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Diffusing Capacity (diffusing + capacity)
Selected AbstractsPulmonary diffusion and aerobic capacity: is there a relation?ACTA PHYSIOLOGICA, Issue 4 2010Does obesity matter? Abstract Aim:, We sought to determine whether pulmonary diffusing capacity for nitric oxide (DLNO), carbon monoxide (DLCO) and pulmonary capillary blood volume (Vc) at rest predict peak aerobic capacity (O2peak), and if so, to discern which measure predicts better. Methods:, Thirty-five individuals with extreme obesity (body mass index or BMI = 50 ± 8 kg m,2) and 26 fit, non-obese subjects (BMI = 23 ± 2 kg m,2) participated. DLNO and DLCO at rest were first measured. Then, subjects performed a graded exercise test on a cycle ergometer to determine O2peak. Multivariate regression was used to assess relations in the data. Results:, Findings indicate that (i) pulmonary diffusion at rest predicts O2peak in the fit and obese when measured with DLNO, but only in the fit when measured with DLCO; (ii) the observed relation between pulmonary diffusion at rest and O2peak is different in the fit and obese; (iii) DLNO explains O2peak better than DLCO or Vc. The findings imply the following reference equations for DLNO: O2peak (mL kg,1 min,1) = 6.81 + 0.27 × DLNO for fit individuals; O2peak (mL kg,1 min,1) = 6.81 + 0.06 × DLNO, for obese individuals (in both groups, adjusted R2 = 0.92; RMSE = 5.58). Conclusion:, Pulmonary diffusion at rest predicts O2peak, although a relation exists for obese subjects only when DLNO is used, and the magnitude of the relation depends on gender when either DLCO or Vc is used. We recommend DLNO as a measure of pulmonary diffusion, both for its ease of collection as well as its tighter relation with O2peak. [source] Decline of neuroadrenergic bronchial innervation and respiratory function in type 1 diabetes mellitus: a longitudinal studyDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 4 2007Raffaele Antonelli Incalzi Abstract Background and aim Type 1 diabetes mellitus complicated by autonomic neuropathy (AN) is characterized by depressed cholinergic bronchomotor tone and neuroadrenergic denervation of the lung. We explored the effects of AN on the rate of decline of pulmonary sympathetic innervation and respiratory function during a 5-year follow-up. Methods Twenty diabetic patients, 11 with AN, were enrolled in 1998 and then followed-up until 2003. During follow-up, glycosylated haemoglobin (HbA1c) was measured every 3 months. In 1998 and 2003 the patients underwent respiratory function tests and a ventilatory scintigraphic study of neuroadrenergic bronchial innervation using 123I-MIBG. Results During follow-up 4 patients, all with AN, were lost, and 1 developed AN. Forced vital capacity (FVC), and diffusing capacity of the lung for carbon monoxide (DLCO) showed comparable rates of decrease in patients with and without AN. The yearly decline of forced expiratory volume in 1 s (FEV1) was about double the physiologic rate, in both AN and AN-free patients. The MIBG clearance significantly increased both in patients with AN (T1/2: 118.88 ± 30.14 min at baseline and 92.10 ± 24.52 min at the end of follow-up) and without AN (135.14 ± 17.09 min and 92.68 ± 13.52 min, respectively), indicating a rapidly progressive neuroadrenergic denervation. The rate of the neuroadrenergic denervation was inversely related to the severity of autonomic dysfunction at baseline (Spearman's rho , 0.62, p = 0.017). Neither respiratory function indexes nor MIBG clearance changes correlated with the overall HbA1c values. Conclusions Neuroadrenergic denervation of the lung parallels the decline of respiratory function indexes in diabetic patients both with and without AN and seems to be independent from the quality of glycemic control. Copyright © 2006 John Wiley & Sons, Ltd. [source] Pulmonary gas exchange abnormalities in liver transplant candidatesLIVER TRANSPLANTATION, Issue 9 2002Rosmawati Mohamed Abnormal diffusing capacity is the commonest pulmonary dysfunction in liver transplant candidates, but severe hypoxemia secondary to hepatopulmonary syndrome and significant pulmonary hypertension are pulmonary vascular manifestations of cirrhosis that may affect the perioperative course. We prospectively assessed the extent of pulmonary dysfunction in patients referred for liver transplantation. A total of 57 consecutive patients with chronic liver disease were evaluated. All patients had a chest radiograph, standing arterial blood gas on room air, pulmonary function testing, and Doppler echocardiogram. Those patients with arterial hypoxaemia (PaO2 < 10 kPa) also underwent 99mTc-macroaggregated albumin lung scan, and nine patients had agitated normal saline injection during echocardiography to define further the existence of pulmonary vascular dilatation. Reduced diffusing capacity for carbon monoxide less than 75% of the predicted value was found in 29 of 57 (51%) patients. Although elevated alveolar-arterial oxygen tension difference was detected in 35% (20/57) of the patients, only four (7%) patients had hypoxemia. We were unable to find evidence of intrapulmonary vascular dilatation either on the lung scan or saline-enhanced echocardiography in any of these patients. Reduction in diffusing capacity for carbon monoxide was noted in 75% (18/24) of patients who were transplanted for primary biliary cirrhosis and was accompanied by widened alveolar-arterial oxygen tension in 10 out of 18 (56%) of patients. This study shows that in liver transplant candidates, diffusion impairment and widened alveolar-arterial oxygen tension difference were frequently detected, especially in patients with primary biliary cirrhosis. [source] Dynamic oxygen-enhanced MRI reflects diffusing capacity of the lungMAGNETIC RESONANCE IN MEDICINE, Issue 6 2002Yoshiharu Ohno Abstract The purpose of this study was to demonstrate the feasibility of dynamic oxygen-enhanced MRI in a clinical setting. We hypothesized that dynamic oxygen enhancement can reflect the regional diffusing capacity of the lung. Ten patients with pulmonary emphysema and seven healthy volunteers were examined with a respiratory-synchronized inversion recovery single-shot turbo spin-echo sequence (TR = 3200,5000 ms, TE = 16 ms, TI = 720 ms, ETS = 4 ms) following 100% oxygen inhalation, using a 1.5 T whole-body scanner. Maximum mean relative enhancement ratios calculated by averaging six defined regions of interest (ROIs) in both lungs were statistically compared between healthy volunteers and patients, and were correlated with diffusing lung capacity (%DLCO). In patients with pulmonary emphysema, maximum mean relative enhancement ratios were significantly decreased compared to those in healthy volunteers (P = 0.0008). Maximum mean relative enhancement ratio had excellent correlation with % DLC0 (r2 = 0.83). Dynamic oxygen-enhanced MRI may reflect the diffusing capacity of the lung; therefore, imaging of oxygen enhancement with MRI may provide maps of the diffusing capacity. Magn Reson Med 47:1139,1144, 2002. © 2002 Wiley-Liss, Inc. [source] Alveolar and bronchial nitric oxide output in healthy childrenPEDIATRIC PULMONOLOGY, Issue 12 2008Anna Sepponen MD Abstract Exhaled nitric oxide (NO) concentration is a marker of pulmonary inflammation. It is usually measured at a single exhalation flow rate. However, measuring exhaled NO at multiple flow rates allows assessment of the flow-independent NO parameters: alveolar NO concentration, bronchial NO flux, bronchial wall NO concentration, and bronchial diffusing capacity of NO. Our aim was to determine the flow-independent NO parameters in healthy schoolchildren and to compare two different mathematical approaches. Exhaled NO was measured at four flow rates (10, 50, 100, and 200 ml/sec) in 253 schoolchildren (7,13 years old). Flow-independent NO parameters were calculated with linear method (flows ,50 ml/sec) and non-linear method (all flows). Sixty-six children (32 boys and 34 girls) with normal spirometry and no history or present symptoms of asthma, allergy, atopy or other diseases were included in the analysis. Median bronchial NO flux was 0.4 nl/sec (mean,±,SD: 0.5,±,0.3 nl/sec) and median alveolar NO concentration was 1.9 ppb (2.0,±,0.8 ppb) with the linear method. Bronchial NO flux correlated positively with height (r,=,0.423; P,<,0.001), FEV1 (r,=,0.358; P,=,0.003), and FVC (r,=,0.359; P,=,0.003). With the non-linear method, median bronchial wall NO concentration was 49.6 ppb (68.0,±,53.3 ppb) and bronchial diffusing capacity of NO was 10.0 pl/sec/ppb (11.8,±,7.5 pl/sec/ppb). The non-linear method gave lower alveolar NO concentration (1.4 [1.5,±,0.7] ppb, P,<,0.001) and higher bronchial NO flux (0.5 [0.6,±,0.3] nl/sec, P,<,0.001) than the linear method, but the results were highly correlated between the two methods (r,=,0.854 and r,=,0.971, P,<,0.001). In conclusion, the multiple flow rate method is feasible in children but different mathematical methods give slightly different results. Reference values in healthy children are of value when applying bronchial and alveolar NO parameters in the diagnostics and follow-up of inflammatory lung diseases. Pediatr. Pulmonol. 2008; 43:1242,1248. © 2008 Wiley-Liss, Inc. [source] Comparison of carbon monoxide (CO) single breath pulmonary diffusing capacity with non-rebreathing, open-circuit CO pulmonary diffusing capacity in healthy childrenPEDIATRIC PULMONOLOGY, Issue 11 2006Oscar E. Suman PhD Abstract Introduction The standard technique for assessing pulmonary diffusing capacity of the lungs (DL) for carbon monoxide (CO) is the single breath (SB) technique. SB_DLco in children can be problematic because it requires a vital capacity >1.5 L. We have developed an open-circuit technique (OC), which uses the wash-in of CO over a series of 8,10 normal breaths that does not require rebreathing. In this study, we compared the SB_DLco against the OC_DLco. Methods Nineteen healthy children between 7 and 18 years performed SB_DLco and OC_DLco tests. The mean SB_DLco was significantly larger than the mean OC_DLco. The mean difference OC_DLco minus SB_ DLco was: ,2.92,±,4.21 ml/min/mm,Hg, though the difference was negatively correlated with the mean of the two (r,=,0.73). The lower mean OC_DLco was in part due to lower lung volume (as measured by alveolar volume (VA)) during the maneuver. In both groups there was a positive correlation between VA and DLco, and the mean VA was ,2.17,±,1.07 L lower using OC compared to SB. The difference was again negatively correlated with the mean (r,=,0.82). The mean OC minus SB difference in DLco/VA was: 6.06,±,1.98 ml/min/mm,Hg/L, though this difference was positively correlated with the mean, r,=,0.76. Conclusions We found a good correlation between both techniques for DLco, VA, and DLco/VA. The OC offers the advantage of minimal subject cooperation, and may be preferable to use in children. Pediatr Pulmonol. 2006, 41:1095,1102. © 2006 Wiley-Liss, Inc. [source] Relationship between induced sputum cytology and inflammatory status with lung structural and functional abnormalities in asbestosisAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 3 2008José Henrique Setta MD Abstract Background Asbestosis is associated with lung cellular and immunological abnormalities. Induced sputum cytology and local and systemic markers of inflammation may be helpful to characterize disease status and progression in these patients. Methods Thirty-nine ex-workers with asbestosis on high-resolution CT (HRCT) and 21 non-exposed controls were evaluated. Sputum cytology and IL-8 in serum and sputum were related to lung function impairment. Results Subjects with asbestosis had reduced sputum cellularity but higher macrophage/neutrophil ratio and % macrophage as compared with controls. Sputum and serum IL-8 were also higher in patients with asbestosis (P,<,0.05). In addition, evidence of lung architectural distorption on HRCT was associated with increased levels of serum IL-8. Interestingly, absolute macrophage number was negatively correlated with total lung capacity (r,=,,0.40; P,=,0.04) and serum IL-8 to lung diffusing capacity (r,=,,0.45; P,=,0.01). Conclusions Occupationally exposed subjects with asbestosis on HRCT have cytologic abnormalities in induced sputum and increased local and systemic pro-inflammatory status which are correlated to functional impairment. Am. J. Ind. Med. 51:186,194, 2008. © 2008 Wiley-Liss, Inc. [source] Adverse effects of asbestos exposure and smoking on lung functionAMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 5 2006Xiaorong Wang MD Abstract Background Exposure to asbestos is a well-recognized cause of both malignant and nonmalignant diseases of lung parenchyma and pleura. This study was conducted to determine the adverse effects of exposure to asbestos and smoking on pulmonary function. Methods Four hundred and sixty-eight workers who were occupationally exposed to asbestos for an average of 13 years were selected from an asbestos-product factory in China. Of them, 85 workers were diagnosed with asbestosis. Additionally, 282 workers who had no experience of exposure to industrial dust were included as a control group. A questionnaire was administered during a face-to-face interview and spirometric maneuvers and single-breath CO diffusing capacity (DLco) were performed. Results Multivariate regression analysis showed that exposure to asbestos was more strongly associated with decreased forced vital capacity (FVC) and DLco, and asbestosis more strongly associated with decreased FVC, while smoking was a major contributing factor to reduced FEV1/FVC. The results were confirmed by a further analysis where the subjects were grouped exclusively by smoking, asbestos exposure, and chest radiographic changes. No interaction or joint effect was observed between asbestos exposure and smoking. Conclusions This analysis suggested that asbestos and smoking might play independent roles, in which asbestos caused mainly a restrictive impairment, and smoking was a major causal factor for airway obstruction in the workers who were intensively exposed to asbestos. Am. J. Ind. Med. 49:337,342, 2006. © 2006 Wiley-Liss, Inc. [source] Normative reference values for lung transfer factor in Isfahan, IranRESPIROLOGY, Issue 4 2006Babak AMRA Objectives and background: Transfer factor or carbon monoxide diffusing capacity (DLCO) is a particularly valuable test of the appropriateness of gas exchange across the alveolocapillary membrane. The purpose of this study is to derive predictive equations for DLCO and its derivative volume-corrected DLCO (DLCO/VA) measured by single-breath method in a large non-smoking population sample in Isfahan. Methodology: We evaluated 1429 randomly selected subjects (732 men, aged 5,85 years). Gender-specific linear prediction equations were developed by multiple regression analysis; with measured DLCO, and DLCO/VA values (mmol/min/kPa), as dependent variables regressed against age (A), height (H) and body surface area (BSA). Results: For both genders, age had negative effects on DLCO, while height had a positive effect on DLCO and DLCO/VA (P < 0.01). The prediction equations for DLCO and DLCO/VA are: ,0.152 × height , 0.056 × age , 11.595' and ,,0.12 × age + 2.467', for men and: ,,0.035 × age , 0.133 × height , 10.707' and ,,0.012 × age , 0.02 × height + 2.755', for women, respectively. Conclusions: Our results therefore provide an original frame of reference for either DLCO or DLCO/VA in Iranian population, obtained from a standardized single-breath technique. [source] Hepatopulmonary syndrome associated with autoimmune liver cirrhosisRESPIROLOGY, Issue 2 2001Nobukazu Takada A 46-year-old woman presented for evaluation of liver dysfunction and dyspnoea. Laboratory examination showed high levels of ,-globulin, immunoglobulin (Ig)G, and antinuclear antibodies. Laparoscopy demonstrated hepatic cirrhosis. Despite normal spirometry, hypoxaemia (which was worse in standing position) and a low diffusing capacity were present. The shunt ratio calculated using arterial blood gas was 6.4%, but was 40% when measured using 99mTc-macroaggregated albumin scanning. The discrepancy between the ratios indicated that hypoxaemia was caused by intrapulmonary vascular dilatation. The patient was diagnosed with hepatopulmonary syndrome associated with autoimmune liver cirrhosis. [source] Disproportional effects of Igf2 knockout on placental morphology and diffusional exchange characteristics in the mouseTHE JOURNAL OF PHYSIOLOGY, Issue 20 2008P. M. Coan Both complete knockout of the Igf2 gene (Igf2null+/,) and knockout of its placental specific transcript alone (Igf2P0+/,) lead to fetal growth restriction in mice. However, in the Igf2null+/, this growth restriction occurs concurrently in gestation with placental growth restriction, whereas, placental growth restriction precedes fetal growth restriction in the Igf2P0+/, mouse. Previous studies have shown that the Igf2P0+/, placenta has proportionate reductions in its cellular compartments and its diffusional exchange characteristics. Yet, nothing is known about the structural development or diffusional exchange characteristics of the Igf2null+/, mouse. Hence, this study compares the structural properties (using stereology) and diffusional exchange characteristics (using measurement of permeability,surface area product, P.S, of three inert hydrophilic tracers) of the Igf2null+/, and the Igf2P0+/, placenta to identify the role of Igf2 in the development of the labyrinthine exchange membrane and its functional consequences. Our data show disproportionate effects of complete Igf2 ablation on the compartments of the placenta, not seen when the placental-specific transcript alone is deleted. Furthermore, although the theoretical diffusing capacity (calculated from the stereological data) of the Igf2null+/, placenta was reduced relative to control, there was no effect of the complete knockout on permeability surface area available for small hydrophilic tracers. This is in contrast to the Igf2P0+/, placenta, where theoretical diffusion capacity and P.S values were reduced similarly. Total ablation of the Igf2 gene from the fetoplacental unit in the mouse therefore results in a disproportionate growth of placental compartments whereas, deleting the placental specific transcript of Igf2 alone results in proportional placental growth restriction. Thus, placental phenotype depends on the degree of Igf2 gene ablation and the interplay between placental and fetal Igf2 in the mouse. [source] Randomized, prospective, placebo-controlled trial of bosentan in interstitial lung disease secondary to systemic sclerosis,ARTHRITIS & RHEUMATISM, Issue 7 2010J. R. Seibold Objective Endothelin is implicated as a participatory pathway in systemic sclerosis (SSc). We tested this hypothesis in a 12-month trial of bosentan, a nonselective endothelin receptor antagonist, as a therapy for SSc-related interstitial lung disease (ILD). Method Patients with SSc and significant ILD were recruited to this prospective, double-blind, randomized, placebo-controlled, parallel group study. The inclusion criteria were designed to select a cohort enriched for patients with active and progressive disease. Exclusion factors included significant pulmonary hypertension. Patients with a diffusing capacity for carbon monoxide of <80% predicted and a 6-minute walk distance of 150,500 meters or a 6-minute walk distance of ,500 meters with a decrease in oxygen saturation received bosentan or placebo. The primary efficacy end point was a change in the 6-minute walk distance from baseline up to month 12. Secondary end points included time to death or worsening results of pulmonary function tests (PFTs). The safety and tolerability of bosentan were also assessed. Results Among the 163 patients, 77 were randomized to receive bosentan, and 86 were randomized to receive placebo. No significant difference between treatment groups was observed for change in the 6-minute walk distance up to month 12. No deaths occurred in this study group. Forced vital capacity and diffusing capacity for carbon monoxide remained stable in the majority of patients in both groups. Significant worsening of PFT results occurred in 25.6% of patients receiving placebo and 22.5% of those receiving bosentan (P not significant). Conclusion No improvement in exercise capacity was observed in the bosentan-treated group compared with the placebo group, and no significant treatment effect was observed for the other end points. Although many outcome variables were stable, bosentan did not reduce the frequency of clinically important worsening. These data do not support the use of endothelin receptor antagonists as therapy for ILD secondary to SSc. [source] High N-terminal pro,brain natriuretic peptide levels and low diffusing capacity for carbon monoxide as independent predictors of the occurrence of precapillary pulmonary arterial hypertension in patients with systemic sclerosisARTHRITIS & RHEUMATISM, Issue 1 2008Y. Allanore Objective To evaluate predictors of pulmonary arterial hypertension (PAH) in a prospective cohort of patients with systemic sclerosis (SSc). Methods Routine clinical assessments as well as measurements of the diffusing capacity for carbon monoxide/alveolar volume (DLCO/VA) ratio and N-terminal pro,brain natriuretic peptide (NT-proBNP) level were performed in a prospective cohort of 101 SSc patients who did not have PAH or severe comorbidities. After a planned 36-month followup, we evaluated the predictive value of these parameters for the development of precapillary PAH, as demonstrated by cardiac catheterization, disease progression, and death. Criteria for cardiac catheterization were a systolic pulmonary artery pressure (PAP) of >40 mm Hg on echocardiography, a DLCO value of <50% without pulmonary fibrosis, and unexplained dyspnea. Results Eight patients developed PAH, 29 had disease progression, and 10 died during a median followup of 29 months. Kaplan-Meier analysis identified the following baseline parameters as being predictors of PAH: DLCO/VA ratio <70% or <60% (P < 0.01 for each comparison), elevated plasma NT-proBNP level (>97th percentile of normal; P = 0.005), echocardiographically estimated systolic PAP >40 mm Hg (P = 0.08), and erythrocyte sedimentation rate >28 mm/hour (P = 0.015). In multivariate analyses, an elevated baseline NT-proBNP level (hazard ratio [HR] 9.97 [95% confidence interval (95% CI) 1.69,62.42]) and a DLCO/VA ratio <60% (HR 36.66 [95% CI 3.45,387.6]) were predictors of the occurrence of PAH during followup. An increased NT-proBNP level together with a decreased DLCO/VA ratio of <70% was highly predictive of the occurrence of PAH during followup (HR 47.20 [95% CI 4.90,450.33]). Conclusion This prospective study identified a decreased DLCO/VA ratio and an increased NT-proBNP as predictors of PAH in SSc. Use of these markers should result in improved PAH risk stratification and allow earlier initiation of therapy. [source] Influence of long-term cigarette smoking on immunoglobulin E-mediated allergy, pulmonary function, and high-resolution computed tomography lung densitometry in elderly patients with asthmaCLINICAL & EXPERIMENTAL ALLERGY, Issue 1 2004F. Mitsunobu Summary Background Smoking is the most important cause of chronic obstructive pulmonary disease (COPD). However, the influence of cigarette smoking on the pathogenesis of asthma in the elderly remains controversial. This study attempted to clarify the influence of cigarette smoking on elderly asthmatics. Methods Forty-eight asthmatics over 70 years old (25 ex-smokers and 23 never-smokers) and 20 patients with COPD over 70 years old (all ex-smokers) were studied to determine the influence of cigarette smoking on IgE-mediated allergy (total IgE, IgE antibodies against inhalant allergens, bronchial hyper-responsiveness (BHR), generation of leukotriene (LT) B4 and C4), pulmonary function, and the relative area of lung showing attenuation values less than ,950 Hounsfield units (RA950) on high-resolution computed tomography scans. Results The incidence of positive IgE antibodies against inhalant allergens, BHR, and the generation of leukotriene B4 (LTB4) by leucocytes were significantly increased in patients with a history of smoking compared with those without. Residual volume (%RV) was significantly increased, and diffusing capacity for carbon monoxide was significantly decreased in ex-smokers with asthma and COPD compared with never-smokers with asthma. Inspiratory RA950 and ratio of expiratory RA950 to inspiratory RA950 were significantly larger in asthmatics with a smoking history than in those without, and in COPD patients than in asthmatics. Conclusion Cigarette smoking enhances the production of IgE antibodies, BHR, and generation of LTB4 by leucocytes in elderly asthmatics. Increased hyper-inflation or emphysematous changes of the lungs expressed by increased RA950, closely related to %RV, was more frequently observed in ex-smokers compared with never-smokers. [source] Anti-topoisomerase II , autoantibodies in systemic sclerosis,association with pulmonary hypertension and HLA-B35CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2000B. Grigolo We have previously detected autoantibodies against topoisomerase II , (anti-topo II ,) in sera from patients with idiopathic pulmonary fibrosis. To determine whether anti-topo II , is also present in systemic sclerosis (SSc) patients with pulmonary involvement, we screened sera from 92 patients and 34 healthy controls. Presence of anti-topo II , was investigated with respect to clinical and serological features, including the frequencies of HLA class I and II alleles. Anti-topo II , was detected in 20/92 (21.7%) patients. No association was found with either anti-topoisomerase I (Scl-70 or anti-topo I) or anti-centromere antibodies. However, anti-topo II , was associated with the presence of pulmonary hypertension (PHT) (as opposed to pulmonary fibrosis), and with a decrease of carbon monoxide diffusing capacity. Anti-topo II , was strongly associated with the presence of the class I antigen HLA-B35. No significant association was found with HLA class II antigens. HLA-B35 also turned out to be associated with the presence of PHT. These results indicate that in SSc patients, the presence of anti-topo II , is associated with PHT, and that the simultaneous presence of HLA-B35 seems to add to the risk of developing PHT. [source] | |||||||||||||