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Biomedical subjects

M Maze

Publications and source records attributed to M Maze.

131 records · Page 8Linked to original sources
PubMedDate not supplied

Clinical interactions with alpha-2-adrenergic agonists in anesthetic practice.

With the continued use of alpha-2-adrenergic agonists in anesthetic practice, careful attention should be given to the potential for drug interactions. Based on a review of the basic and applied pharmacology of this class of compound, we have made recommendations for the safe and efficacious use of alpha-2-adrenergic agonists in the clinical setting.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Dissociation of hypnotic-anesthetic actions of alpha 2 agonists from cyclic AMP in the rat.

alpha 2 adrenergic agonists are used clinically for their anesthetic, analgesic, and sympatholytic actions in surgical patients. All alpha 2 adrenergic receptors, when activated by alpha 2-adrenergic agonists, are able to inhibit adenylate cyclase. We have examined the alpha 2-adrenoceptor-mediated anesthetic actions of dexmedetomidine, a highly selective alpha 2-adrenergic agonist, after pretreatment of the animals with rolipram, a cyclic AMP (cAMP)-specific phosphodiesterase inhibitor, cAMP accumulation and monoamine turnover were measured in the locus coeruleus (LC) and hippocampus (HC) following administration of rolipram [275 mg/kg, intraperitoneally (IP)] and dexmedetomidine (100-500 mg/kg, IP). The hypnotic response to dexmedetomidine was also measured in these animals. In other experiments, rats were stereotactically cannulated in the LC with an indwelling catheter, and after the second day, the tail-flick analgesic response to dexmedetomidine (3.5 mg/0.2 ml LC), following rolipram (275 mg/kg, IP) pretreatment, was assessed. In the presence of elevated cAMP levels, the hypnotic, analgesic, and sympatholytic effects of dexmedetomidine persisted. These data suggest that adenylate cyclase activity does not mediate the cellular responses to alpha 2-adrenergic agonists but instead may act in concert with other alpha 2-adrenoceptor-coupled effector mechanisms to transduce the anesthetic actions of these agents.

Adrenergic alpha-2 Receptor Agonists↗
PubMedDate not supplied

Chronic treatment with dexmedetomidine desensitizes alpha 2-adrenergic signal transduction.

Tolerance to the hypnotic response was induced in rats by chronically infusing dexmedetomidine, a novel alpha 2-adrenergic agonist. The alpha 2-adrenoceptor affinity for dexmedtomidine and para-iodoclonidine was significantly reduced in tolerant rats, while Bmax was uncharged. The ability of pertussis toxin (PTX) to ribosylate guanine nucleotide regulatory proteins (G proteins) ex vivo was reduced in tolerant rats; the quantity of PTX-sensitive G proteins was unchanged. Forskolin-stimulated adenylyl cyclase was less sensitive to inhibition by dexmedetomidine in the tolerant rats; however, acute intraperitoneal injection of dexmedetomidine still reduced cyclic adenosine monophosphate levels in tolerant rats. Both the decrease in ribosylation and the lower alpha 2-adrenoceptor binding affinity may reflect a decrease in the ability of the G protein to couple to the alpha 2-adrenoceptors in the locus coeruleus of tolerant rats. In this state, the alpha 2 adrenoceptors are less capable of transducing the effector response (inhibition of adenylyl cyclase).

Adenylate Cyclase Toxin↗