Reference : Effects of Inhaled Nitric Oxide on Pulmonary Hemodynamics in a Porcine Model of Endot...
Scientific journals : Article
Human health sciences : General & internal medicine
Effects of Inhaled Nitric Oxide on Pulmonary Hemodynamics in a Porcine Model of Endotoxin Shock
Lambermont, Bernard mailto [Centre Hospitalier Universitaire de Liège - CHU > > Frais communs médecine >]
D'Orio, Vincenzo mailto [Université de Liège - ULiège > Département des sciences cliniques > Médecine d'urgence - bioch. et phys. hum. normales et path.]
Kolh, Philippe mailto [Université de Liège - ULiège > Département des Sciences biomédicales et précliniques > Service de biochimie et de physiologie humaines, normale et pathologique > >]
Gérard, Paul mailto [Université de Liège - ULiège > Département de mathématique > Statistique (aspects expérimentaux) >]
Marcelle, Roland [Université de Liège - ULiège > > Relations académiques et scientifiques (Médecine) >]
Critical Care Medicine
Yes (verified by ORBi)
[en] OBJECTIVE: To evaluate the effects of inhaled nitric oxide (NO) on pulmonary circulation in a porcine endotoxin shock model. DESIGN: Prospective, randomized trial. SETTING: Laboratory at a large university medical center. SUBJECTS: Twelve pathogen-free pigs weighing 15 to 31 kg. INTERVENTIONS: After surgical preparation, all pigs received a 0.5 mg/kg endotoxin infusion over 30 mins. One hour after the start of endotoxin, NO inhalation (40 ppm) was initiated in six pigs, whereas the six remaining pigs served to control the progression of shock in this model. Consecutive changes in systemic and pulmonary hemodynamics, including characteristic resistance, vascular compliance, peripheral vascular resistance, and inductance, were continuously assessed during the experimental protocol using a four-element Windkessel model of the pulmonary circulation. MEASUREMENTS AND MAIN RESULTS: Endotoxin insult resulted in a biphasic pulmonary artery pressure increase from 14 +/- 2 to 32 +/- 4 mm Hg. Inhaled NO reversed the resistance to blood flow in small pulmonary arteries from 596 +/- 69 to 424 +/- 36 dyne-sec/ cm5. In contrast, the vascular capacitance of the entire pulmonary circuit, which decreased from 2.4 +/- 0.2 to 0.8 +/- 0.1 mL/mm Hg throughout endotoxin challenge, remained insensitive to NO administration. CONCLUSION: In endotoxin-induced pulmonary hypertension, inhaled NO may function as a modulator of distal pulmonary arterial tone but fails to act as a regulator of larger capacitance pulmonary vessels.
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