ABSTRACT NO: 016
Introduction: Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator in animal models of acute  and recurrent pulmonary microembolism . However, the vasoconstrictor mechanism affected by iNO in this situation is still unknown. Therefore, in this study, we compared the effects of iNO with inhalation of 100% oxygen (O2) and the combination of both in an animal model of sustained pulmonary hypertension following recurrent pulmonary microembolism.
Methods: Twelve anaesthetized pigs (12.5 ± 1.1 kg BW) were subjected to three pulmonary microembolizations by i.v. injection of polydextrane microspheres (15 mg kg−1; ∅ 300 μm) on days 0, 7 and 49 respectively. One week later (day 56), the mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR) were measured at the baseline (FiO2 = 0.21; iNO = 0 ppm), during inhalation of O2 (FiO2 = 1.0; iNO = 0 ppm), iNO (FiO2 = 0.21; iNO = 40 ppm) and O2 + iNO (FiO2 = 1.0; iNO = 40 ppm).
Results: Compared with the baseline (29 ± 2.4 mmHg), mPAP decreased significantly with inhalation of O2 (24 ± 2.1 mmHg), iNO (23 ± 2.3 mmHg) and O2 + iNO (22 ± 2.1 mmHg) (P < 0.05 vs. baseline respectively). FIGURE
Conclusions: O2 and iNO are pulmonary vasodilators in this model. Their effects are not additive. Hypoxic pulmonary vasoconstriction seems to be the major vasoconstricting mechanism causing increased pulmonary vascular tone.
1 Böttiger BW et al. Chest
2 Weimann J et al. J Crit Care
The publication of this supplement has been supported by the sponsors of the Third ISMG Meeting: Abbott, AGA, AstraZeneca, Dräger, Janssen, Medex Medical, Messer Austria, Ohmeda, Pharmacia & Upjohn, Scott Medical Products, Siemens