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Bernard Aguilaniu

Publications and source records attributed to Bernard Aguilaniu.

6 recordsLinked to original sources
PubMed2007

Air trapping in mild and moderate asthma: effect of inhaled corticosteroids.

BACKGROUND: Air trapping reflects small airway obstruction in asthma and can be assessed quantitatively by high-resolution computed tomography (HRCT). Hydrofluoroalkane-beclomethasone dipropionate (HFA-BDP) is deposited across all sizes of airways, including the small ones. However, its long-term effect on air trapping remains unknown in uncontrolled asthma. OBJECTIVES: To compare the effect of inhaled corticosteroids of different particle size - HFA-BDP and fluticasone propionate (FP) - on lung attenuation in mild-to-moderate uncontrolled asthma. METHODS: A randomized study was performed to analyze the effect of HFA-BDP (400 microg/d) or FP (500 microg/d) given over a period of 3 months to patients with uncontrolled mild-to-moderate asthma. HRCT was performed with spirometric gating, and lung attenuation was measured at residual volume and at pulmonary total capacity. The difference between inspiratory and expiratory attenuation was calculated as an air trapping index. RESULTS: Twenty-five out of 58 patients had abnormal air trapping and could be included in the study. Lung attenuation significantly diminished in the posterior zones of the lung after a 3-month treatment with HFA-BDP or FP, but the difference between the groups was not significant. Adjusted mean variations of the air trapping index from baseline to treatment completion were 34.3 (11.2, 57.3) and 27.3 (6.4, 48.2) for the HFA-BDP and FP groups, respectively. However, the reduction of air trapping area was more pronounced in the group treated with HFA-BDP. CONCLUSION: Inhaled corticosteroids decrease air trapping in uncontrolled asthma regardless of their particle size. CLINICAL IMPLICATIONS: In mild-to-moderate asthma, air trapping assessed by HRCT may be a new outcome related to the control of the disease.

Administration, Inhalation↗
PubMed2006

Stage-related changes in functional capacity in Hodgkin's disease: assessment by cardiopulmonary exercise testing before initiation of treatment.

Our aim was to examine indices of cardiorespiratory capacity at rest and during exercise before initiation of therapy for Hodgkin's disease. We prospectively studied 24 patients divided into two groups according to the disease stage. Group 1 included eight patients in stage IA and four in stage IIA; group 2 included four patients in stage IIB, six in stage III, and two in stage IV. All patients underwent detailed cardiopulmonary evaluations at rest using electrocardiogram, echocardiogram, spirometry, and measurement of pulmonary diffusing capacity (DLCO), and during exercise using a cardiopulmonary exercise test. Groups 1 and 2 were similar with respect to sex distribution (eight women and four men in each), mean age (35+/-36 vs37+/-4.6 years), body mass index, and hemoglobin concentration (12.7+/-0.2 vs 12.1+/-0.3 g l-1). All patients had a normal cardiovascular status. All patients in group 1 had normal cardiorespiratory measurements at rest and during exercise. Forced vital capacity was significantly lower in group 2 (84.8+/-2.7% predicted) than in group 1 (105+/-3%, P<0.0001), without abnormalities in DLCO or in resting and exercise oxygen diffusion. Likewise, percentage predicted VO2max (65+/-4 vs 97+/-6, P<0.0002), oxygen pulse at peak exercise (0.12+/-0.01 vs 0.17+/-0.01, P<0.001), and DeltaVO2/DeltaW slope (8.4+/-0.3 vs 10.2+/-0.4, P<0.003) were significantly lower in group 2 than in group 1. Functional capacity during exercise was markedly reduced in patients suffering from Hodgkin's disease in advanced stages. This loss of exercise capacity appeared mainly related to a peripheral disorder.

Adult↗
PubMed2006

Bicarbonate infusion and pH clamp moderately reduce hyperventilation during ramp exercise in humans.

To test the hypothesis that the decrease in plasma pH contributes to the hyperventilation observed in humans in response to exercise at high workloads, five healthy male subjects performed a ramp exercise [maximal workload: 352 W (SD 35)] in a control situation and when arterialized plasma pH was maintained at the resting level (pH clamp) by intravenous infusion of sodium bicarbonate [129 mmol (SD 23), beginning at 59% maximal workload (SD 5)]. Bicarbonate infusion did not modify O(2) consumption (Vo(2)) but significantly (P < 0.05) increased arterial Pco(2), plasma bicarbonate concentration, and respiratory exchange ratio (P < 0.05). At the three highest workloads, pulmonary ventilation (Ve) and Ve/Vo(2) were approximately 5-10% lower (P < 0.05) when bicarbonate was infused than in the control situation, and hyperventilation was reduced by 15-30%. These data suggest that the decrease in plasma pH is one of the factors that contribute to the hyperventilation observed at high workloads.

Acid-Base Equilibrium↗
PubMed2006

Lactic acid buffering, nonmetabolic CO2 and exercise hyperventilation: a critical reappraisal.

It has been suggested that hyperventilation and the disproportionate increase in VCO2 versus VO2 above the ventilatory threshold (V(TH)) in ramp exercise are due to the production of nonmetabolic CO2 in muscle because of lactic acid buffering by plasma bicarbonate entering the cell in exchange with lactate [Wasserman, K., 1982. Dyspnea on exertion. Is it the heart or the lungs? JAMA 248, 2039-2043]. According to this model, plasma standard bicarbonate concentration decreases in a approximately 1:1 ratio with the increase in plasma lactate concentration, 1 mmol of CO2 is generated above that produced by aerobic metabolism for each mmol of lactic acid buffered, and nonmetabolic CO2 produced in the muscle is partly responsible for hyperventilation because of the resulting increase in the CO2 flow to the lungs. The present report shows that this model is not consistent with experimental data: (1) bicarbonate is not the main buffer in the muscle; (2) the decrease in standard bicarbonate concentration is not the mirror image of the increase in lactate concentration; (3) buffering by bicarbonate does not increase CO2 production in muscle (no nonmetabolic CO2 is produced in tissues); (4) the CO2 flow to the lungs, which should not be confused with VCO2 at the mouth, does not increase at a faster rate above than below V(TH). The disproportionate increase in VCO2 at the mouth above V(TH) is due to hyperventilation (not the reverse) and to the low plasma pH which both reduce the pool of bicarbonate readily available in the body.

Acid-Base Equilibrium↗
PubMed2002

Impaired exercise response in sarcoid patients with normal pulmonary functio.

BACKGROUND AND AIM OF THE WORK: Sarcoidosis is a granulomatous disease with frequent pul monary involvement. Patients generally exhibit a 25-30% reduction in maximal aerobic capacit (VO2max). As most investigations have included patients with both normal and abnormal resting pulmonary function tests (PFT), the mechanisms responsible for this limitation remain unclear. We initiated a prospective study to characterize the cardio-respiratory response to exercise in sarcoid patients with normal resting PFT. METHODS: 19 untreated male patients with biopsy-proven sarcoidosis and 19 age- an sex-matched sedentary healthy controls (38 +/- 8.7 vs 37 +/- 8.7 yrs ; Body Mass Index: 24 +/- 3.05 vs 23 +/- 3.05) were included in the study. All patients had normal resting PFT including diffusing capacity for CO (DLCO) > 80% predicted and normal cardiac status at rest as assessed by EKG and echocardiography. A maximal cycling test was performed in all subjects. RESULTS: True maximal effort was obtaine in all subjects (plasma lactate 9.1 +/- 2.6 vs 11.0 +/- 2.2 mmol l(-1), pH 7.35 +/- 0.04 vs 7.34 +/- 0.04) (patients vs controls). Patients exhibited a 30% lower maximal workload and/or VO2max (2,128 +/- 413 vs 2,909 +/- 387 ml x min(-1)) than controls. Maximal ventilation (79 +/- 21.7 vs 110 +/- 21.7 l x min(-1)) and tital volume (VT) (2,313 +/- 517 ml vs 2,856 +/- 339) were significantly lower in patients than in controls while dead space t tital volume ratio (VD/V(T)) (0.18 +/- 0.09 vs 0.11 +/- 0.04) was higher in patients than in controls. PaO2, PAiO2, and PAi-aO2 at VO2max were not significantly different between patient and controls. Peak exercise EKG was normal in all but one patient. Interestingly, heart rate was significantly lower in patients for all relative exercise intensities > or = 60% VO2max including maximum (159 +/- 21.7 vs 182 +/- 13) CONCLUSION: The present observations indicate a significant maximal exercise limitation in sarcoid patients without significant pulmonary impairment which could be related at least in part to an impaired heart rate response to exercise.

Adult↗