Hirosato Kikuchi

Decomposition of enflurane in soda lime

The stability of enflurane in soda lime was examined. A product of enflurane decomposition was detected after the reaction of enflurane with soda lime, but not in the absence of soda lime. The production of this compound, identified as 1-chloro-1,2-difluorovinyl difluoromethyl ether by gas chromatography-mass spectrometry, increased with time and temperature. The same decomposition product was produced by the reaction of enflurane with potassium, sodium, or calcium hydroxides, and it was also detected in the gas phase at a maximum concentration of 1.29 ppm at 420 min after 5% enflurane circulated with 200 ml/min carbon dioxide gas in a closed anesthesia circle system with a soda lime canister and a model lung. We concluded that enflurane was decomposed to 1-chloro-1,2-difluorovinyl difluoromethyl ether by soda lime.

Clinical Classification and Incidence of Malignant Hyperthermia in Japan

Denborough and Lovell [1] first described malignant hyperthermia (MH) as an inherited syndrome in 1960. At present, it is generally accepted that MH is triggered by many anesthetics. Succinylcholine chloride (SCC) and volatile anesthetics have been especially implicated as important triggering drugs [2,3]. With these triggering drugs, induced hypermetabolism produces tachycardia, increased O2 consumption and CO2 production, premature ventricular contraction, hypotension and hypertension, cyanosis, tachypnea, muscle rigidity, and hyperthermia as the signs of MH. Also seen as complications of MH are electrolyte imbalances, myoglobinuria, hyperkalemia, creatine phosphokinase (CPK) elevation, impaired coagulation, renal failure, and severe metabolic and respiratory acidosis.

Malignant hyperthermia with normal calcium-induced calcium release rate of sarcoplasmic reticulum in skeletal muscle

tance of suxamethonium 100 mg. Pancuronium was used as an intraoperative muscle relaxant. The surgery lasted approximately 2 h, 30min. His rectal temperature increased from 37.8°C just after the induction of anesthesia to 39°C just before the end of surgery. His temperature increased further after the reversal of the pancuronium with atropine and neostigmine. He became tachypneic and his skin color revealed cyanotic change in the peripheral regions of his extremities and in his lips. His temperature transiently reached 40.5°C, in spite of whole-body cooling carried out with a cooling mat and ethanol evaporation. Analysis of his arterial blood gas revealed pH 6.55, base excess (BE) 29.8mEq/l. He showed almost complete recovery 7h after whole-body cooling and the intravenous administration of bicarbonate (530mEq in total). In the recent series of operations, performed at our institution, an emergency appendectomy operation was performed (first operation) without any problem, with the patient under spinal anesthesia combined with epidural anesthesia. Postoperative pathological examination diagnosed appendicular cancer. Eighteen days after the first operation, right hemicolectomy was performed (second operation). Anesthesia was induced with 120 mg of propofol, after the intravenous administration of dantrolene 60mg, and was maintained with fentanyl, propofol, epidural block, and N2O—O2. His airway was managed with a laryngeal mask. His rectal temperature decreased from 36°C to 35.2°C during the 2-h, 23-min operation. Results for serum electrolytes, serum creatine kinase (CK), arterial blood gas analysis, and urinary analysis were all normal. Two hours after the end of the operation, his temperature had increased to 38.2°C in the intensive care unit (ICU), and this was associated with shivering. Intramuscular sulpyrine and intravenous flurbiprofen decreased his temperature slightly. Sixty milligrams of dantrolene, however, was ineffective. His temperature had gradually returned to normal by day 6 after the operation.

What Is Malignant Hyperthermia

As the contents of this Free Discussion Session was to be transcribed from the tape recording and then become a part of the proceedings, the Chairperson requested at the outset that each speaker kindly give his name and affiliation. Unfortunately, not all gave their name as requested and therefore it was not possible to verify all the statements with the respective speakers. Thus, the organizers made editorial changes and identified speakers other than the chairpersons as A, B, C... and were not able to check the transcription with each of the speakers. However, utmost care has been exercised by the editors to ensure accuracy, but it is feared that the discussion made may not have necessarily been transcribed precisely.

Enzyme inhibition by analgesic and hypnotic agents on anaerobic dehalogenation of halothane.

Enzyme inhibition on anaerobic dehalogenation of halothane by various analgesic or hypnotic agents was investigated in vitro using rat liver microsomal fraction. The production rate of chloro-difluoro-ethylene (CDE) and chloro-trifluoroethane (CTE), anaerobic metabolites of halothane, was measured when various concentrations of analgesic or hypnotic agents (fentanyl, morphine, pentazocine, buprenorphine, ketamine, diazepam, chlorpromazine and hydroxyzine) were supplemented. Inhibitor constant (Ki) of each agent was calculated and compared with each other. The activity of NADPH-cytochrome c reductase (fp2) and NADH-ferricyanide reductase (fp1) was measured when each agent was added. The values of inhibitor constants (Ki) for CDE and CTE formation were in the following order from large to small values; morphine (656 μM and 2570 μM), chlorpromazine (49.7 μM and 68.1 μM), ketamine (24.9 μM and 64.4 μM), fentanyl (23.9 μM and 34.6 μM), hydroxyzine (19.2 μM and 50.8 μM), diazepam (17.0 μM and 13.9 μM), buprenorphine (11.2 μM and 22.4 μM), and pentazocine (1.96 μM and 6.67 μM) respectively. Pentazocine inhibited the formation of CDE 300 fold greater than morphine. The activity of fp2 and fp1 did not change by the addition of these analgesic or hypnotic agents. These results indicate that various analgesic or hypnotic agents, which are commonly used with halothane in clinical anesthesia, suppress the anaerobic dehalogenation of halothane in vitro. They also imply that the suppression of production of halothane metabolites is the result of direct enzyme inhibition on cytochrome P-450, since these agents did not affect the activity of fpz and fPI which are flavoproteins existing in the microsomal electron transport system.