The rostral ventrolateral medulla (RVLM) controls the vascular system and may contribute to postoperative
hypertension. It comprises
adrenergic cardiovascular neurons, a site for action of alpha2-adrenergic agonists. Because alpha2 agonists minimize perioperative circulatory activation, we asked the following question: do alpha2 agonists, such as
clonidine and
mivazerol, blunt the
catecholamine activation observed in the RVLM on emergence from
anesthesia?
Halothane-anesthetized, paralyzed rats had their ventilatory, circulatory, and
acid-base stability controlled. All pressure points and incisions were infiltrated with
local anesthetics. With in vivo electrochemistry, a
catechol signal was recorded in the RVLM during 150 min of stable
halothane anesthesia (saline-
halothane group); for 120 min after
halothane discontinuation (saline-emergence group); after emergence and administration of the reference alpha2 agonist,
clonidine 7 microg/kg or 21 microg/kg I.V. (50% or 90% effective dose [ED50 or ED90], respectively); and after emergence and administration of a new alpha2 agonist,
mivazerol 20 microg/kg or 150 microg/kg I.V. (ED50 or ED90). Under
halothane, dose-response curves for the RVLM
catecholamine signal were constructed for
mivazerol and an alpha2 antagonist,
idazoxan (ED50 2.3 mg/kg I.V.). Stable
halothane anesthesia (n = 5) led to no change in mean arterial pressure (MAP), heart rate (HR), or
catechol signal (
CAOC). During emergence from
anesthesia, the MAP, HR, and
CAOC increased (n = 5).
Clonidine led to a near total suppression of the RVLM
catecholamine activation noticed on emergence from
anesthesia (n = 5).
Hypertension was partially blunted with
clonidine 7 microg/kg (n = 5).
Tachycardia was partially blunted with
mivazerol 20 microg/kg (n = 5). Pretreatment with
idazoxan suppressed all the effects of
mivazerol (n = 5).
IMPLICATIONS: On emergence from
anesthesia, alpha2 agonists modify the activity of
adrenergic cardiovascular neurons located within the vasomotor center, as assessed by in vivo electrochemistry. We provide a rationale for the use of alpha2 agonists on emergence from
anesthesia in coronary/hypertensive patients.