Reversion of Pulmonary Hypertension Induced by Hypoxia With Inhaled Nitric Oxide (No) in An Animal Model 15

NO is a potent vasodilator than has been identified as the endothelium derived relaxing factor. It is possible that in certain conditions such as Persistent Pulmonary Hypertension (PPH) of the newborn and the postoperative period of several congenital cardiac disease NO release may be impaired. There is no specific agent for PPH treatment to induce selective and sustained pulmonary vasodilation. Recent reports show that inhaled NO improves oxygenation in children with severe Pulmonary Hypertension (PH). The purpose of the study was to evaluate the effect of increasing doses of NO in animals with PH induced by acute hypoxia. Meterial and Methods: The experimental design was prospective, descriptive and controlled. A model of PH was created by inducing hypoxia with low inspired FiO₂ in 4 piglets under 45 days old which were intubated and received anesthesia with fentanyl and pancuronium. Catheters in the external yugular vein, carotid artery and pulmonary artery were placed in the animals. NO was administered in varying doses between 5 and 80 ppm. Continuous measurement of NO and Nitric dioxide(NO₂) with a portable analyzer of electrochemical cells (Pulmonox II) was performed. Methemoglobin and bleeding time were determined at baseline levels and at different doses of NO. The comparison of changes between the different doses of NO and baseline levels was evaluated by Student t test, a p value of <0.05 was considered significant.Table

Table 1

Conclusions: NO inhalation at doses of 5ppm or more reverts PH in the animal model, with no significant changes in SAP methemoglobin levels and bleeding.