Effects of Inhaled Nitric Oxide on Right Ventricular Function in Endotoxin Shock

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Abstract
Sepsis has been shown to cause right ventricular (RV) dysfunction, which may be related to pulmonary hypertension and increased RV afterload. This study evaluates the effects of inhaled nitric oxide (NO), a selective pulmonary vasodilator, on RV function in a porcine model of endotoxemia. After an infusion of Escherichia coli lipopolysaccharide (LPS; 200 microg/kg), animals were resuscitated with saline (1 mL/kg/min) and observed for 3 hours while being mechanically ventilated (Fiosub 2 = 0.6, tidal volume = 12 mL/kg, and peak end-expiratory pressure = 5 cm Hsub 2 O). The LPS group (n = 5) received no additional treatment. The NO group (n = 5) received inhaled NO (40 ppm) for the last 2 hours. The control group (n = 5) received only saline without LPS. Hemodynamic data and blood gases were collected hourly for 3 hours. LPS resulted in pulmonary hypertension and RV dysfunction as indexed by a decreased RV ejection fraction and increased RV end-diastolic volume. In haled NO significantly decreased pulmonary hypertension and significantly increased RV ejection fraction and oxygen delivery without adverse effects. In conclusion, inhaled NO significantly improved pulmonary hypertension and RV dysfunction in a porcine model of endotoxemia and should be a useful therapeutic modality in selected septic patients.