Cardiopulmonary effects of dexmedetomidine in sevoflurane-anesthetized sheep with and without nitric oxide inhalation

Objective-To determine whether inhaled nitric oxide (NO) prevents pulmonary hypertension and improves oxygenation after IV administration of a bolus of dexmedetomidine in anesthetized sheep. Animals-6 healthy adult sheep. Procedure-In a crossover study, sevoflurane-anesthetized sheep received dexmedetomidine (2 mu g/kg, IV) without NO (DEX treatment) or with inhaled NO (DEX-NO treatment). Cardiopulmonary variables, including respiratory mechanics, were measured before and for 120 minutes after bolus injection of dexmedetomidine. Results-Dexmedetomidine induced a transient decrease in heart rate and cardiac output. A short-lived increase in mean arterial pressure (MAP) and systemic vascular resistance (SVR) was followed by a significant decrease in MAP and SVR for 90 minutes. Mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance increased transiently after dexmedetomidine injection. The PaO2 was significantly decreased 3 minutes after injection and reached a minimum of (mean SEM) 13.3 78 kPa 10 minutes after injection. The decrease in PaO2 was accompanied by a sudden and prolonged decrease in dynamic compliance and a significant increase in airway resistance, shunt fraction, and alveolar dead space. Peak changes in MPAP did not differ between the 2 treatments. For the DEX-NO treatment, PaO2 was significantly lower and the shunt fraction significantly higher than for the DEX treatment. Conclusions and Clinical Relevance-Inhalation of NO did not prevent increases in pulmonary arterial pressures induced by IV administration of dexmedetomidine. Preemptive inhalation of NO intensified oxygenation impairment, probably through increases in intrapulmonary shunting.