Abstract

alpha 2-Adrenergic receptors are found on large and small cerebral vessels, but their role in control of cerebral blood flow (CBF) and cerebral vascular reactivity is unclear. We assessed the effects of dexmedetomidine (DEX), a highly selective alpha 2-adrenergic agonist, on the cerebrovascular response to hypercapnia in dogs anesthetized with either pentobarbital (PENTO) or isoflurane (ISO), drugs which produce different levels of CBF at a similar level of cerebral oxygen consumption (CMRO2). Dogs were anesthetized with either PENTO, 30 mg/kg, n = 6, or ISO 1.4% end-tidal, n = 7. CBF (radiolabeled microspheres) was determined during normocapnia and hypercapnia at baseline (pre-DEX), after DEX (10 micrograms/kg, intravenous bolus, plus an additional 5 micrograms/kg during hypercapnia), and after administration of a selective alpha 2-adrenergic receptor antagonist (atipamezole, 500 micrograms/kg, intravenous bolus). In the PENTO group, CBF increased from 31 +/- 3 to 137 +/- 24 mL.min-1.100 g-1 in response to hypercapnia (PCO2 approximately 90 mmHg) at pre-DEX and there was no change in normocapnic CBF or hypercapnic blood flow after DEX or atipamezole. In the ISO group, at pre-DEX, CBF increased from 86 +/- 8 to 166 +/- 19 mL.min-1.100 g-1 in response to hypercapnia (PCO2 approximately 90 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

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