Kagawa K, Mammoto T, Hayashi Y, Kamibayashi T, Mashimo T, Yoshiya I
Department of Anesthesiology, Osaka University, Faculty of Medicine, Osaka Medical Center for Cancer and Cardiovascular Disease, Suita, Japan.
Anesthesiology. 1997 Oct;87(4):963-7. doi: 10.1097/00000542-199710000-00032.
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.
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 microg/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 alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 microg/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 microg/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated.
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.
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.
最近有证据表明，α2肾上腺素能受体激动剂的几种药理作用不仅通过激活α2肾上腺素能受体介导，还通过咪唑啉受体介导，咪唑啉受体是中枢神经系统中的非肾上腺素能受体。然而，咪唑啉受体对麻醉的影响尚不清楚，阐明这两种受体对麻醉的影响很重要。
72只大鼠用氟烷麻醉，氟烷的麻醉需求量以最低肺泡浓度（MAC）评估。在右美托咪定（0、10、20和30微克/千克，腹腔注射[IP]）存在的情况下测定氟烷的MAC，右美托咪定是一种对咪唑啉受体亲和力较弱的选择性α2肾上腺素能受体激动剂。然后，作者评估了对咪唑啉受体亲和力较小的α2肾上腺素能受体拮抗剂萝芙木碱（20毫克/千克，腹腔注射）对右美托咪定（30微克/千克）降低MAC作用的抑制作用。此外，还研究了选择性咪唑啉受体激动剂利美尼定（20、50、100、1000微克/千克，腹腔注射）对氟烷MAC的影响。
右美托咪定剂量依赖性地降低氟烷的MAC，右美托咪定的这种降低MAC的作用被萝芙木碱完全阻断。单独使用利美尼定不会改变氟烷的MAC。
目前的数据表明，右美托咪定的麻醉节省作用很可能是通过α2肾上腺素能受体介导的，刺激咪唑啉受体对氟烷的麻醉需求量几乎没有影响。
