Is the inhaled nitric oxide useful in pulmonary embolism? An experimental study

Background

In perioperative and critical patients, inhaled nitric oxide (NO) decreased pulmonary artery pressure and pulmonary vascular resistance in several diseases [1]. In the presence of pulmonary vasoconstriction, the higher pulmonary vascular resistance then the greater the inhaled NO vasodilator effect. Recently it has been demonstrated that inhaled NO could attenuate the pulmonary vasoconstriction caused by active mediators in an experimental model of massive air pulmonary embolism (PE) [2].

Objective

The goal of study is to investigate the effects (hemodynamics and in gas exchange) of inhaled NO in a massive pulmonary embolism model in dogs.

Materials and methods

We performed a prospective study in four groups of adult mongrel dogs in two phases. Phase 1 (normoventilated with FiO₂ 0.21): Group A (control), nine dogs; Group B (NO inhaled), nine dogs. Phase 2 (normoventilated with an hypoxic mixture [FiO₂ 0.16]): Group C (control), five dogs; Group D, six dogs (NO inhaled). Pulmonary embolism was induced by the modified Fisher's method [3]. Inhalation of NO was started 15 min prior to induction of PE and was kept constant throughout the experiment. Mean pulmonary artery pressure (PAPm), central venous pressure (CVP) and mean systemic arterial blood pressure (SAPm), cardiac output, arterial and mixed venous blood samples were obtained in basal conditions, hypoxic period previous embolism, after started NO inhalation and 5, 15, 30 and 45 min after embolism induction. Results as expressed as mean ± standard deviation. Nonparametric test (Mann–Whitney U test and Wilcoxon test) were used. Statistical significance was set at P < 0.05.

Results

In phase 1 no significant differences in all variables measured at any time were found. There was an improvement in gas exchange. In phase 2 NO inhalation both improved gas exchange and reduced PAPm in the hypoxic ventilation prior to PE. After pulmonary embolism we observed a reduction in PAPm and improve arterial oxygenation but no statistical differences were found. No significant intergroup differences were found with regard to CO, PVC. A trend to lower cardiac output was observed in the group of inhaled NO.

Conclusions

Our data suggest that in pulmonary embolism induced by Fisher's method, inhaled NO did not modify either pulmonary haemodynamics or oxygenation. We have shown that inhaled NO improved the hypoxic induced pulmonary hypertension without effects in systemic arterial pressure.