclude that elevated airway NO at baseline in asthma is reduced by inhaled PBS. Thus airway NO may be, in part, due to nitrite conversion to NO and is consistent with airway pH dysregulation in asthma.

Administration, Inhalation↗
PubMed2005

Vascular endothelial dysfunction and mortality risk in patients with chronic heart failure.

BACKGROUND: Endothelial function is known to be impaired in subjects with chronic heart failure (CHF), but the association between endothelial function and subsequent mortality risk in CHF has not been previously reported. METHODS AND RESULTS: Biomarkers of endothelial function in the systemic arterial circulation (flow-mediated dilation [FMD] in the brachial artery) and the pulmonary circulation (exhaled nitric oxide [NO] production during submaximal exercise) were prospectively assessed in 259 subjects with New York Heart Association class II-III CHF. In subjects with FMD measurements (n=149), there were 12 deaths and 5 urgent transplantations over a median follow-up period of 841 days. In subjects with exhaled NO production measurements (n=110), there were 18 deaths and 1 urgent transplantation over a median follow-up period of 396 days. Both decreased FMD and decreased exhaled NO production were associated with increased risk of death or urgent transplantation after adjustment for other known CHF prognostic factors (age, etiology of CHF, functional class, left ventricular ejection fraction) in Cox multivariate proportional-hazards models (adjusted hazard ratio [HR] estimate for a 1% decrease in FMD=1.20; 95% confidence interval [CI], 1.03 to 1.45; P=0.027; adjusted HR estimate for a 1-ppb/min decrease in exhaled NO production=1.31, 95% CI, 1.01 to 1.69, P=0.04). CONCLUSIONS: Endothelial dysfunction in CHF, as assessed by FMD in the brachial artery and exhaled NO production during submaximal exercise, is associated with an increased mortality risk in subjects with both ischemic and nonischemic CHF.

Biomarkers↗
PubMed1995

Effect of preinspiratory maneuver on the single-breath DLCO.

We have observed in some patients with pulmonary disease and normal subjects that the difference between two successive measurements for single-breath DLCO amounted to 10%. By scrutinizing data from these subjects, we observed that they spontaneously changed their preinspiratory maneuver just before inhaling the test gas mixture. The purpose of the present work is to assess the influence of five different preinspiratory maneuvers on DLCO. Nine healthy males were investigated. They performed at random the five following maneuvers: (A) rapid exhalation from functional residual capacity (FRC) to residual volume (RV), (B) rapid exhalation from FRC to RV and long apnea at RV, (C) rapid exhalation from FRC to RV and short apnea at RV, (D) slow exhalation at a constant speed from FRC to RV, and (E) curvilinear exhalation from FRC to RV. The DLCO values after maneuver B were higher than those after the four other maneuvers; there was a significant relationship between DLCO and the duration of the preinspiratory maneuver. The data are best explained by an alteration in the distribution of the inspired gas mixture to areas with different diffusing capacities. In conclusion, the preinspiratory maneuvers must be standardized in order to improve the reproducibility of the single-breath DLCO measurements.

Adult↗
PubMed2003

Multiple single-breath measurements of nitric oxide in the intubated patient.

Multiple flow rate measurements of exhaled nitric oxide (NO) have been advocated to fractionate NO from alveolar and bronchial sources. The aim of this study was to develop a method by which multiple single-breath exhalations at various flow rates could be performed in intubated, mechanically ventilated patients. Nine patients without lung disease were studied awake and after intubation, during general anesthesia. A suction ejection system connected to a restrictor valve was used to control the exhalation flow rate. From these measurements the fraction of alveolar NO (FANO), the fraction of airway wall NO (FawNO), and the airway wall transfer rate (DNO) were calculated. The fraction of exhaled NO was reduced by 50% after intubation. DNO was also reduced by intubation (from 10 +/- 1.3 to 6.4 +/- 2.1 nl second(-1) ppb(-1) x 10(-3)) whereas neither FawNO nor FANO was affected. The peak NO concentration after 20 seconds of apnea during general anesthesia was similar to calculated FawNO. The vacuum aspiration method used in this study allowed for reproducible multiple single-breath measurements and calculation of alveolar and bronchial NO parameters. Further studies will reveal whether this methodology will improve the value of exhaled NO analysis in intubated, mechanically ventilated patients with pulmonary disease.

Adult↗
PubMed2006

Longitudinal monitoring of lung injury in children after acute chlorine exposure in a swimming pool.

RATIONALE: Acute exposure to chlorine gas results in respiratory impairment, but few data are available on the pathobiology of the underlying lung damage. OBJECTIVES: To assess lung function and potential lung damage pathways in the acute phase and longitudinally over a 15-mo follow-up after acute chlorine exposure. METHODS: Ten previously healthy children were accidentally exposed to chlorine gas at a swimming pool because of an erroneous servicing procedure. The fraction of nitric oxide in exhaled air (Fe(NO)), exhaled breath condensate compounds, and serum Clara cell-specific protein CC16 were repeatedly measured. MAIN RESULTS: In the acute phase, all patients had respiratory distress (one child required mechanical ventilation) and reduced lung function (median and interquartile range: FVC, 51 [43-60]% predicted; FEV(1), 51 [46-60]% predicted). This was accompanied by low Fe(NO) (4.7 [3.9-7.9] ppb), high exhaled breath condensate leukotriene B(4) (LTB(4)) levels (24.4 [22.5-24.9] pg/ml), and increased serum CC16 levels (mean +/- SEM, 23.4 +/- 2.5 microg/L). Lung function returned to normal in 15 d (FVC, 97% predicted [82-108], and FEV(1), 92% predicted [77-102]). Fe(NO) reached normal values after 2 mo (12.6 [11.4-15] ppb), whereas LTB(4) levels were still increased (12 [9.3-17.1] pg/ml). CONCLUSION: Children acutely exposed to chlorine in a swimming pool presented a substantial lung function impairment associated with biochemical exhaled breath alterations, represented mainly by an increase in LTB(4) and a reduction in Fe(NO). Although lung function and Fe(NO) improved within a few weeks, the increased levels of exhaled LTB(4) persisted for several months.

Accidents↗
PubMedDate not supplied

Non-invasive assessment of airway inflammation in ship-engine workers.

Smoking is harmful for respiratory function. In young to middle-aged men the damage is insidious and difficult to demonstrate. The respiratory impairment could increase under specific stressful conditions in the professional environment. On the hypothesis that exhaled markers are useful for assessing airway susceptibility to inhaled irritants, we measured exhaled markers and lung function in smoking and non-smoking engine-driver military coastguards before and after a patrol at sea. Eighteen men, mean age 39 yrs (range 23-58 yrs), 8 smokers, underwent spirometry, exhaled and nasal nitric oxide (eNO, nNO), exhaled carbon monoxide (CO) and exhaled breath condensate (EBC) for measures of hydrogen peroxide (H2O2), leukotriene B4 (LTB4), proteins (Prots), 8-isoprostanes (8-IsoPs), nitrite (NO2-) and nitrosothiols (RS-NOs) at baseline and after an 8-hour patrol navigation on board small, high-speed diesel-powered ships. At baseline, the smokers showed higher middle flows and CO levels, lower eNO and nNO than non-smokers, but similar levels of EBC markers; geometric means (95% confidence interval), CO: 23.6 (14.5 to 38.3) vs. 3.5 (2.5 to 5.3) ppm; eNO: 7.9 (4.8 to 12.9) vs. 26.7 (15.7 to 45.5) ppb, p=0.000. After navigation, Prots, 8-IsoPs and RS-NOs (but not lung function variables or other markers) significantly increased only in smokers; baseline vs post-navigation RS-NOs: 0.27 (0.11 to 0.65) vs. 1.30 (0.58 to 2.89) micromol, p=0.012. The respiratory consequences of a stressing environment in engine-driver military coastguards who actively smoke are better assessed by measuring EBC markers than by eNO, nNO or lung function. By increasing airway inflammation from oxidative-stress, tobacco smoking appears to interact with other chemical or physical factors elicited during sea navigation. Precisely what these factors are deserves further investigation.

Adult↗
PubMed2006

Diagnostic accuracy of canine scent detection in early- and late-stage lung and breast cancers.

BACKGROUND: Lung and breast cancers are leading causes of cancer death worldwide. Prior exploratory work has shown that patterns of biochemical markers have been found in the exhaled breath of patients with lung and breast cancers that are distinguishable from those of controls. However, chemical analysis of exhaled breath has not shown suitability for individual clinical diagnosis. METHODS: The authors used a food reward-based method of training 5 ordinary household dogs to distinguish, by scent alone, exhaled breath samples of 55 lung and 31 breast cancer patients from those of 83 healthy controls. A correct indication of cancer samples by the dogs was sitting/lying in front of the sample. A correct response to control samples was to ignore the sample. The authors first trained the dogs in a 3-phase sequential process with gradually increasing levels of challenge. Once trained, the dogs' ability to distinguish cancer patients from controls was then tested using breath samples from subjects not previously encountered by the dogs. The researchers blinded both dog handlers and experimental observers to the identity of breath samples. The diagnostic accuracy data reported were obtained solely from the dogs' sniffing, in double-blinded conditions, of these breath samples obtained from subjects not previously encountered by the dogs during the training period. RESULTS: Among lung cancer patients and controls, overall sensitivity of canine scent detection compared to biopsy-confirmed conventional diagnosis was 0.99 (95% confidence interval [CI], 0.99, 1.00) and overall specificity 0.99 (95% CI, 0.96, 1.00). Among breast cancer patients and controls, sensitivity was 0.88 (95% CI, 0.75, 1.00) and specificity 0.98 (95% CI, 0.90, 0.99). Sensitivity and specificity were remarkably similar across all 4 stages of both diseases. CONCLUSION: Training was efficient and cancer identification was accurate; in a matter of weeks, ordinary household dogs with only basic behavioral "puppy training" were trained to accurately distinguish breath samples of lung and breast cancer patients from those of controls. This pilot work using canine scent detection demonstrates the validity of using a biological system to examine exhaled breath in the diagnostic identification of lung and breast cancers. Future work should closely examine the chemistry of exhaled breath to identify which chemical compounds can most accurately identify the presence of cancer.

Animals↗
PubMed2001

Inhaled fluticasone decreases bronchial but not alveolar nitric oxide output in asthma.

Exhaled nitric oxide (NO) concentration is a noninvasive measure of airway inflammation and is increased in asthma. Inhaled glucocorticoids decrease exhaled NO concentration, but the relative contributions of alveolar and bronchial levels to the decrease in exhaled NO concentration are unknown. Alveolar NO concentration and bronchial NO flux can be separately approximated by measuring exhaled NO at several exhalation flow rates. The effect of steroid treatment on alveolar and bronchial NO output in asthma was studied. Alveolar NO concentration and bronchial NO flux were assessed in 16 patients with asthma before and during treatment with inhaled fluticasone for 8 weeks and in 16 healthy controls. Before the treatment, asthmatics had increased bronchial NO flux (mean+/-SEM: 3.6+/-0.4 versus 0.7+/-0.1 nL x s(-1), p<0.001) but normal alveolar NO concentration (1.2+/-0.5 versus 1.0+/-0.2 parts per billion (ppb), p>0.05) compared with controls. Inhaled fluticasone decreased bronchial NO flux from 3.6+/-0.4 to 0.7+/-0.1 nL x s(-1) (p<0.01) but had no effect on alveolar NO concentration (before: 1.2+/-0.5; after: 1.2+/-0.1 ppb, p>0.05). The forced expiratory volume in one second improved, whereas asthma symptom score and serum levels of eosinophil cationic protein and eosinophil protein X decreased during the treatment. In conclusion, inhaled fluticasone decreases bronchial but not alveolar nitric oxide output simultaneously with clinical improvement in patients with asthma.

Administration, Inhalation↗
PubMed2002

Nitric oxide but not carbon monoxide is continuously released in the human nasal airways.

Results from different laboratories indicate that nitric oxide (NO) and carbon monoxide (CO) coexist in the human airways both in health and disease. These gases are present in exhaled human breath and high concentrations of NO as well as CO have been reported in the nasal airways. In addition, exhaled CO and NO are increased in patients with airways inflammation. NO and CO were measured simultaneously in orally exhaled air and in air sampled from the nose in 18 healthy subjects using chemiluminescence (for NO) and infrared (for CO) techniques at different fixed flow rates. The acute effects of smoking on airway release of NO and CO were also studied. Nasal NO was detected in all subjects and the concentrations were highly flow-dependent (mean+/-SEM: 236+/-23 and 527+/-49 parts per billion (ppb), at 2 and 0.5 L x min(-1), respectively). In contrast, no evidence of CO release in the nasal airways regardless of sample flow rate was found. In fact, additional experiments indicated a net absorption of CO when low levels of this gas were flushed through the nasal cavity. Nasal CO also remained undetectable after smoking. Both NO (22+/-2 ppb) and CO (1.1+/-0.1 parts per million) were consistently found in orally exhaled air. CO, but not NO, levels increased acutely after smoking a cigarette. The authors conclude that the patterns of nitric oxide and carbon monoxide release in the airways seem to differ profoundly in healthy subjects. Orally exhaled air contains both nitric oxide and carbon dioxide whereas nasal air contains nitric oxide only.

Adult↗
PubMed2003

Increased eNO and pulmonary iNOS expression in eNOS null mice.

Nitric oxide (NO) is a major regulatory molecule of the cardiovascular system; however, measurement of vascular NO synthesis in vivo represents a major challenge. NO stemming from the lower respiratory tract has been used as a marker of vascular endothelial function. Experimental evidence for this concept is lacking. Therefore, the aim of the present study was to investigate this relationship. Lower respiratory tract exhaled NO concentration, together with systemic and pulmonary artery pressure, was measured in endothelial nitric oxide synthase (NOS) (eNOS) null mice (eNOS-/-). Similar studies were performed in inducible NOS (iNOS) null mice (iNOS-/-). Defective endothelial NO synthesis in eNOS-/- mice (evidenced by systemic and pulmonary hypertension) was associated with augmented exhaled NO levels (12.5 +/- 1.9 versus 9.8 +/- 1.2 parts per billion (ppb), eNOS-/- versus wild type), whereas normal endothelial NO synthesis in iNOS-/- mice was associated with decreased exhaled NO levels (4.3 +/- 1.5 ppb). Augmented exhaled NO levels in eNOS-/- mice were associated with upregulation of iNOS expression in the lung. These results indicate that inducible nitric oxide synthase is a major determinant of gaseous nitric oxide production in the lung, and lower respiratory tract exhaled nitric oxide does not always represent a marker of vascular endothelial nitric oxide synthesis.

Animals↗
PubMed1992

Time dependence of lung mechanics in preterm lambs.

The passive exhalation flow-volume plots of preterm lambs exhibit curvature. To explain this curvature, we proposed two mathematical models that could predict the measured passive exhalation flow-volume data well. One model takes into account the flow and volume dependence of resistance and compliance. The second model emphasizes the time dependence of lung mechanics and considers the respiratory system viscoelastic properties and the analogy of the lung to two electronic resistor-capacitor circuits connected in parallel. We attempted to determine which of the two models is more valid by analyzing passive exhalation flow-volume data that were obtained while briefly obstructing flow midway through deflation. In 14 preterm lambs (130 d gestation), the flow of exhaled gas increased from 76 +/- 35 mL/s when measured just before obstruction to 90 +/- 30 mL/s when measured immediately after release of the obstruction (p less than 0.0001). This finding suggests that a time-dependent phenomenon was taking place during obstruction and is inconsistent with the model based upon the flow and volume dependence of resistance and compliance. We made similar measurements in four near-term (143-146 d gestation) and four full-term lambs (9-12 d of age). Their flow-volume curves were relatively linear, and they showed no increases in flow after removal of the obstruction. The results of this study strongly suggest that time-dependent phenomena caused the curvilinearity in the passive exhalation flow-volume plots of preterm lambs. We suspect that the time-dependent phenomena is associated with the premature lung and with parenchymal lung disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed2003

Nitric oxide airway diffusing capacity and mucosal concentration in asthmatic schoolchildren.

Asthmatic patients show increased concentrations of nitric oxide (NO) in exhaled air (Feno). The diffusing capacity of NO in the airways (Dawno), the NO concentrations in the alveoli and the airway wall, and the maximal airway NO diffusion rate have previously been estimated noninvasively by measuring Feno at different exhalation flow rates in adults. We investigated these variables in 15 asthmatic schoolchildren (8-18 y) and 15 age-matched control subjects, with focus on their relation to exhaled NO at the recommended exhalation flow rate of 0.05 L/s (Feno0.05), age, and volume of the respiratory anatomic dead space. NO was measured on-line by chemiluminescence according to the European Respiratory Society's guidelines, and the NO plateau values at three different exhalation flow rates (11, 99, and 382 mL/s) were incorporated in a two-compartment model for NO diffusion. The NO concentration in the airway wall (p < 0.001), Dawno (p < 0.01), and the maximal airway NO diffusion rate (p < 0.001) were all higher in the asthmatic children than in control children. In contrast, there was no difference in the NO concentration in the alveoli (p = 0.13) between the groups. A positive correlation was seen between the volume of the respiratory anatomic dead space and Feno0.05 (r = 0.68, p < 0.01), the maximal airway NO diffusion rate (r = 0.71, p < 0.01), and Dawno (r = 0.56, p < 0.01) in control children, but not in asthmatic children. Feno0.05 correlated better with Dawno in asthmatic children (r = 0.65, p < 0.01) and with the NO concentration in the airway wall in control subjects (r < 0.77, p < 0.001) than vice versa. We conclude that Feno0.05 increases with increasing volume of the respiratory anatomic dead space in healthy children, suggesting that normal values for Feno0.05 should be related to age or body weight in this age group. Furthermore, the elevated Feno0.05 seen in asthmatic children is related to an increase in both Dawno and NO concentration in the airway wall. Because Dawno correlates with the volume of the respiratory anatomic dead space in control subjects and Feno0.05 correlates with Dawno in asthmatic children, we suggest that Dawno partly reflects the total NO-producing surface area and that a larger part of the bronchial tree produces NO in asthmatic children than in control children.

Adolescent↗
PubMed1998

Mechanics of lung ventilation in a large aquatic salamander, siren lacertina

Lung ventilation in Siren lacertina was studied using X-ray video, measurements of body cavity pressure and electromyography of hypaxial muscles. S. lacertina utilizes a two-stroke buccal pump in which mixing of expired and inspired gas is minimized by partial expansion of the buccal cavity during exhalation and then full expansion after exhalation is complete. Mixing is further reduced by the use of one or two accessory inspirations after the first, mixed-gas cycle. Exhalation occurs in two phases: a passive phase in which hydrostatic pressure and possibly lung elasticity force air out of the lungs, and an active phase in which contraction of the transverse abdominis (TA) muscle increases body cavity pressure and forces most of the remaining air out. In electromyograms of the lateral hypaxial musculature, the TA became active 200-400 ms before the rise in body cavity pressure, and activity ceased at peak pressure. The TA was not active during inspiration, and no consistent activity during breathing was noted in the external oblique, internal oblique and rectus abdominis muscles. The finding that the TA is the primary expiratory muscle in S. lacertina agrees with findings in a previous study of another salamander, Necturus maculosus. Together, these results indicate that the use of the TA for exhalation is a primitive character for salamanders and support the hypothesis that the breathing mechanism of salamanders represents an intermediate step in evolution between a buccal pump, in which only head muscles are used for ventilation, and an aspiration pump, in which axial muscles are used for both exhalation and inhalation.

Journal Article↗
PubMed1998

Respiratory nitric oxide levels in experimental human influenza.

BACKGROUND: Exhaled oral nitric oxide (NO), a reported marker of inflammation in the respiratory tract, can be elevated by "upper respiratory tract infections." However, the responsible viruses and the time course of this rise in NO are not clear. OBJECTIVE: To determine the expired nasal and oral NO levels during experimentally induced influenza A infection in 14 healthy volunteers without a history of asthma, rhinitis, or sinusitis. METHODS: After being housed in individual rooms, susceptible volunteers were inoculated with 10(6) 50% tissue culture infective dose of influenza A/Texas/36/91/(H1N1) virus on a single occasion by intranasal drops. Volunteers remained in the isolation unit for 8 days and returned for follow-up 21 days after inoculation. Symptom scores and nasal washing for viral culture were obtained daily. NO samples from the mouth and nose were obtained on days 0 through 4, 8, and 21 by having the patient perform a slow vital capacity maneuver through a plastic tube into a Mylar balloon. RESULTS: All patients had influenza virus cultured from nasal washings (12 of 14 on day 1, 14 of 14 by day 5). Patient symptom scores peaked on day 3 (mean+/-SE; 15.4+/-3.2) and returned to baseline by day 8. Preinfection exhaled nasal NO (right, 28.4+/-3.7 parts per billion [ppb]; left, 27.7+/-4.6 ppb) was significantly higher than oral NO (5.8 ppb; p<0.001). Exhaled oral NO was significantly elevated on day 8 postinoculation (12.9+/-0.8 ppb; p<0.01 Bonferroni) and returned to baseline at follow-up. Nasal NO levels showed a slight decrease on days 2 to 4 but returned to baseline by day 8. CONCLUSION: Experimental influenza virus infection can increase oral but not nasal exhaled NO levels. The timing of exhaled NO changes suggests that NO does not contribute to illness manifestations directly.

Adolescent↗