Effect of two anaesthetic regimens on airway nitric oxide production in horses

There is evidence that halothane inhibits nitric oxide synthase in vitro, but the effect of intravenous anaesthetic agents is less clear. This study was undertaken to compare the rate of exhaled nitric oxide production (VNO) in spontaneously breathing horses anaesthetized with halothane or an intravenous regimen. Seven adult horses were studied twice in random order. After premedication with romifidine 100 microg kg(-1), anaesthesia was induced with ketamine 2.2 mg kg(-1) and maintained with halothane in oxygen (HA) or by an intravenous infusion of ketamine, guaiphenesin and romifidine (IV). Inhaled and exhaled nitric oxide (NO) concentrations, respiratory minute ventilation (VE), pulmonary artery pressure (PPA), fractional inspired oxygen concentration (FIO2), end-tidal carbon dioxide concentration (E'CO2), cardiac output (Q) and partial pressures of oxygen and carbon dioxide in arterial blood (PaO2, PaCO2) were measured. Exhaled nitric oxide production rate was significantly lower (40 min, P<0.01; 60 min, P<0.02) during HA [40 min, 1.4 (SD 1.4) pmol l(-1) kg(-1) min(-1); 60 min, 0.7 (0.7) pmol l(-1) kg(-1) min(-1)] than during IV [40 min, 9.3 (9.9) pmol l(-1) kg(-1) min(-1); 60 min, 12.5 (13.3) pmol l(-1) kg(-1) min(-1)). Mean pulmonary artery pressure was significantly higher (40 min, P<0.01; 60 min, P<0.001) during HA [40 min, 5.9 (1.1) kPa; 60 min, 5.9 (0.9) kPa] compared with IV (40 min, 4.4 (0.4) kPa; 60 min, 4.4 (0.5) kPa]. NO is reduced in the exhalate of horses anaesthetized with halothane compared with an intravenous regimen. It is suggested that increased mean pulmonary artery pressure during halothane anaesthesia may be linked to the differences in NO production.