Effects of inhaled nitric oxide 10 ppm in spontaneously breathing horses anaesthetized with halothane

Inhaled nitric oxide, a selective pulmonary vasodilator, is known to improv e arterial oxygenation after cardiopulmonary bypass and during acute respir atory distress syndrome in humans. During general anaesthesia with spontane ous ventilation, healthy adult horses develop large alveolar-arterial oxyge n tension differences. In this study, we have determined the effects of inh aled nitric oxide (10 parts per million (ppm)) on venous admixture and pulm onary haemodynamics in horses anaesthetized with halothane. Seven adult hor ses were studied twice in random sequence. After premedication with romifid ine 100 mu g kg(-1), anaesthesia was induced with ketamine 2.2 mg kg(-1) an d maintained with 1.1 MAC (0.95%) of halothane in oxygen. Horses breathed s pontaneously. After 65 min, each horse had nitric oxide 10 ppm added to the inspired gas for 20 min (procedure HA+NO) or anaesthesia was continued wit h halothane in oxygen (procedure HA). Cardiac output, minute ventilation, a rterial and mixed venous oxygen and carbon dioxide tensions, and mean pulmo nary and carotid arterial pressures were measured for 100 min. Shunt fracti on and pulmonary and systemic vascular resistances were calculated. Shunt f raction (SF) and mean pulmonary artery pressure (P-PA (mean)) were not diff erent between the two groups after 65 min of general anaesthesia (HA: SF 0. 20 (SD 0.06), P-PA mean 45 (8) mm Hg; HA+NO: SF 0.21 (0.04), P-PA (mean) 44 (7) mm Hg) or after 85 min (HA: SF 0.22 (0.07), P-PA mean 45 (8) mm Hg; HA +NO: SF 0.20 (0.03), P-PA mean 43 (7) mm Hg). There were no significant eff ects of time or nitric oxide inhalation on any other variable. There was a significant correlation (r = 0.80, P < 0.05) between calculated shunt fract ion 65 min after induction of anaesthesia and body weight.