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Surfactant dysfunction after inhalation of nitric oxide
Journal of Applied Physiology (Bethesda, Md. : 1985)
|June 1, 1996
Summary
Inhaled nitric oxide (NO) impairs lung surfactant function by altering proteins in the epithelial lining fluid, leading to reduced surface activity. This effect was observed in rats exposed to NO, impacting surfactant performance.
Area of Science:
- Pulmonary Physiology
- Biochemistry
- Toxicology
Background:
- Surfactant dysfunction contributes to respiratory distress.
- Nitric oxide (NO) is a signaling molecule with potential roles in lung function.
- The impact of inhaled NO on surfactant activity requires further investigation.
Purpose of the Study:
- To investigate the effects of inhaled nitric oxide (NO) on the functional properties of pulmonary surfactant.
- To determine if NO alters the protein components of bronchoalveolar lavage (BAL) fluid and their interaction with surfactant.
Main Methods:
- Young rats were exposed to air, 95% oxygen, NO, or 95% oxygen plus NO for 24 hours.
- Surfactant function was assessed by measuring minimum surface tension and surface activity of BAL fluid.
- Proteins in BAL fluid were analyzed for quantity, molecular weight distribution, and hemoglobin oxidation state.
Main Results:
- Inhaled NO increased the minimum surface tension of surfactant at low phosphatidylcholine concentrations.
- NO exposure altered BAL proteins, enhancing their ability to inhibit surfactant surface activity.
- In vitro NO exposure converted hemoglobin to methemoglobin in BAL proteins, suggesting a mechanism for surfactant inactivation.
Conclusions:
- Inhaled nitric oxide impairs lung surfactant function.
- Alterations in BAL proteins, specifically the conversion to methemoglobin, contribute to NO-induced surfactant dysfunction.
- These findings suggest a novel mechanism by which NO can negatively impact lung physiology.
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