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

There is evidence that halothane inhibits nitric oxide synthase in vitro, b ut the effect of intravenous anaesthetic agents is less clear. This study w as undertaken to compare the rate of exhaled nitric oxide production ((V) o ver dot (NO)) in spontaneously breathing horses anaesthetized with halothan e or an intravenous regimen. Seven adult horses were studied twice in rando m order. After premedication with romifidine 100 mug kg(-1), anaesthesia wa s induced with ketamine 2.2 mg kg(-1) and maintained with halothane in oxyg en (HA) or by an intravenous infusion of ketamine, guaiphenesin and romifrd ine (IV). Inhaled and exhaled nitric oxide (NO) concentrations, respiratory minute ventilation (VE), pulmonary artery pressure (PPA), fractional inspi red oxygen concentration (FIO2), end-tidal carbon dioxide concentration (E' (CO2)), cardiac output ((Q) over dot) and partial pressures of oxygen and c arbon dioxide in arterial blood (Pao,, Pace,) 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 pu lmonary 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 w ith 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 intraveno us regimen. It is suggested that increased mean pulmonary artery pressure d uring halothane anaesthesia may be linked to the differences in NO producti on.