The α2-adrenergic receptor agonist dexmedetomidine produces an anesthetic state in a variety of species. Although its effects on cerebral blood flow and the electroencephalogram have been investigated, the effect of this drug on intracranial pressure (IGP) has not been reported previously. Dexmedetomidine therefore as intravenously administered to 24 New Zealand white rabbits that had been anesthetized with halothane and mechanically ventilated to maintain a constant arterial CO2 tension (PaCO2) between 34 and 39 mm Hg. After placement of an arterial catheter and ventricular cannula, baseline measurements of monitored variables, including heart rate, mean arterial blood pressure, ICP, end-tidal CO2, body temperature, and arterial blood gases, were recorded. Dexmedetomidine (20, 80, or 320 μg/kg IV) or saline solution was then infused over a 10-min period. The ICP transiently decreased by 31% in the 20-μg/kg group (from a mean value of 9.4 ± 1.3 [SEM] to 6.5 ± 1.0 mm Hg, P < 0.05). In the 320-μg/kg group, ICP remained unchanged over the course of the study despite a significant increase in arterial blood pressure (32 mm Hg). The effects of dexmedetomidine on ICP were next investigated in the presence of intracranial hypertension produced by a cryogenic lesion (mean baseline ICP 16.8 mm Hg). In addition to the previously monitored variables, sagittal sinus blood flow was measured by the hydrogen clearance technique before and after the administration of dexmedetomidine (320 μg/kg IV). In these experiments, dexmedetomidine was associated with a 14% decrease in sagittal sinus blood flow that was not statistically significant. There was no change in ICP after the administration of dexmedetomidine in this model of intracranial hypertension. From these studies, we conclude that dexmedetomidine has minimal effects on ICP in halothane-anesthetized rabbits.
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine