Pulmonary Gas Exchange Capacity Research Articles

Respiratory Rate as a Factor in Lung Injury-Not Just What You Set, but How You Set.

Respiratory Rate as a Factor in Lung Injury-Not Just What You Set, but How You Set.

Influence of prenatal maternal corticosteroid therapy on clinical and metabolic features and pulmonary function of preterm newborn puppies

Although the effects of antenatal corticosteroid therapy in clinical improvement and pulmonary maturation in preterm have been described, little is known on premature newborn puppies. This study aimed to evaluate the effect of maternal administration of a single dose of prenatal betamethasone on lung function of preterm newborn puppies in the first hours of life, especially from the clinical point of view and acid-base balance. A prospective study was conducted involving 21 puppies allocated into three experimental groups: Term Group (63 days post-ovulation), Preterm-Treated Group (57 days post-ovulation and maternal administration of a single dose of 0.5 mg/kg of betamethasone) and Preterm-Control Group (57 days post-ovulation). Puppies were analyzed clinically through the Apgar score, heart rate, respiratory rate and neurological tests (muscular tone and irritability reflex) and for oximetry and blood acid-base balance in distinct experimental moments. Premature puppies had marked degree of prematurity, reversed by maternal administration of betamethasone. Prenatal corticosteroid therapy promoted better pulmonary and metabolic condition, with more efficient compensatory response to acid-base imbalance and better pulmonary gas exchange capacity. Therefore, prenatal treatment with betamethasone can be adopted as clinical lung maturation protocol for pregnancies at risk in order to prevent low vitality and increase neonatal survival.

Mycoplasma pneumoniae, pneumonies et asthme

Mycoplasma pneumoniae is an intracellular pathogen, devoid of cell wall, able to invade airway epithelial cells. Infection mayeither remain asymptomatic or induce bronchitis and pneumonia. M. pneumoniae is the first-ranking aetiological agent of community-acquired pneumonias in children over five years of age. Clinical features are usually mild, but this should not preclude the initiation of a treatment, in order to avoid serious sequelae such as impairment of pulmonary gas exchange capacity. In children at high-risk of asthma, infection with M. pneumoniae can induce exacerbation. A survey was performed in children admittedto hospital Saint-Vincent-de-Paul (Paris) for an episode of severe asthma exacerbation with persistent hypoxemia. Mycoplasma infection was identified in 26% of children with a history of asthma and 50% of those for whom the exacerbation was the presenting manifestation of the disease. Furthermore, if the Mycoplasma infection was atypical, asthma exacerbation recurred within one month. M. pneumoniae should be considered not only as a preeminent agent of respiratory infection in children, but also as a triggering factor in exacerbation and even inception of asthma. As a consequence, it is mandatory to carefully search for and actively treat Mycoplasma infection in children.

Pulmonary gas exchange capacity is reduced during normovolaemic haemodilution in healthy human subjects.

To test the hypothesis that a physiological compensatory mechanism maintains respiratory gas exchange during normovolaemic haemodilution. Pulmonary gas exchange capacity was evaluated in seven healthy subjects by measuring the lung diffusion of carbon monoxide (DLCO). During the measurement, various breath-holding times, inspiratory volumes, and sitting or supine positions, were randomly selected in an attempt to alter pulmonary capillary perfusion. KCO was calculated as the percentage of theoretical values of the ratio of DLCO by alveolar volume and normalized by sex, age, and height. Normovolaemic haemodilution (NH) was performed by bleeding an average blood volume of 1 L with simultaneous Dextran 60 replacement to obtain an haematocrit below 35%. After NH, haemoblogin concentration [Hb] decreased from 14.94 +/- 0.96 to 12.5 +/- 0.98 g.dl-1 (P < 0.001). KCO decreased (P < 0.02) but remained closely correlated to [Hb] at every lung volume (P < 0.02). Breathholding time and body position had no effect. Moderate NH impairs pulmonary gas exchange capacity in awake, resting healthy subjects. There is no evidence of any compensatory mechanism since the KCO vs [Hb] relationship is unchanged.

Adaptation of the growing lung to increased V̇ O 2: III. The effect of exposure to cold environment in rats

This study was undertaken to further test the hypothesis that increased V̇ O 2 operates as a stimulus for enhanced lung growth leading to a pulmonary diffusing capacity adapted to the body's O 2 requirements. V̇ O 2 was augmented by raising 4-week-old rats for 3 weeks at 11°C ambient temperature, with controls kept at 24°C; this led to an increase in V̇ O 2 averaged over 24 h by 64%. In contrast to previous experiments with waltzing mice this regime did not affect body growth, as the final body weights were identical in both groups. In the cold-exposed rats the lung volume was larger by 24%, due to an increase by 26% in air volume (at about TLC), 13% in capillary blood volume and 19% in tissue volume. The alveolar and capillary surface areas were increased by 18%, and D m and D l by 17% and 21% respectively. It is concluded that the hypothesis of adaptation of pulmonary gas exchange capacity to increased V̇ O 2 cannot be rejected. Whilst in previous experiments some doubts had to be retained as to the specificity of the stimulus, because of its rather marked effect on body weight, this reservation does not hold in this case. The structural modifications which lead to increased D l in the various experimental models are discussed.

CONCENTRATION-TIME PRODUCT (CT) AS AN EXPRESSION OF DOSE IN SUBLETHAL EXPOSURES TO PHOSGENE.

Abstract Rats were exposed to phosgene at concentrations of 0.5 to 4.0 ppm for time periods ranging from five minutes to eight hours, using various combinations of concentrations and time to give a range of equal CT products. Response was expressed in terms of impaired pulmonary gas exchange capacity as measured by the decreased rates of uptake of carbon monoxide and ether. Beginning changes in pulmonary performance were noted following exposures to CT products as low as 30 ppm-min. Following doses greater than 180 ppm-min., death became increasingly likely, with associated reduction in CO uptake to less than 50% of normal. There was no indication that concentration contributed more than exposure time to the magnitude of change in pulmonary performance over the range of CT values studied.