Biomedical subjects

Tony G Babb

Publications and source records attributed to Tony G Babb.

4 recordsLinked to original sources

PubMed2006

The confounding effects of thoracic gas compression on measurement of acute bronchodilator response.

RATIONALE: Improvement in FEV(1) is a main endpoint in clinical trials assessing the efficacy of bronchodilators. However, the effect of bronchodilators on maximal expiratory flow may be confounded by thoracic gas compression (TGC). OBJECTIVE: To determine whether TGC confounds effect of albuterol on FEV(1). METHODS: We evaluated the response to albuterol inhalation in 10 healthy subjects, 9 subjects with asthma, and 15 subjects with chronic obstructive pulmonary disease (COPD) with mean (SD) age in years of 38 (SD, 11), 45 (SD, 11), and 64 (SD, 8), respectively. Lung mechanics were measured at baseline and 20 minutes after inhalation of 180 micro g of albuterol. We then applied a novel method to calculate FEV(1) corrected for the effect of TGC (NFEV(1)). RESULTS: Prior to albuterol administration, NFEV(1) was significantly higher than FEV(1). However, post-albuterol inhalation, FEV(1) increased more than NFEV(1) because of reduced TGC. In multiple regression analysis, the changes in TGC, inspiratory lung resistance, and ratio of residual volume to total lung capacity postalbuterol predicted more than 75% of FEV(1) improvement in patients with COPD. CONCLUSION: Improvements in FEV(1) after albuterol in patients with COPD are due to reduction of lung resistance, hyperinflation, and TGC. The latter is negligible during tidal breathing. Thus, although reduction of lung resistance and hyperinflation may result in improved dyspnea with a bronchodilator, the contribution of TGC reduction to improvement of FEV(1) may not exert any meaningful clinical effect during tidal breathing. This fact has to be taken into consideration when assessing the efficacy of new bronchodilators.

Adult↗

PubMed2006

Layers of exercise hyperpnea: modulation and plasticity.

Despite the fundamental biological significance of the ventilatory response to mild or moderate physical activity (the exercise hyperpnea), we still know remarkably little concerning its underlying mechanisms. Part of the difficulty in revealing those mechanisms may arise due to confusion between multiple mechanistic layers, each contributing to the impressive degree of regulation achieved. The primary, feedforward exercise stimulus or stimuli increase ventilation in approximate proportion to changes in metabolic rate. Chemoreceptor feedback then minimizes deviations from optimal blood gas regulation, most often preventing excessive hypocapnia in non-human mammals. Recent evidence has accumulated, suggesting that adaptive control strategies including modulation and plasticity may adjust the feedforward and/or feedback contributions when blood gas homeostasis proves inadequate. In this review, we present evidence from a goat model of exercise hyperpnea concerning the existence of modulation and plasticity, and specifically mechanisms known as short-term and long-term modulation of the exercise ventilatory response. Throughout the review, we consider available evidence concerning the relevance of these mechanisms to humans. Plasticity is a property only recently recognized in the neural system subserving respiratory control, and the application of these concepts to the exercise ventilatory response in humans is in its infancy. Modulation and plasticity may confer an ability of individuals to adapt their exercise ventilatory response so that it remains appropriate in the face of life-long changes in endogenous (e.g. development, aging, onset of disease) or exogenous (e.g. altitude, wearing a breathing apparatus during physical exertion) physiological conditions.

Adaptation, Physiological↗

PubMed2006

Urine acid-base compensation at simulated moderate altitude.

Acute exposure to high altitude elicits respiratory alkalosis, and this is partially corrected by renal compensation. To determine the time course and magnitude of renal compensation during short-term moderate altitude exposure, we measured urine gas tensions and acid-base status in 48 healthy men and women at four levels of simulated altitude exposures. Each subject was exposed in pseudorandom order to simulated altitudes of 1780, 2085, 2455, and 2800 m in a decompression chamber for 24 h, separated by 1 week at sea level. Fresh urine was collected anaerobically at sea level and after 6 and 24 h of each altitude exposure. Urine pH increased significantly (p < 0.01) after 6 h at all altitudes and returned to baseline values by 24 h at the lowest altitudes. In contrast, urine pH remained elevated at the highest altitudes. The mean value of urine HCO at sea level was 1.67 +/- 0.25 mmol/L, increased significantly after 6 h at all altitudes, and then returned to near baseline after 24 h at three lower altitudes (1780, 2085, and 2455 m). However, it remained elevated at 2800 m. PCO2 in urine was significantly increased after 6 h and returned to baseline after 24 h at all altitudes. These results suggest that (1) short-term low to moderate altitude exposure results in a marked HCO diuresis, which may be caused by inhibition of the secretion of renal tubular H+, and (2) renal HCO compensation was completed by 24 h at low to moderate altitude, but still incomplete at higher altitude.

Acid-Base Equilibrium↗

PubMed2003

Obesity: associations with acute mountain sickness.

BACKGROUND: Although few retrospective studies of high altitude have reported that obesity might be associated with the development of acute mountain sickness (AMS), this association has not been studied prospectively. OBJECTIVE: To determine whether obesity is associated with the development of AMS. DESIGN: Obese and nonobese men were compared at a simulated altitude of 3658 m (12 000 ft). SETTING: 24 hours in a hypobaric environmental chamber. PARTICIPANTS: 9 obese and 10 nonobese men. MEASUREMENTS: Percentage body fat (by hydrostatic weighing), Lake Louise AMS score, and Sao2 level (by pulse oximetry) were measured. RESULTS: Average AMS scores increased more rapidly with time spent at simulated high altitudes for obese men than for nonobese men (P < 0.001). The response of Sao2 with exposure differed between nonobese and obese men. After 24 hours in the altitude chamber, seven obese men (78%) and four nonobese men (40%) had AMS scores of 4 or more. CONCLUSION: Obesity seems to be associated with the development of AMS, which may be partly related to greater nocturnal desaturation with altitude exposure.

Adult↗