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Interactions Between Neuronal Histamine and Halothane Anesthesia in Rats
Author(s) -
Mammoto Tadanori,
Yamamoto Yumiko,
Kagawa Kiyokazu,
Hayashi Yukio,
Mashimo Takashi,
Yoshiya Ikuto,
Yamatodani Atsushi
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.69010406.x
Subject(s) - thioperamide , halothane , histaminergic , histamine , microdialysis , anesthetic , anesthesia , histidine decarboxylase , antagonist , chemistry , endocrinology , pharmacology , medicine , histamine h3 receptor , central nervous system , receptor , biochemistry , amino acid , histidine
Using an in vivo microdialysis method, we measured the release of histamine in the anterior hypothalamic area (AHy) of rats under several concentrations of halothane anesthesia (1, 0.5, and 0.2%). The release of histamine increased to 341 and 325% at halothane concentrations of 0.5 and 0.2%, compared with the basal level at anesthesia induced by 1% halothane. α‐Fluoromethylhistidine (100 mg/kg i.v.), a specific and irreversible inhibitor of histidine decarboxylase, reduced the histamine release to <35% of the basal value at 1% halothane anesthesia in the AHy, and also decreased the anesthetic requirement for halothane, evaluated as the minimum alveolar concentration (MAC), by 26%. Furthermore, pyrilamine (20 mg/kg i.v.), a brain‐penetrating H 1 antagonist, and zolantidine (20 mg/kg i.v.), a brain‐penetrating H 2 antagonist, reduced the MAC for halothane by 28.5 and 16%, respectively. Although thioperamide (5 mg/kg i.v.), an antagonist of presynaptic H 3 autoreceptor, induced an approximate twofold increase in the level of histamine release in conscious freely moving rats, the same dose of thioperamide had little effect on the release of histamine under 1% halothane anesthesia in the AHy. Furthermore, thioperamide did not change the anesthetic requirement (MAC) for halothane. The present findings indicate that halothane anesthesia inhibits the release of neuronal histamine and that histaminergic neuron activities change the anesthetic requirement (MAC) for halothane through H 1 as well as H 2 receptors.