Inhaled nitric oxide prevents left ventricular impairment during endotoxemia

We evaluated the effect of longterm inhalation of nitric oxide (NO) on card iac contractility after endotoxemia by using the end-systolic elastance of the left ventricle (LV) as a load-independent contractility index. Chronic instrumentation in 12 pigs included implantation of two pairs of endocardia l dimension transducers to measure LV volume and a micromanometer to measur e LV pressure. One week later, the animals were divided into a control grou p (n = 6) or a NO group (n = 6). All animals received intravenous Escherich ia coli endotoxin (10 mu g.kg(-1).h(-1)) and equivalent lactated Ringer sol ution. NO inhalation (20 parts/million) was begun 30 min after the initiati on of endotoxemia and was continued for 24 h. In both groups, tachycardia, pulmonary hypertension, and systemic hyperdynamic changes were noted. The e nd-systolic elastance in the control group was significantly decreased beyo nd 7 h. NO inhalation maintained the end-systolic elastance at baseline lev els and prevented its impairment. These findings indicate that NO exerts a protective effect on LV contractility in this model of endotoxemia.