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

Sabine B. R. KästnerEquine Clinic, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.

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Susanne KullEquine Clinic, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.

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Annette P. N. KutterEquine Clinic, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.

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Jolanda BollerEquine Clinic, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.

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Regula Bettschart-WolfensbergerEquine Clinic, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.

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Mirja K. HuhtinenOrion Pharma Animal Health, Orion Corp, Turku, Finland.

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 DVM, PhD

Abstract

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 µg/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 ± 7.8 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. (Am J Vet Res 2005;66:1496–1502)

Abstract

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 µg/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 ± 7.8 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. (Am J Vet Res 2005;66:1496–1502)