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John A Clements

Publications and source records attributed to John A Clements.

4 recordsLinked to original sources
PubMed2005

Hyaluronan reduces surfactant inhibition and improves rat lung function after meconium injury.

Hyaluronan (HA), an ionic polymer, is normally present in the alveolar subphase and is known to decrease lung surfactant inactivation caused by serum in vitro. In this study, we examined whether HA can ameliorate the inactivating effects of meconium in vitro and in vivo. Surface activities of various mixtures of Survanta, HA, and meconium were measured using a modified pulsating bubble surfactometer. With meconium, almost all surface activity measures were improved by the addition of HA of several molecular weights at a concentration of 0.25%. Anesthetized, paralyzed rats were maintained on positive-pressure ventilation. After lung injury by instillation of meconium, they were treated with Survanta, Survanta with HA, or control mixtures. Serial measures of blood gases and peak inspiratory pressure were recorded for the duration of the experiment. When the Survanta plus HA group was compared with the Survanta alone group, arterial oxygen tension averaged 117% higher, peak inspiratory pressure was 27% lower at the end of the experiment, and lung compliance also showed significant improvement. These results indicate that HA added to Survanta decreases inactivation caused by meconium in vitro and improves gas exchange and pulmonary mechanics of animals with meconium-induced acute lung injury.

Animals↗
PubMed2004

Hyaluronan decreases surfactant inactivation in vitro.

Hyaluronan (HA) is an anionic polymer and a constituent of alveolar fluid that can bind proteins, phospholipids, and water. Previous studies have established that nonionic polymers improve the surface activity of pulmonary surfactants by decreasing inactivation of surfactant. In this work, we investigate whether HA can also have beneficial effects when added to surfactants. We used a modified pulsating bubble surfactometer to measure mixtures of several commercially available pulmonary surfactants or native calf surfactant with and without serum inactivation. Surface properties such as equilibrium surface tension, minimum and maximum surface tensions on compression and expansion of a surface film, and degree of surface area reduction required to reach a surface tension of 10 mN/m were measured. In the presence of serum, addition of HA dramatically improved the surface activities of all four surfactants and in some cases in the absence of serum as well. These results indicate that HA reduces inactivation of surfactants caused by serum and add evidence that endogenous HAs may interact with alveolar surfactant under normal and abnormal conditions.

Anions↗
PubMed2004

Coagulation-dependent mechanisms and asthma.

In several clinical disorders, there are interactions between inflammation-dependent tissue injury and thrombin formation, fibrin deposition, and impaired fibrinolysis. New evidence generated from a mouse model of allergic airway hyperreactivity suggests that disordered coagulation and fibrinolysis may contribute to the pathogenesis of asthma. The inflammatory mechanisms that lead to airway smooth muscle contraction and airway hyperresponsiveness may be associated with accumulation of extravascular fibrin, plasma exudates, and inflammatory cells that can lead to airway closure.

Asthma↗