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*

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

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

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

BACKGROUND: Paraquat is a widely used herbicide, known to cause lethal toxicity in humans. Most studies about paraquat have concentrated on systemic toxicity, however several cases of paraquat-induced dermatitis have been reported. OBJECTIVE: The purpose of this study was to confirm the cutaneous toxic effect of paraquat and to select potential antidotes in paraquat-induced dermatitis. METHODS: Keratinocyte toxicity due to paraquat and the toxicity reduction capacity of several drugs were investigated in eitro. Topical effects of these drugs on paraquat-induced dermatitis in guinea pig skin was also investigated. RESULTS: Over 50% of keratinocytes failed to survive at a concentration of 2X10-4M paraquat by a neutral red uptake assay. Skin irritation by paraquat was observed at 2% concentration by non-invasive methods as well as a skin biopsy. Dexamethasone, glutathione and tocopherol showed some capacity to reduce paraquat-induced keratinocyte toxicity in vitro. Only dexamethasone, however, showed a reduction of cutaneous blood flow volume and dermal inflammatory cell infiltration in the guinea pig study. CONCLUSION: This result indicates the possible in eitro protective effect of paraquat toxicity in glutathione and tocopherol. Dexamethasone was capable of reducing paraquat-induced cytotoxicity and dermatitis both in vitro and in vivo.
Animals ; Antidotes* ; Biopsy ; Dermatitis ; Dexamethasone ; Glutathione ; Guinea Pigs ; Humans ; In Vitro Techniques ; Keratinocytes ; Neutral Red ; Paraquat* ; Skin* ; Tocopherols

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