Reference

Changes in the alkaloid composition and acute toxicity of Aconitum roots during processing

Changes in the alkaloid composition and acute toxicity of Aconitum roots during processing. Hikino, Hiroshi; Yamada, Chizuko; Nakamura, Kazuko; Sato, Hiroshi; Ohizumi, Yasushi; Endo, Katsuya (Pharm. Inst., Tohoku Univ., Sendai, Japan). Yakugaku Zasshi, 97(4), 359-66 (Japanese) 1977. CODEN: YKKZAJ. DOCUMENT TYPE: Journal CA Section: 63 (Pharmaceuticals) Section cross-reference(s): 4, 11 Raw tubers of A. japonicum and A. carmichaeli, which are the sources of processed aconite roots used widely as an Oriental medicine in Japan, contain mesaconitine (I) [2752-64-9] or hypaconitine (II) [6900-87-4] as the main poisonous principle and are highly toxic. When they are processed at 120.degree. for 40 min (to Kako-bushi), a greater part of the poisonous aconitines is hydrolyzed into the much less poisonous benzoylaconines and, together with the postulated co-occurrence of substances which reduce the toxicity of the aconitines, the tubers become essentially innocuous. The processed aconite roots (Shirakawabushi), prepd. by a variety of procedures (immersion into salt water, coating with lime or ash, and/or some heat tratment), show variation in the alkaloid content and compn., and still exhibit considerable toxicity. The processed aconite roots (Ho-bushi), prepd. by immersion into salt water and heat treatment, have also been shown to be converted into benzoylaconines and further the alkaloid content has been significantly reduced. It is quite probable that, in the processed aconite roots (Ho-bushi), not only the poisonous alkaloids but also other active principles have been much decreased owing to chem. degrdn. by heat treatment as well as by phys. loss due to extn. during processing, which is to be clarified by future pharmacol. examns. When raw tubers are heated at 100.degree. in the presence of water (conditions employed for decoction), the content of the aconitines is gradually diminished and the toxicity reduced rapidly, a fact which confirms that raw tubers become far less toxic by means of sufficient heating under these conditions.

Mechanism of analgesic action of mesaconitine

Mechanism of analgesic action of mesaconitine. I. Relationship between analgesic effect and central monoamines or opiate receptors. Murayama, Mitsuo; Ito, Tomoko; Konno, Chohachi; Hikino, Hiroshi (Pharm. Inst., Tohoku Univ., Sendai 980, Japan). Eur. J. Pharmacol., 101(1-2), 29-36 (English) 1984. CODEN: EJPHAZ. ISSN: 0014-2999. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The contribution of the central monoamines and the opiate receptor to mesaconitine (MA)(I) [2752-64-9]-induced analgesia was investigated by means of pharmacol. and neurochem. methods in which morphine (Mor) was used for comparison. The analgesic action of intracerebral MA detd. by the acetic acid-induced writhing method and the tail flick method was dose-dependent, indicating that its activity is elicited through the central nervous system. MA-induced analgesia was decreased by a-methyl-p-tyrosine (a-MT), 6-hydroxydopamine, diethyldithiocarbamate, disulfiram, and reserpine, and increased by methamphetamine and norepinephrine (NE). The mode of action of MA was similar to that of Mor except for the results obtained upon combined administration with l-dopa, dopamine, a-MT, or chem. related to 5-hydroxytryptamine. In addn., MA promoted the a-MT-induced decrease in NE levels in hippocampus, medulla oblongata plus pons and spinal cord. Levallorphan did not affect the analgesic activity of MA, showing that its activity is not mediated via the opiate receptors. Thus, the analgesic activity of MA is closely related to responses involving the central catecholaminergic system, in particular, the noradrenergic system.