No abstract available.
Antidotes* ; Emergencies*

"Jajie" means antidote in Dai language. As an important part of theories of Dia ethnic medicine, "Jajie" focuses on antidote before treatment. With wide application and exact effect, "Jajie" plays an important role in preventing and treating diseases, especially liver disease, digestive system diseases, metabolic diseases, skin diseases and so on. Therefore, systematic collection, analysis and studies on Dai ethnic medicine "Jajie" is an important content in the development of the theory of Dai ethnic medicine as well as new drugs. This essay briefs the general situation of "Jajie" and the advance of its studies, and gives comments on Jajie's development.
Antidotes ; therapeutic use ; China ; ethnology ; Humans ; Medicine, Chinese Traditional

To investigate the therapeutic effect of high-dosage gamma-aminobutyric acid (GABA) on acute tetramine (TET) poisoning, 50 Kunming mice were divided into 5 groups at random and the antidotal effects of GABA or sodium dimercaptopropane sulfonate (Na-DMPS) on poisoned mice in different groups were observed in order to compare the therapeutic effects of high-dosage GABA with those of Na-DMPS. Slices of brain tissue of the poisoned mice were made to examine pathological changes of cells. The survival analysis was employed. Our results showed that both high-dosage GABA and Na-DMPS could obviously prolong the survival time, delay onset of convulsion and muscular twitch, and ameliorate the symptoms after acute tetramine poisoning in the mice. Better effects could be achieved with earlier use of high dosage GABA or Na-DMPS. There was no significant difference in prolonging the survival time between high-dose GABA and Na-DMPS used immediately after poisioning. It is concluded that high-dosage GABA can effectively antagonize acute toxicity of teramine in mice. And it is suggested that high-dosage GABA may be used as an excellent antidote for acute TET poisoning in clinical practice. The indications and correct dosage for clinical use awaits to be further studied.
Acute Disease ; Antidotes/*administration & dosage ; Antidotes/therapeutic use ; Bridged Compounds/*poisoning ; Random Allocation ; Rodenticides/*poisoning ; Unithiol/therapeutic use ; gamma-Aminobutyric Acid/*administration & dosage ; gamma-Aminobutyric Acid/therapeutic use

When the skin and soft tissue necrosis occurs due to extravasation of intravenously administrated biological active materials and drugs, no specific mode of treatment modality is known except for supportive management or debridement and skin graft. This experiment was designed to determine the effective dosage of hyaluronidase and triamcinolone acetonide on the extravasation necrosis caused by calcium gluconate and to establish the optimal time of administration of the antidotes. Initially 0.4 ml of 10% calcium gluconate was injected subcutaneously into the rabbit back. Study I was designed to observe the skin change in 8 groups including control group with no treatment and treated groups with normal saline, saline with hyaluronidase(dosage: 150, 300, 600 unit), saline with triamcinolone acetonide(1 mg, 2 mg), and 150 unit hyaluronidase and 1 mg triamcinolone acetonide (all in volume 0.2 ml, treatment delay: immediate, 15-minutes, 30-minutes, 1-hour, 3-hours delay). The sizes of skin necrosis and induration were measured and compared between each group. Study II was designed to examine the histologic findings of the skin and evaluate the effect of hyaluronidase and triamcinolone acetonide on tissue damage. The sizes of induration and necrosis are smaller in all treated groups than non-treated group and the statistically significant protective effect on reducing the size of necrosis was found in groups treated with the drugs within 15 minutes to 30 minutes(p < 0.05). The most effective protection was obtained by the immediate injection of 150 unit dosage of hyaluronidase with 1 mg triamcinolone acetonide. This study suggests that intralesional injection of hyaluronidase and triamcinolone acetonide within half hour delay for the treatment of extravasation necrosis of calcium gluconate is the most effective, probably due to their diffusion, antiinflammatory effect and role in facilitating the resorption of calcium in the tissue.
Antidotes ; Calcium Gluconate* ; Calcium* ; Debridement ; Diffusion ; Hyaluronoglucosaminidase* ; Injections, Intralesional ; Necrosis ; Skin ; Transplants ; Triamcinolone Acetonide* ; Triamcinolone*

Acute Disease ; Animals ; Antidotes ; therapeutic use ; Mice ; Organophosphate Poisoning ; Poisoning ; drug therapy ; Rats

Organophosphate (OP) pesticides are the most common source of human toxicity globally, causing high mortality and morbidity despite the availability of atropine as a specific antidote and oximes to reactivate acetylcholinesterase. The primary toxicity mechanism is inhibition of acetylcholinesterase (AchE), resulting in accumulation of the neurotransmitter, acetylcholine, and abnormal stimulation of acetylcholine receptors. Thus, the symptoms (muscarinic, nicotinic, and central nervous system) result from cholinergic overactivity because of AchE inhibition. OP can also cause rhabdomyolysis, pancreatitis, parotitis, and hepatitis. OP therapy includes decontamination, supportive therapy, and the use of specific antidotes such as atropine and oximes. However, there has been a paucity of controlled trials in humans. Here we evaluated the literature for advances in therapeutic strategies for acute OP poisoning over the last 10 years.
Acetylcholine ; Acetylcholinesterase ; Antidotes ; Atropine ; Decontamination ; Hepatitis ; Humans ; Neurotransmitter Agents ; Oximes ; Pancreatitis ; Parotitis ; Pesticides ; Receptors, Cholinergic ; Rhabdomyolysis

Unexpected occurrence of local anesthetic toxicity is not rare and can cause fatal complications that do not respond to any known drug of intervention. Recently, the successful use of lipid emulsion for local anesthetic toxicity has been reported and recommended as a rescue method for cardiac or neurologic complications. We report a case of seizure attack and respiratory arrest successfully recovered with the use of intravenous lipid emulsion. Clinicians must be aware of the beneficial role of lipid emulsion in cases of local anesthetic toxicity.
Anesthetics, Local ; Ankle* ; Antidotes ; Fat Emulsions, Intravenous ; Neurotoxicity Syndromes ; Resuscitation* ; Seizures

OBJECTIVETo investigate the activity of ChE in rats poisoned by dimehypo and then treated with pralidoxime methylchloride or unithiol.

METHODRats were divided into control group (dimehypo); intervention groups [dimehypo plus pralidoxime methylchloride or dimehypo plus unithiol (sodium dimercaptopropanesulphonate)]. Rats were dosed with 4 different doses of dimehypo: 1/16, 1/8, 1/4 and 1/2 of LD50 respectively(the LD50 of dimehypo is 342 mg/kg). After being poisoned with dimehypo orally, rats were immediately injected intramuscularly with pralidoxime methylchloride or unithiol. The activity of ChE in blood was detected before and 1/2, 1, 2, 4 and 24 h after poisoning in dimehypo and intervention groups.

RESULTThe ChE activity of four dose subgroups at 1 h after poisoning were (1.04 +/- 0.21), (0.84 +/- 0.12), (0.71 +/- 0.12), (0.66 +/- 0.07) U/ml respectively; the ChE activity of pralidoxime methylchloride intervention groups were (1.01 +/- 0.18), (1.17 +/- 0.11), (1.01 +/- 0.04), (1.03 +/- 0.12) U/ml respectively; and the ChE activity of unithiol intervention groups were (1.15 +/- 0.15), (1.26 +/- 0.27), (1.08 +/- 0.08), (1.04 +/- 0.12) U/ml respectively. The inhibited ChE in blood was recovered by either treatment with pyraldoxime methylchloride or unithiol. These two drugs had similar effects of recovering the activity of ChE(P > 0.05), but at higher doses(1/4 and 1/2 of LD50) the effects of both were not so good.

CONCLUSIONPralidoxime methylchloride and unithiol could partly recover the activity of ChE inhibited by dimehypo.

Animals ; Antidotes ; pharmacology ; Cholinesterase Inhibitors ; poisoning ; Cholinesterases ; blood ; Dose-Response Relationship, Drug ; Insecticides ; poisoning ; Pralidoxime Compounds ; pharmacology ; Rats ; Unithiol ; pharmacology

Aconitum is a genus of various species of flowering plants that belongs to the Family Ranunculaceae. Most Aconitum sp. have extremely toxic alkaloid substances such as aconitine, mesaconitine and hypaconitine. Among these substances, aconitine can cause fatal cardiotoxicity by activating sodium channels followed by calcium channels in myocardial cells. Even though there have been various therapeutic plans suggested comprising antidotes based on diverse case reports and studies, there is no confirmatory treatment protocol for aconite poisoning. Here, we report an aconite poisoning patient who had refractory ventricular tachyarrhythmia that did not respond to intravenous amiodarone therapies even though they were sustained for over 2 hours, but showed successful recovery following intravenous fat emulsions (IFE) therapy.
Aconitine ; Aconitum* ; Amiodarone ; Antidotes ; Calcium Channels ; Cardiotoxicity ; Clinical Protocols ; Fat Emulsions, Intravenous ; Flowers ; Humans ; Poisoning* ; Ranunculaceae ; Sodium Channels ; Tachycardia

Aconitum is a genus of various species of flowering plants that belongs to the Family Ranunculaceae. Most Aconitum sp. have extremely toxic alkaloid substances such as aconitine, mesaconitine and hypaconitine. Among these substances, aconitine can cause fatal cardiotoxicity by activating sodium channels followed by calcium channels in myocardial cells. Even though there have been various therapeutic plans suggested comprising antidotes based on diverse case reports and studies, there is no confirmatory treatment protocol for aconite poisoning. Here, we report an aconite poisoning patient who had refractory ventricular tachyarrhythmia that did not respond to intravenous amiodarone therapies even though they were sustained for over 2 hours, but showed successful recovery following intravenous fat emulsions (IFE) therapy.
Aconitine ; Aconitum* ; Amiodarone ; Antidotes ; Calcium Channels ; Cardiotoxicity ; Clinical Protocols ; Fat Emulsions, Intravenous ; Flowers ; Humans ; Poisoning* ; Ranunculaceae ; Sodium Channels ; Tachycardia