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Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic, haemodynamic and neuroendocrine responses to electrical neuromuscular stimulation were measured in five normal and five malignant hyperthermia-susceptible pigs. Normal animals recovered after stimulation but susceptible pigs showed malignant hyperthermia-like responses. Catecholamine levels were higher in malignant hyperthermia-sensitive than in normal pigs at all sampling times.
Res Vet Sci 1985 Sep
PMID:Electrical stimulation triggers porcine malignant hyperthermia. 407 Jul 95

A comparative study of two patients, one affected by haemorrhagic shock and encephalopathy (HSE) and the other by heatstroke is reported. Both presented shock, disseminated intravascular coagulation, neurological damage and hepatopathy. A lowered alpha 1-antitrypsin concentration as well as a slightly increased circulating immune complexes and complement consumption were observed in the HSE patient but not in the heatstroke one. In both, cultures for bacteria were negative, the viral serology was non-specific and hepatitis A and B studies were negative. HSE patient died. A possible relationship between HSE, heatstroke, malignant hyperthermia and halothane hepatitis is postulated. Fever, potentially hepatotoxic drugs or unknown agents (HSE) might trigger this clinical picture.
An Esp Pediatr 1985 Sep
PMID:[Hemorrhagic shock and encephalopathy. Its possible relation with heat stroke]. 407 88

The methods used to screen patients for malignant hyperpyrexia at present are not sufficiently accurate. This paper reports more specific methods of detecting patients liable to develop malignant hyperpyrexia. A motor-point muscle biopsy is performed for histopathological examination and to detect muscle contracture in vitro after exposure to halothane and suxamethonium.
Br Med J 1972 Sep 02
PMID:Screening for malignant hyperpyrexia. 506 39

Work in pigs has shown that malignant hyperpyrexia during anaesthesia may occur without suxamethonium having been given. A virtually constant feature in reported cases and in our own observations is that all subjects developing hyperpyrexia had received nitrous oxide and halothane.
Br Med J 1968 Sep 07
PMID:Hyperpyrexia during anaesthesia. 566 93

The time-course of Ca2+ release from sarcoplasmic reticulum isolated from muscles of normal pigs and those of pigs susceptible to malignant hyperthermia were investigated using stopped-flow spectrophotometry and arsenazo III as a Ca2+ indicator. Several methods were used to trigger Ca2+ release: (a) addition of halothane (e.g., 0.2 mM); (b) an increase of extravesicular Ca2+ concentration ([Ca2+0]); (c) a combination of (a) and (b), and (d) replacement of ions (potassium gluconate with choline chloride) to produce membrane depolarization. The initial rates of Ca2+ release induced by either halothane or Ca2+ alone, or both, are at least 70% higher in malignant hyperthermic sarcoplasmic reticulum than in normal. The amount of Ca2+ released by halothane at low [Ca2+0] in malignant hyperthermic sarcoplasmic reticulum is about twice as large as in normal sarcoplasmic reticulum. Membrane depolarization led to biphasic Ca2+ release in both malignant hyperthermic and normal sarcoplasmic reticulum, the rate constant of the rapid phase of Ca2+ release induced by membrane depolarization being significantly higher in malignant hyperthermic sarcoplasmic reticulum (k = 83 s-1) than in normal (k = 37 s-1). Thus, all types of Ca2+ release investigated (a, b, c and d) have higher rates in malignant hyperthermic sarcoplasmic reticulum than normal sarcoplasmic reticulum. These results suggest that the putative Ca2+ release channels located in the sarcoplasmic reticulum are altered in malignant hyperthermic sarcoplasmic reticulum.
Biochim Biophys Acta 1984 Sep 05
PMID:Kinetic studies of Ca2+ release from sarcoplasmic reticulum of normal and malignant hyperthermia susceptible pig muscles. 608 5

Syndrome malin refers to neuroleptic malignant syndrome (NMS), a combination of extrapyramidal symptoms, hyperthermia, autonomic dysfunction, hypertension, and coma, which has been reported primarily with haloperidol administration, but also with fluphenazine, thiothixene, and thioridazine. NMS is much more severe than typical extrapyramidal reactions to neuroleptic agents and can result in fatality. The syndrome is not dose related and can begin within hours of initiation of therapy or after months of treatment. Treatment of NMS has been mainly supportive in the past. Recent reports have suggested benefits from the use of bromocriptine and amantadine (dopaminergic agonists), based on a possible etiology of neuroleptic-induced dopaminergic blockade. Dantrolene also has been utilized successfully in NMS on the hypothesis that the syndrome is similar to anesthetic-induced malignant hyperthermia. These agents provide a more specific treatment for this potentially lethal syndrome.
Drug Intell Clin Pharm 1983 Sep
PMID:Therapy of syndrome malin. 613 52

For the past 25 years, halothane has been the primary anesthetic agent at Children's Hospital, Columbus, Ohio. To confirm our impression that adverse reactions to halothane are rarely a problem in children, we examined the records of 200,311 cases conducted with halothane from June 1, 1958, through May 31, 1983. Life-threatening complications due to side effects were identified in fifteen patients, and could be grouped into three areas: hepatitis (one), malignant hyperthermia (ten), and cardiac arrhythmias (four). No child died or sustained permanent sequelae. In eleven instances, other drugs (succinylcholine, atropine, cocaine, and epinephrine) possibly contributed to the adverse reactions.
Anesth Analg 1984 Sep
PMID:Halothane and children: the first quarter century. 646 80

The methods of gathering information to determine the safety of anesthesia and to establish the risk of mortality and morbidity include anecdotal tales, in-hospital audit and peer review, reports to medical protective societies, retrospective studies, reviews of specific problems and prospective studies. All these methods have limitations and, in particular, do not readily differentiate the anesthetic from the surgical contributions. However, it appears that over the past 30 years the risk of death directly attributable to anesthesia has decreased from 1 in 2680 to about 1 in 10 000. The main causes of death are faulty anesthetic techniques due to human error, drug overdose, coexistent disease and failure of immediate postoperative care. Equipment failure, poor preoperative assessment, halothane-associated hepatitis and malignant hyperthermia, although often cited in the literature, are rarely the cause of problems associated with anesthesia.
Can Med Assoc J 1984 Sep 01
PMID:Anesthesia in 1984: how safe is it? 646 15

Purebred Pietrain malignant hyperthermia (MH)-susceptible pigs (n = 102) were subjected to halothane (0%, 1%, 2%, 3%, 4%, and 5%) in oxygen. The number of pigs in each group exhibiting muscle rigidity (MH(+) reaction) and the reaction times were recorded, as were the number of deaths resulting from MH. Mortality was not affected by the halothane concentration. However, halothane concentration did markedly affect the number of MH(+) reactions and the reaction times. False-negative reactions were apparent in the pigs at halothane concentrations less than 3%. Increasing the halothane concentration incrementally to 5% (from 0%) significantly (P less than 0.05) decreased reaction times between treatment groups. The reductions in reaction times which occurred in the pigs given the 3%, 4%, and 5% halothane concentrations (62.1, 56.2, and 50.05)--although significant (P less than 0.05)--would indicate that 3% halothane would generally be sufficient for MH testing.
Am J Vet Res 1984 Sep
PMID:Halothane testing for malignant hyperthermia in swine: dose-response effects. 649 30

Using the skinned fiber preparation, the response to caffeine was studied on the skeletal muscle of malignant hyperthermia or other neuromuscular diseases. The sensitivity to caffeine was increased in the muscle of malignant hyperthermia. The sensitivity also was increased in Duchenne muscular dystrophy or asymptomatic patients with raised serum creatine kinase activity. Judging from the interaction between caffeine and the contractile system, the abnormal response originated from the sarcoplasmic reticulum in malignant hyperthermia. In Duchenne muscular dystrophy, the contractile system also might be involved in the increased sensitivity. Since the disease spectrum presenting abnormal responses is broad, it is suggested that muscle fibers become sensitive to caffeine when they are degenerating or regenerating.
Muscle Nerve 1983 Sep
PMID:Malignant hyperthermia and related neuromuscular diseases: caffeine contracture of the skinned muscle fibers. 663 64


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