piperidines and Coma

At least four doses of quinine followed by a single dose of mefloquine or by a single dose of sulfadoxine-pyrimethamine are two highly effective regimens for chloroquine-resistant falciparum malaria. Mefloquine alone is valuable in ambulant patients. Chloroquine-sensitive falciparum malaria can be treated with a course of chloroquine. Vivax and all other types of malaria should be treated with sequential chloroquine and primaquine. Quinine, by intravenous infusion, is the most effective drug for severe falciparum malaria. The optimum intravenous dose varies between 5 mg/kg and 10 mg/kg administered over four hours. Intravenous or oral quinine should be administered about every 12 hours and the total daily dose of quinine should rarely exceed 20 mg/kg. Intravenous fluid input should be controlled in falciparum malaria to prevent pulmonary oedema. Established renal failure is best treated by dialysis. The value of adrenocortical steroids for falciparum coma has not been established. Fresh blood transfusion may be helpful in small doses for severe anaemia and to replace clotting factors. Anticoagulants, such as heparin, should not be used in falciparum malaria.

Topics: Anemia; Antimalarials; Blackwater Fever; Child; Child, Preschool; Chloroquine; Coma; Drug Combinations; Drug Resistance, Microbial; Hemorrhage; Humans; Kidney Failure, Chronic; Malaria; Piperidines; Plasmodium falciparum; Plasmodium vivax; Primaquine; Pulmonary Edema; Quinine; Quinolines; Sulfadoxine

Topics: Adrenal Hyperplasia, Congenital; Adrenal Insufficiency; Amides; Anesthesia, Epidural; Anesthetics, Intravenous; Anesthetics, Local; Child; Chromosomes, Human, Pair 21; Coma; Gene Deletion; Genetic Diseases, X-Linked; Glycerol Kinase; Hip; Humans; Hypoadrenocorticism, Familial; Hypoglycemia; Male; Muscular Dystrophy, Duchenne; Osteotomy; Piperidines; Remifentanil; Ropivacaine

Topics: Aged; Analgesics, Opioid; Anesthesia; Anesthesia, General; Anesthetics, Intravenous; Coma; Deep Brain Stimulation; Humans; Male; Parkinson Disease; Piperidines; Propofol; Remifentanil

Topics: Abdominal Injuries; Adsorption; Adult; Anesthesia, Local; Anesthetics, Local; Bupivacaine; Coma; Conscious Sedation; Female; Fetal Death; Fetofetal Transfusion; Fetoscopy; Humans; Hypnotics and Sedatives; Infant, Newborn; Infusions, Intravenous; Laser Coagulation; Myoclonus; Myometrium; Piperidines; Placenta; Pregnancy; Pregnancy Complications; Punctures; Remifentanil; Trismus

Rapid administration of large doses of ammonia leads to death of animals, which is largely prevented by pretreatment with N-methyl-D-aspartate (NMDA) receptor antagonists. The present study focuses on a subunit(s) of NMDA receptor involved in ammonia-induced death by use of NMDA receptor GluRepsilon subunit-deficient (GluRepsilon(-/-)) mice and the selective GluRepsilon2 antagonist CP-101,606. Acute ammonia intoxication was induced in mice (eight per group) by a single intraperitoneal (i.p.) injection of ammonium chloride. Appearance of neurological deteriorations depended on the doses of ammonium chloride injected. While wild-type, GluRepsilon1(-/-), GluRepsilon4(-/-), and GluRepsilon1(-/-)/epsilon4(-/-) mice all died by ammonium chloride at 12 mmol/kg during the first tonic convulsions, two of eight GluRepsilon3(-/-) mice survived. Pretreatment of wild-type mice with CP-101,606 prevented two mice from ammonia-induced death. Pretreatment of GluRepsilon3(-/-) mice with CP-101,606 prevented the death of three mice and prolonged the time of death of non-survivors. Similarly, the neuronal form of nitric oxide synthase (NOS) inhibitor 7-nitroindazole (7-NI) as well as the nonselective NOS inhibitor L-NMMA, but not the inducible NOS inhibitor 1400W, partially prevented the death of mice and prolonged the period of death. Furthermore, ammonium chloride prolonged the increase in intracellular free Ca2+ concentration ([Ca2+]i) and subsequent NO production induced by NMDA in the cerebellum. These results suggest that activation of NMDA receptor containing GluRepsilon2 and GluRepsilon3 subunits and following activation of neuronal NOS are involved in acute ammonia intoxication which leads to death of animals.

Topics: Ammonia; Animals; Calcium; Cerebellum; Coma; Dizocilpine Maleate; Dose-Response Relationship, Drug; Enzyme Inhibitors; Excitatory Amino Acid Antagonists; Injections, Intraperitoneal; Mice; Mice, Inbred C57BL; Mice, Knockout; Nitric Oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type I; Piperidines; Receptors, N-Methyl-D-Aspartate; Seizures

The protective effects of TJ-8007 (Tsumura-Zokumeito, Traditional chinese medicine) against cerebral anoxia were investigated with various experimental models in mice and rats. 1) In histotoxic anoxia, TJ-8007 (0.3-3.0 g/kg, p.o.) dose-dependently demonstrated a protective effect on coma induced by a sublethal dose of KCN (1.8 mg/kg, i.v.) in mice. Ifenprodil (30 mg/kg, p.o.) tended to reduce the coma time, but papaverine (100 mg/kg, p.o.) showed a negative effect. 2) TJ-8007 (0.3-3.0 g/kg, p.o.) dose-dependently tended to prolong the survival time of mice subjected to a lethal dose of KCN (3.0 mg/kg, i.v.), TJ-8007 also improved the survival rate at the dose of 3.0 g/kg. Ifenprodil (30 mg/kg, p.o.) or papaverine (100 mg/kg, p.o.) exerted a similar effect on the survival time, but did not affect the mortality. 3) In the normobaric hypoxia with a gas mixture of 96% N2 and 4% O2, TJ-8007 (0.3-3.0 g/kg, p.o.) did not affect the survival time of mice. On the other hand, papaverine (100 mg/kg, p.o.) prolonged the survival time, and phenytoin (100 mg/kg, p.o.) showed a marked protective effect, but ifenprodil (30 mg/kg, p.o.) produced an adverse effect. 4) In the asphyxic anoxia induced by stopping artificial respiration of immovable rats, TJ-8007 (1.0, 3.0 g/kg, p.o.) showed a protective effect on the fall of systemic blood pressure and on the decline of heart rate; furthermore, it dose-dependently prolonged the disappearance time of cortical activity. Also, phenytoin (100 mg/kg, p.o.) tended to protect against the fall of blood pressure and prolonged the cortical resistance time.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Brain Damage, Chronic; Coma; Drugs, Chinese Herbal; Hypoxia, Brain; Male; Medicine, Chinese Traditional; Medicine, East Asian Traditional; Mice; Papaverine; Phenytoin; Piperidines; Plant Extracts; Potassium Cyanide; Rats; Rats, Inbred Strains

The anti-anoxic effect of sufoxazine was investigated in various cerebral anoxia models with mice, in comparison with those of various cerebroactive drugs. Sufoxazine reduced dose-dependently the duration of coma induced by a sublethal dose of KCN (1.8 mg/kg, i.v.), significantly stimulating recovery from the coma at 5 mg/kg, i.p. and 30 mg/kg, p.o. It also protected against a lethal dose of KCN (2.5 mg/kg, i.v.). Sufoxazine prolonged the survival time of mice subjected to hypobaric and normobaric hypoxia. Dihydroergotoxin and ifenprodil gave similar protection in the KCN-induced anoxia models, but produced adverse effects in the hypoxia models. Calcium hopantenate exerted similar but weak protection only at a dose as high as 300 mg/kg, i.p. These findings suggest that sufoxazine has an anti-anoxic action superior to those of the other cerebroactive drugs used.

Topics: Animals; Atmospheric Pressure; Coma; Dihydroergotoxine; Drug Therapy, Combination; gamma-Aminobutyric Acid; Hypoxia, Brain; Mice; Morpholines; Pantothenic Acid; Physostigmine; Piperidines; Potassium Cyanide

Topics: Aged; Androstanes; Coma; Diazepam; Female; Humans; Neuromuscular Nondepolarizing Agents; Piperidines; Respiration, Artificial; Tetanus

Topics: Coma; Diarrhea; Female; Humans; Infant; Parasympatholytics; Piperidines

Topics: Atropine; Coma; Depression; Depressive Disorder; Drug Combinations; Glycolates; Hallucinogens; Humans; Piperidines; Pyrrolidines

Topics: Ascomycota; Barbiturates; Coma; Piperidines; Poisoning; Thiazoles