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The Effect of Imidazoline Receptors and α2-adrenoceptors on the Anesthetic Requirement (MAC) for Halothane in Rats

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Abstract

Background:

Recent evidences have documented that several pharmacologic actions of alpha2 -adrenoceptor agonists are mediated via activation of not only alpha2 -adrenoceptors, but also by imidazoline receptors, which are nonadrenergic receptors in the central nervous system. However, the effect of imidazoline receptors on the anesthesia is not well known, and it is important to clarify the effects of both receptors on anesthesia.

Methods:

Seventy-two rats were anesthetized with halothane, and the anesthetic requirement for halothane was evaluated as minimum alveolar concentration (MAC). The MAC for halothane was determined in the presence of dexmedetomidine (0, 10, 20, and 30 micro gram/kg, intraperitoneally [IP]), a selective alpha2 -adrenoceptor agonist with weak affinity for imidazoline receptors. Then, the authors evaluated the inhibitory effect of rauwolscine (20 mg/kg, IP), an alpha sub 2 -adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 micro gram/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 micro gram/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated.

Results:

Dexmedetomidine decreased the MAC for halothane dose-dependently, and this MAC-reducing action of dexmedetomidine was completely blocked by rauwolscine. Rilmenidine alone did not change the MAC for halothane.

Conclusions:

The present data indicate that the anesthetic sparing action of dexmedetomidine is most likely mediated through alpha2 -adrenoceptors, and the stimulation of imidazoline receptors exerts little effect on the anesthetic requirement for halothane.

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