Anisodine is isolated from the roots of the plant Solanaceae Anisodus tanguticus
(Maxim.) Pasch. (Scopolia tangutica Maxim.), which has a common name of
Zhang-Liu-Shen, growing at the plateau with an altitude of 1700–4300?m and richly
distributed in Tibet, Sichuan, Qinghai, Gansu, and other provinces in China.
Appearance: white crystals or crystalline powder. Flash point: 253.2?°C. Melting
point: 126–128? °C (acetone-H2O), 190–192? °C (95% ethanol), and 197–200? °C
(absolute ethanol). MS m/e (%): 319(51), 154(14), 138(100), 96(5), 95(5), 94(36),
97(15), 96(5), 42(15), 137(25), and 119(23).
Anisodine hydrobromide was an originally created new drug in China. It was separated from the herbal medicine Anisodus tanguticus from Qinghai province. In the
early 1960s, Anisodus tanguticus was given the common name of Zhang-Liu-Shenin Qinghai province, similar to the common name Zhang Liu of Radix Phytolaccae.
As a result, the root was misused as Radix Phytolaccae until the occurrence of atropine poisoning symptoms. Histological identification found that it is Anisodus tanguticus (Maxim.) Pasch, not Radix Phytolaccae. In order to make full use of the wild
plant’s resources and develop the products of henbane drugs in China, the Chinese
Academy of Medical Sciences carried out the systemic research on the plant .
Anisodine hydrobromide is recorded in the second volume of national standards for
chemical drugs of the People’s Republic of China. The formulation consists of
injection and tablet.
It is used clinically for treatment of migraine, retinal vascular spasm, ischemic
lesions, shrinking of the optic nerve, retina, and choroid, etc. It could improve the
functional recovery after acute paralysis induced by inflammation of the nervous
system and cerebrovascular disease, paralysis agitants, and carbon monoxideinduced toxic encephalopathy. It was also used for intravenous combined anesthesia, organophosphorus poisoning, bronchitis, asthma, and prevention and treatment
of seasickness.
Central anticholinergic effects: anisodine competes with acetylcholine in the M
cholinergic receptor to prevent acetylcholine binding M cholinergic receptor, thus
blocking the nerve impulse transmission and interfering with the physiological
function based on the cholinergic neurotransmission. It has similar or slightly
weaker effects than that of atropine on electrical activity of the brain, on pain caused
by tremorine, and on tremor caused by arecoline in mice. Its effect is 19 times
weaker than those of scopolamine .
Peripheral anticholinergic effects: anisodine possesses antispasmodic and antiasthma effects and inhibits saliva secretion and mydriasis, which are weaker than
those of atropine.
It acts against organic phosphate pesticide poisoning.
Anti-shock effect: anisodine prolonged significantly the survival time of animals
or reduced mortality in patients with clinical shock through directly relieving vasospasm of vascular smooth muscle, antagonizing adrenaline-induced vasoconstriction, and improving microcirculation .
Anti-cerebral ischemic disease: the effect of anisodine on cerebral blood circulation is mainly to regulate vasomotor, decrease cerebral vascular resistance, and
increase cerebral blood flow, thereby improving the symptoms of cerebral
ischemia.
In the past, anisodine was mainly used in the treatment of various diseases of the
central nervous system.
It had a certain therapeutic effect on patients with very low vision and deservesclinical application . When used for ischemic optic neuropathy treatment, anisodine significantly promoted the recovery of the visual field, with the effective rate as
high as 82.14% compared with conventional therapeutic regimen using corticosteroids combined with vasodilators, thrombolytic agents, vitamins, and antibiotics.
