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Diffusing capacity of the lung for nitric oxide (), otherwise known as the transfer factor, was first measured in 1983. This document standardises the technique and application of single-breath This panel agrees that 1) pulmonary function systems should allow for mixing and measurement of both nitric oxide (NO) and carbon monoxide (CO) gases directly from an inspiratory reservoir just before use, with expired concentrations measured from an alveolar "collection" or continuously sampled rapid gas analysers; 2) breath-hold time should be 10 s with chemiluminescence NO analysers, or 4-6 s to accommodate the smaller detection range of the NO electrochemical cell; 3) inspired NO and oxygen concentrations should be 40-60 ppm and close to 21%, respectively; 4) the alveolar oxygen tension ( ) should be measured by sampling the expired gas; 5) a finite specific conductance in the blood for NO (θNO) should be assumed as 4.5 mL·min·mmHg·mL of blood; 6) the equation for 1/θCO should be (0.0062· +1.16)·(ideal haemoglobin/measured haemoglobin) based on breath-holding and adjusted to an average haemoglobin concentration (male 14.6 g·dL, female 13.4 g·dL); 7) a membrane diffusing capacity ratio (/) should be 1.97, based on tissue diffusivity.

The aim of the present study was to calculate reference equations for carbon monoxide and nitric oxide transfer, measured in two distinct populations.The transfer factor of the lung for nitric oxide (TL,NO) and carbon monoxide (TL,CO) were measured in 303 people aged 18-94 yrs. Measurements were similarly made in two distant cities, using the single-breath technique. Capillary lung volume (Vc) and membrane conductance, the diffusing capacity of the membrane (Dm), for carbon monoxide (Dm,CO) were derived.The transfer of both gases appeared to depend upon age, height, sex and localisation. The rate of decrease in both transfers increased after the age of 59 yrs. TL,NO/alveolar volume (VA) and TL,CO/VA were only age-dependent. The mean TL,NO/TL,CO was 4.75 and the mean Dm/Vc was 6.17 min ; these parameters were independent of any covariate. Vc and Dm,CO calculations depend upon the choice of coefficients included in the Roughton-Forster equation. Values of 1.97 for Dm,NO/Dm,CO ratio and 12.86 min?kPa -1 for 1/red cell CO conductance are recommended.The scatter of transfer reference values in the literature, including the current study, is wide. The present results suggest that differences might be due to the populations themselves and not the methods alone.KEYWORDS: Ageing, capillary lung volume, carbon monoxide, diffusion, nitric oxide, pollution T he measurement of the transfer of gases through the lung is one of the few tests aimed at investigating alveolar function. The 1957 model and equation of ROUGHTON and FORSTER [1] permitted the transfer of carbon monoxide through the aveolocapillary structure to be split into two resistances, one for the alveolar membrane (1/membrane conductance, the diffusing capacity of the membrane (Dm), for carbon monoxide (Dm,CO)) and the other for the blood reacting with the gas (1/HCOVc), where HCO is the red cell conductance at a concentration, set by the pioneers of the method, of 14.9 g?dL -1 [2] and Vc the capillary lung volume:where TL,CO is the transfer factor of the lung for carbon monoxide. The first technique used to solve this equation with two unknowns, Dm and Vc, was to measure two transfers of CO, one under conditions of normoxia the other under hyperoxia. Breathing O 2 , by reducing HCO, lowers the TL,CO. GUENARD et al.[3] first published measurements of Dm and Vc using transfer factor of the lung for nitric oxide (TL,NO) and TL,CO and assuming HNO to be infinity, i.e. TL,NO5Dm,NO.The transfer of CO is dependant upon both Dm and Vc with HCO as a finite value.The relationship between Dm for nitric oxide (Dm,NO) and Dm,CO introduces a constant a: Dm,NO5aDm,CO. Therefore, the measurement of NO transfer alone permits the calculation of Dm,CO and, by introducing the latter into the CO transfer equation, of Vc.Most published reference values for Dm and Vc have been derived from the first two-step technique; one used the NO/CO method in a population of 127 healthy adults with a mean¡SD age of ,40¡12 yrs [4] and another focused on NO transfer in a population of 1...

The phosphodiesterase-5 inhibitor sildenafil has been reported to improve hypoxic exercise capacity, but the mechanisms accounting for this observation remain incompletely understood. Sixteen healthy subjects were included in a randomized, double-blind, placebo-controlled, cross-over study on the effects of 50-mg sildenafil on echocardiographic indexes of the pulmonary circulation and on cardiopulmonary cycle exercise in normoxia, in acute normobaric hypoxia (fraction of inspired O2, 0.1), and then again after 2 weeks of acclimatization at 5000 m on Mount Chimborazo (Ecuador). In normoxia, sildenafil had no effect on maximum VO2 or O2 saturation. In acute hypoxia, sildenafil increased maximum VO2 from 27 +/- 5 to 32 +/- 6 mL/min/kg and O2 saturation from 62% +/- 6% to 68% +/- 9%. In chronic hypoxia, sildenafil did not affect maximum VO2 or O2 saturation. Resting mean pulmonary artery pressure increased from 16 +/- 3 mmHg in normoxia to 28 +/- 5 mmHg in normobaric hypoxia and 32 +/- 6 mmHg in hypobaric hypoxia. Sildenafil decreased pulmonary vascular resistance by 30% to 50% in these different conditions. We conclude that sildenafil increases exercise capacity in acute normobaric hypoxia and that this is explained by improved arterial oxygenation, rather than by a decrease in right ventricular afterload.