Effects of intratracheal captopril on severely meconium-injured piglet lungs

Severe meconium aspiration syndrome (MAS) may cause intractable respiratory failure in neonates. Targeting the renin-angiotensin system may be an effective way to treat such pulmonary dysfunction. Captopril has the potential to mitigate the severity of lung injury by inhibiting angiotensin-converting enzyme.

Twelve newborn piglets were intratracheally instilled with human meconium to induce severe MAS and were randomly treated with IT administration of captopril (0.5 mg/kg) (IT-Cap group, n = 6), or sham air instillation (Control group, n = 6). Cardiopulmonary profiles were monitored for a total of 5 hours. Pulmonary history was examined to compare lung injury severity between groups.

There were no significant differences between the two study groups in gas exchange and lung compliance, peak inspiratory pressure, heart rate, and mean arterial blood pressure over the 5-h experimental period, but there were trends toward lower blood pressure and pH in the IT-Cap group. Histopathological examinations revealed significantly higher lung injury scores in the dependent site of the control group than in the nondependent site of the control group and both sites of the IT-Cap group.

Intratracheal captopril did not present significant beneficial effects on severe meconium-injured lungs within 5 hours after injury. Further studies with different disease severities and dosing strategies are required.