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
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