Exposure to cyclic oxygen sufficient for development of oxygen-induced retinopathy does not induce bronchopulmonary dysplasia in rats.

Bronchopulmonary dysplasia and retinopathy of prematurity affect premature infants exposed to supplemental oxygen. Susceptibility to oxygen-induced retinopathy in the rat is heritable, with inbred Dark Agouti (DA) rats being more susceptible than Fischer 344 (F344) rats. To establish if hyperoxic exposure sufficient to induce florid retinopathy would induce strain-specific lung changes, newborn DA and F344 rats were exposed to cyclic hyperoxia or room air for up to 18 days.

Lung mechanics are both dose and tidal volume dependant in LPS-induced lung injury.

Endotoxin stimulus plays a significant role in various forms of acute lung injury (ALI) which may be exacerbated by mechanical ventilation. Here, we identify the temporal pathophysiologic sequence following inhaled lipopolysaccharide (LPS) and subsequently examine both LPS dose and V(T) relationships. Rats received intratracheal LPS (3, 9 or 15 mg/kg) prior to mechanical ventilation (V(T)=6, 9 or 12 ml/kg) and measurement of forced impedance mechanics for up to 4h.

Reduced surface tension normalizes static lung mechanics in a rodent chronic heart failure model.

Rationale: Chronic elevation of pulmonary microvascular pressure in chronic heart failure results in compensatory changes in the lung that reduce alveolar fluid filtration and protect against pulmonary microvascular rupture.

Objectives: To determine whether these compensatory responses may have maladaptive effects on lung function.

Methods: Six weeks after myocardial infarction (chronic heart failure model) rat lung composition, both gross and histologic; air and saline mechanics; surfactant production; and immunological mediators were examined.

Hypercapnic acidosis modulates inflammation, lung mechanics, and edema in the isolated perfused lung.

Objective: Low tidal volume (V(T)) ventilation strategies may be associated with permissive hypercapnia, which has been shown by ex vivo and in vivo studies to have protective effects. We hypothesized that hypercapnic acidosis may be synergistic with low V(T) ventilation; therefore, we studied the effects of hypercapnia and V(T) on unstimulated and lipopolysaccharide-stimulated isolated perfused lungs.

Materials And Methods: Isolated perfused rat lungs were ventilated for 2 hours with low (7 mL/kg) or moderately high (20 mL/kg) V(T) and 5% or 20% CO(2), with lipopolysaccharide or saline added to the perfusate.