Requests: If you need specific information on this remedy - e.g. a proving or a case info on toxicology or whatsoever, please post a message in the Request area www.homeovision.org/forum/ so that all users may contribute.
Animal studies comparing solanine with K-strophantidine revealed similar effects. Exposure of neonatal rat cells to solanine caused an initial increased contraction rate followed by cessation (Bergers & Alink, 1980). Isolated frog muscle showed an increased intropy. Toxic intravenous doses caused ventricular fibrillation in rabbits. In addition, in rabbits, toxic intra-peritoneal (I.P) doses caused mild to moderate inhibition of both specific and non-specific cholinesterase (Patil et al, 1972).
Variability in the toxic alkaloid and nitrate concentrations of the plants in different situations accounts for the conflicting reports of their being harmless in some cases and harmful in others (Cooper & Johnson, 1984).
In vivo: in rabbits, the intra-peritoneal administration caused mild to moderate inhibition of specific and non-specific cholinesterases (Patil et al., 1972). Intravenously, it caused ventricular fibrillation (Nishie et al, 1971).
In sick animals, blood-tinged serum and edema is seen around the kidneys, and blood dots if the animal lives for several days. Histological lesions in the kidneys consisted on: tubular toxic necrosis, focal hemorrhages and edema. Lesions in the digestive tract are: hemorrhagic gastritis and enteritis with ulcers (Scineca & Oehme, 1985).
It has limited medicinal uses: in liniments, poultices and decoctions for external use (Martindale, 1982). It has also been used in folkloric medicine as sedative and anticonvulsant. Solanine hydrochloride has been used as an agricultural insecticide (Merck, 1989).
Possible teratogenic effect has been reported, associated to solanine-containing potatoes (Solanum tuberoseum), but not to solanum nigrum. Many workers investigated whether solanidan alkaloids might be teratogenic, and although some effects were reported in chick embryos and hamsters, most workers found not terata in rats, rabbits and mice (Keeler & Tu, 1983).
The active principles affect mainly the heart, the central nervous system and the gastrointestinal tract. Symptoms may appear rapidly: nausea, vomiting, abdominal pains, diarrhoea, headache, mydriasis, flushed and warm skin, delirium, psychomotor agitation, coma, paralysis, circulatory and respiratory depression, loss of sensation and even death.
Unripe, green fruits should always be considered poisonous.
The course of poisoning is rapid: symptoms appear soon after Ingestion of the unripened fruits. Symptomatology is rarely delayed beyond six hours. In severe poisoning, death usually occurs within 24 hours.
Death may occur from cardiac arrhythmias and from respiratory failure.
If the patient survives after 24 hours, the prognosis is favorable due to the rapid elimination of the toxin through faeces and urine.
Systematic description of clinical effects
Cardiovascular: Tachycardia and cardiac arrhythmia occur, followed by circulatory depression.
Respiratory: Respiration depression may occur.
CNS: Altered mental status manifested as drowsiness, headache, hallucinations, delirium, psychomotor agitation or restlessness, coma and death.
Peripheral nervous system: Paralysis may occur.
Autonomic nervous system: Skin is warm and flushed. Initial tachycardia can occur.
Gastrointestinal: Nausea, vomiting, diarrhoea, abdominal pains.
11.1 Case reports from literature
A 10-year-old girl was brought to the hospital with loss of
consciousness of unknown origin. The mother denied any
possibility of poisoning. The child's sister later
confessed that, on the previous day, the patient had eaten
15 to 20 black berries. The plant, when examined, turned out
to be black nightshade. The child's mental status alternated
between sleepiness and restlessness. Later, it was found out
that due to severe headache, the child herself took four to
six sleeping tablets (Polster, 1953).