• Media type: E-Article
  • Title: Cardiopulmonary effects of dexmedetomidine in sevoflurane-anesthetized sheep with and without nitric oxide inhalation
  • Contributor: Kästner, Sabine B. R.; Kull, Susanne; Kutter, Annette P. N.; Boller, Jolanda; Bettschart-Wolfensberger, Regula; Huhtinen, Mirja K.
  • imprint: American Veterinary Medical Association (AVMA), 2005
  • Published in: American Journal of Veterinary Research
  • Language: Not determined
  • DOI: 10.2460/ajvr.2005.66.1496
  • ISSN: 0002-9645
  • Keywords: General Veterinary ; General Medicine
  • Origination:
  • Footnote:
  • Description: <jats:title>Abstract</jats:title><jats:p><jats:bold>Objective</jats:bold>—To determine whether inhaled nitric oxide (NO) prevents pulmonary hypertension and improves oxygenation after IV administration of a bolus of dexmedetomidine in anesthetized sheep.</jats:p><jats:p><jats:bold>Animals</jats:bold>—6 healthy adult sheep.</jats:p><jats:p><jats:bold>Procedure</jats:bold>—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.</jats:p><jats:p><jats:bold>Results</jats:bold>—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 PaO<jats:sub>2</jats:sub>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 PaO<jats:sub>2</jats:sub>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, PaO<jats:sub>2</jats:sub>was significantly lower and the shunt fraction significantly higher than for the DEX treatment.</jats:p><jats:p><jats:bold>Conclusions and Clinical Relevance</jats:bold>—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. (<jats:italic>Am J Vet Res</jats:italic>2005;66:1496–1502)</jats:p>
  • Access State: Open Access