• The Korean Journal of Physiology
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• v.19 no.2
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• pp.155-160
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• 1985

Dantrolene sodium(DS) is a long acting skeletal muscle relaxant which has been successfully used to control muscle spasticity in patients with various neurological disorders. However, its use is associated with hepatotoxicity. Tissue sulfhydryl group has many important roles for cellular integration and glutathione serves as a substrate for the detoxification metabolism. The purpose of this study were to investigate the effect of DS on tissue sulfhydrl group and glutathione content. Foully albino rats were divided into two groups ; saline treated (control) and DS treated groups. DS dissolved in saline was administered orally. All rats were sacrificed after 7. 14. 21 and 28 days of DS ana saline treatment by dacapitation ana liver was removed for the enzyme preparation. Total and nonprotein sulfhydryl were measured by the method of Sedlak and Lindsay (1968). Total glutathione content was assayed according to the method described by Tietze (1969) and glutathione reductase was assayed according to the method of Racker (1955), The results obtained are summarized as follows : DS administration significantly depressed the total, protein and nonprotein sulfhydryl content in liver. There were significant reduction of both total glutathione content and glutathione reductase activity in liver. On the basis of the above results it may be speculated that the toxicity of DS are well correlated with tissue sulfhydryl content and glutathione reductase activity.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.19 no.1
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• pp.109-114
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• 1997

Malignant hyperthermia is a hypermetabolic, fatal syndrome triggered by anesthetic drugs that occurs frequently in genetically susceptible persons. It is characterized by tachycardia, rapidly increasing temperature, skeletal muscle rigidity, respiratory and metabolic acidosis, cyanosis etc. It has been noted that the majority of cases of malignant hyperthermia are fatal unless early diagnosis and treatment are performed. Thus, the accurate prediction of preanesthetic susceptibility and early diagnosis of malignant hyperthermia is necessary to appropriate treatment. Dantrolene sodium has been shown to be effective in the prevention and treatment of malignant hyperthermia. We experienced a case of malignant hyperthermia, which is presented of a 32-year-old healthy male patient in whom a orthognatic surgery was performed under $O_2-N_2O$-enfl-rane anesthesia with induction by pentobarbital and succinylcholine. We discuss this case with reviewing the history, incidence, etiology, pathophysiology, clinical signs & biochemical changes, prevention & treatment.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.27 no.4
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• pp.381-387
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• 2005

Malignant hyperthermia is a catastrophic, hypermetabolic syndrome that arises in susceptible individuals when they are exposed to certain inhalational anesthetics or muscle relaxants. It is characterized by hyperthermia, tachycardia, acidosis, and muscle rigidity. It has been noted that the majority of cases of malignant hyperthermia are fatal unless early diagnosis and treatment are performed. We experienced a 24 year old male Malignant hyperthermia presented for orthognathic surgery under $O_2-N_2O$-sevoflurane anesthesia without succinylcholine. Two half hours after induction, tachycardia developed and was followed by unstable blood pressure and hyperpyrexia. Anesthesia was terminated and vigorous emergency treatment was attempted. The patient was treated by the intravenous administration of dantrolene sodium. The diagnosis of an acute malignant hyperthermia reaction by clinical criteria can be difficult because of the nonspecific nature and variable incidence of many of the clinical signs and laboratory findings. So the malignant hyperthermia clinical grading scale is recommended for use as an aid to the objective definition of this disease. This clinical grading system provides a new and comprehensive clinical case definition for the malignant hyperthermia syndrome. We recently encountered a case of delayed malignant hyperthermia during sevoflurane anesthesia that was successfully treated by the intravenous administration of dantrolene sodium. In conclusion, exposure to sevoflurane should be avoided in patients thought to be susceprible to malignant hyperthermia.

• Animal cells and systems
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• v.1 no.1
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• pp.77-80
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• 1997

DOantrolene is a primary specific therapeutic drug for prevention and treatment of malignant hyperthermia symptoms. The mechanisms underlying the therapeutic effects of the drug are not well understood. The present study aimed at the characterization of the effects of azumolene, a water soluble dantrolene analogue, on ryanodine binding to sarcoplasmic reticulum (SR) from normal and malign::lnt hyperthermia susceptible (MHS) swine muscles. Characteristics of $[^3H]ryanodine$ binding were clearly different between the two types of SR. Kinetic analysis of eH]ryanodine binding to SR in the presence of $2{\mu}M$ $Ca^{2+}$ showed that association constant $(K_{ryanodine}_7$ is significantly higher in MHS than normal muscle SR $(2.83 vs. 1.32{\times}10^7 M^{-1}$, whereas the maximal ryanodine binding capacity $(B_{max})$ is similar between the two types of SR. Addition of azumolene $(e.g. 400{\mu}M)$ did not significantly alter both $K_{ryanodine}$ and $B_{max}$ of $[^3H]$ryanodine binding in both types of SR, indicating that the azumolene effect was not on the ryanodine binding sites. Addition of caffeine activated $[^3H]$ ryanodine binding in both types of SR, and caffeine sensitivity was significantly higher in MHS muscle SR than normal muscle SR $(K_{caffeine}:3.24 vs. 0.82 {\times} 10^2 M^{-l}). Addition of azumolene $(e.g.400{\mu}M)$ decreased Kcaffeine without significant change in $B_{max}$ in both types of SR suggesting that azumolene competes with caffeine binding site(s). These results suggest that malignant hyperthermia symptoms are caused at least in part by greater sensitivity of the MHS muscle SR to the $Ca^{2+}$ release drug(s), and that azumolene can reverse the symptoms by reducing the drug affinity to $Ca^{2+}$ release channels.