Enflurane* ; Metabolism* ; Methoxyflurane* ; Panax*

Ginseng has been believed to be a powerful tonic by oriental people for a long time and is one of the most popular folk medicine in oriental countries. Intraperitoneal injection of ginseng into rats and mice has been reported to Increase the rates of hepatic RNA and protein synthesis, increase proliforation of rough RES of liver, and enhance alcohol metabolism. We have carried out a study to see the effects of red ginseng powder and extract on in vivo and in vitro metabolism of enflurane and methoxyflurane in male Fisher 344 rats. Red ginseng powder was dissolved in deionized water and dosed for two weeks ad libitum in rats. Hepatic microsomes were prepared and oxidative defluorination of enflurane and methoxyflurane were measured in vitro. Using red ginseng extract, studies were done of both acute and chronic treatment in rats. In chronic experiments, they were dosed with several dosages three times a day for three days; on the fourth day enflurane was administered i.p. and one hour later fluoride levels were mesured in plasma and hepatic microsomes were prepared for in vitro studies as above. In the acute experiment enflurane was administered intraperitoneally eighteen hours after single oral dosage of ginseng and plasma defluorination was measured. There were no statistically significant differences in hepatic microsomal cytochrome P-450 content or defluorination of enflurane and methoxyflurane between control and experimental groups using either red ginseng extract or powder. The results showed that ginseng ingestion did not affect the metabolism of enflurane and methoxyflurane.
Animal ; Enflurane/metabolism* ; Male ; Methoxyflurane/metabolism* ; Panax/metabolism* ; Plants, Medicinal* ; Rats ; Rats, Inbred F344

Enflurane is metabolized in the liver by the hepatic microsomal enzyme system, cytochrome P-450 (P450IIE1) and induces enzyme system during enflurane exposure. Enhanced biotransformation might occur after enflrane itself and pathologic conditions, such as fasting, diabetes, chemical diabetes. Increased inorganic fluoride, one of the enflurane metabolites could impair renal function. The possibility of increased enflurane defluorination in the diabetic patient, group 1 (control, n= 6), group 2 (blood sugar level below 200mg%, n=6) and group 3 (blood sugar level above 200 mg%, n=5), was investigated by measuring the serum and urine F in the preoperative period and 1 MAC-hr, 2 MAC-hr, immediate postoperative and 24th postoprative hour. In the preoperative, iaunediate postoperative and 24th postoperative hour, the changes of renal function were measured by the BUN and creatinine. The results were as follows: 1) In the diabetic groups, serum fluoride ion increased significantly after enflumane anesthesia at a11 time intervals. Between control and group 3, there were significant difference of aerum inorganic fiuoride after enflurane anesthesia. 2) Urine fluoride levels increased significantly after enflurane anesthesia in all groups 3) There were no changes in renal function after enflurane anestheaia. Our study indicated that enflurane dose not harm diabetic patients.
Anesthesia ; Biotransformation ; Creatinine ; Cytochrome P-450 Enzyme System ; Enflurane* ; Fasting ; Fluorides ; Humans* ; Liver ; Metabolism* ; Preoperative Period

The liver is the major site of endogenous and exogenous drug metabolism. The primary result of drug metabolism is the production of more water-soluble and therefore more easily excreted drug metabolites. Drugs are sometimes biotransformed into more reactive metabolites, which may lead to toxicity. Volatile anesthetics, like most drugs, undergo metabolism in the body and are sometimes associated with toxic reactions. Here, author will discuss the metabolism and hepatic toxicity of inhaled anesthetics. Toxicity and liver injury have been reported after repeated exposure on subsequent occasions to different fluorinated anesthetics. This phenomenon of cross-sensitization has also been reported with the chlorofluorocarbon(CFC) replacement agents, the hydrochlorofluorocarbons(HCFCs). Halothane, enflurane, sevoflurane, isoflurane, desflurane are all metabolized to trifluoroacetic acid, which have been reported to induce liver injury in susceptible patients. The propensity to produce liver injury appears to parrel metabolism of the parent drug: halothane(20%) >>>> enflurane(2.5%) >> sevoflurane(1%) > isoflurane(0.2%) > desflurane(0.02%). The use of any anesthetic must be based on its benefits and risks, how it may produce toxicity, and in which patients it may be most safely administered. Nonhalogenated inhaled anesthetics (nitrous oxide, xenon) chemically inert and not metabolized in human tissue. The perfect anesthetic agents dose not exist. But ongoing research attempts to uncover emerging toxicities. Xenon is not currently approved for clinical use. Other than the expense associated with its use, it may be the most ideal anesthetic agent. In general, surgical manipulation or disturbance of the surgical site appears to be more important in decreasing hepatic blood flow than current anesthetic agents such as isoflurane, sevoflurane, and desflurane or technique. However, the clinician is challenged to balance new information with current clinical practices and choice the safest, most effective agents for each patient.
Anesthetics* ; Enflurane ; Halothane ; Humans ; Isoflurane ; Liver* ; Metabolism ; Parents ; Risk Assessment ; Trifluoroacetic Acid ; Xenon

To evaluate the importance of enflurane metabolism, we selected eleven hepatitis B surface antigen positive, special antigen, antibody negative patients who were schedule for elective surgery. Their physical status were ASA class I or II, liver function tests shoused normal state, and they had no previous history of operation or liver disease. The result were concluded that the influence of enflurane anesthesia on liver function was not significant for anesthesia & surgery.
Anesthesia* ; Appointments and Schedules ; Enflurane* ; Hepatitis B Surface Antigens ; Humans ; Liver ; Liver Diseases ; Liver Function Tests ; Metabolism

Serum Ta and T were measured in 34 patients scheduled elective surgery with general anesthesia, who were divided into two groups (enflurane group' 12, propofol group' 22). No clinical signs of thyroid disturbances could be observed preoperatively in the patients. Anesthesia was induced with thiopental 5 mg/kg in enflurane group; propofol 2 mg/kg in propofol group, and maintained with Oz 2 L/min, NH 2 L/min, enflurane (1.0-2.596) in enflurane group,' 2 L/ min, N 4 L/min and continuous controlled infusion of pmpofol (50-150 mcg/kg/min) in propofol group. Blood samples were collected 5 minutes after arrival in operating room, 1 minute after induction, 5 minutes after intubation, 1 minute after skin incision, during operation and 10 minutes after extubation. Blood samples were centrifused and serum was taken from each sample. Determinations of Ta and T4 were performed using enhanced chemiluminescence immunoassay (ELIA). Comparisons of our results were made using repeated measuves analysis of variance, paired students t-test and statistically significant when p value was less than 0.05. The results are summarized as follows' 1) In enflurane group, serum Ta levels showed a decreasing tendency after extubation compared to baseline. Decreasing serum T4 after administration of thiopental could be considered statistically significant and serum T levels showed a decreasing tendency after extubation compared to baseline. 2) In propofol gnup, serum Tz levels showed a decreasing tendency after extubation compared to baseline. Rises in serum Te after incision and extubation could be considered statistically significant. Based on these results, no direct negative influence of propofol need be expected on Tg metabolism in euthyroid patients. However, the changes in these hormones, although with in the physiological range here, indicate that propofol may adversely influence their levels in the presence of manifested thyroid disease.
Anesthesia ; Anesthesia, General* ; Enflurane* ; Humans ; Immunoassay ; Intubation ; Luminescence ; Metabolism ; Operating Rooms ; Propofol* ; Skin ; Thiopental ; Thyroid Diseases ; Thyroid Gland ; Thyroxine ; Triiodothyronine

The halogenated anesthetics, halothane, enflurane and isoflurane undergo biotransformation in man. They produce inorganic fluoride ion as a metabolite, which is well known as the cause of methoxyflurane induced nephrotoxicity. This study was done to investigate the rapidity and extent of biotransformation of volatile anesthetics for 2 hours of operation. Thirty patients were randomly divided into halothane, enflurane and isoflurane group according to anesthetics. Blood and urine sampling was done before operation, post-induction 10 min, 20 min, 30 min, 1 hour, 1 hour 30 min and 2 hours for the measurement of inorganic fluoride ion. Aspartate aminotransferase, alanine aminotransferase, blood urea nitrogen and creatinine levels were measured before and 24 hours after operation. The results were as follows ; 1) The values of blood fluoride ion in halothane and isoflurane group were decreased with time during operation and there was no change in enflurane group. 2) The values of urine fluoride ion in three groups were increased with time during operation. The rate of increase was the greatest in enflurane group. 3) There were no changes in the value of AST, ALT, BUN and creatinine. The above results suggest that the biotransformation of volatile anesthetics to inorganic fluoride ion was the greatest in enflurane, but the level was insufficent to cause renal dysfunction during 3.18 hour operation.
Alanine Transaminase ; Anesthetics* ; Aspartate Aminotransferases ; Biotransformation* ; Blood Urea Nitrogen ; Creatinine ; Enflurane ; Fluorides ; Halothane ; Humans ; Isoflurane ; Metabolism ; Methoxyflurane

BACKGROUND: The effects of calcium chloride (CaCl2) on regional mechanical function, coronary blood flow (CBF) and myocardial oxygen consumption (MVO2) were examined in normal and stunned myocardium in an open-chest canine model. The effects were compared with those of epinephrine. METHODS: Thirty-one dogs were acutely instrumented under enflurane anesthesia to measure aortic and left ventricular pressure, pulmonary and left anterior descending (LAD) coronary flow, and subendocardial segment length the in LAD region. CaCl2 (0.1, 0.25, 0.5, 0.75 mg/ml of LAD flow, n = 16) or epinephrine (4, 10, 20, 30 ng/ml of LAD flow, n = 15) was directly infused into the LAD before (normal) and after 15 min of its occlusion and reperfusion (stunned). Simultaneous measurements of arterial and coronary venous contents of oxygen and lactate were made to calculate oxygen (EO2) and lactate (Elac) extraction ratio during CaCl2 or epinephrine infusion. RESULTS: Both CaCl2 and epinephrine infusions in normal myocardium resulted in dose-dependent increases in mechanical functions and MVO2. These changes were accompanied by parallel increases in CBF, resulting in no changes of EO2 with CaCl2, while CBF increased more than MVO2 with epinephrine, resulting in a decrease in EO2. After ischemia and reperfusion, mechanical functions and Elac were significantly depressed, but similar mechanical responses to both agents with resultant unaltered EO2 were observed. Elac was decreased further during epinephrine, while it remained unaltered during CaCl2 infusion in stunned myocardium. CONCLUSIONS: CaCl2, similar to epinephrine, exerts positive inotropic and lusitropic effects in normal and stunned myocardium in dogs. In addition, CaCl2 has no direct effect on coronary vascular tone in either normal or stunned myocardium, while epinephrine causes direct vasodilation in normal but not in stunned myocardium.
Anesthesia ; Animals ; Calcium Chloride* ; Calcium* ; Dogs ; Enflurane ; Epinephrine* ; Ischemia ; Lactic Acid ; Metabolism* ; Myocardial Stunning* ; Myocardium ; Oxygen ; Oxygen Consumption ; Reperfusion ; Vasodilation ; Ventricular Pressure

BACKGROUND: Epinephrine is frequently administered during cardiac surgery. The vascular response to epinephrine might be altered by ischemia and reperfusion, since altered vascular control has been demonstrated even after a short period of ischemia. To test the hypothesis, the effects of epinephrine on regional myocardial contractility, coronary blood flow (CBF) and myocardial oxygen consumption (MVO2) were investigated before and after ischemia in an open-chest canine myocardium. METHODS: Fifteen dogs were acutely instrumented under enflurane anesthesia to measure aortic and left ventricular pressures, pulmonary and left anterior descending (LAD) blood flows via Doppler flowmeter, and subendocardial segment length in the region supplied by LAD. Incremental doses of epinephrine (4, 10, 20, 30 ng/mL of LAD flow) were infused directly into LAD before (normal) and after a 15 min of LAD occlusion and subsequent 30 min-reperfusion (stunned). Segment shortening (%SS), as an index of regional myocardial contractility was evaluated. Simultaneous arterial and coronary venous contents of oxygen and lactate were measured during epinephrine (0.0, 4, 10, and 30 ng/mL) infusion. Effectiveness of metabolic vasodilation was determined from oxygen extraction ratio (EO2). RESULTS: Epinephrine infusions before ischemia resulted in dose-dependent increases in %SS and MVO2. These changes were accompanied by excessive increases in CBF, resulting in decreased EO2. After the ischemia and reperfusion, %SS was depressed and lactate extraction (Elac) was reduced, but similar mechanical responses to epinephrine were observed. However, in the stunned myocardium, CBF increased in parallel with increases in MVO2, resulting in unaltered EO2. Epinephrine infusion further decreased Elac dose-dependently in stunned myocardium. Heart rate and left ventricular systolic and diastolic pressures were little but similarly affected during epinephrine infusions before and after myocardial ischemia. CONCLUSIONS: The results suggest that epinephrine exerts positive inotropic effects in both normal and stunned myocardium, and that epinephrine causes direct coronary vasodilation in normal myocardium, but this effect is abolished in stunned myocardium in dogs. It is also suggested that epinephrine infusion depresses Elac dose-dependently in stunned myocardium.
Anesthesia ; Animals ; Dogs* ; Enflurane ; Epinephrine* ; Flowmeters ; Heart Rate ; Ischemia ; Lactic Acid ; Metabolism* ; Myocardial Ischemia ; Myocardial Stunning* ; Myocardium ; Oxygen ; Oxygen Consumption ; Reperfusion ; Thoracic Surgery ; Vasodilation ; Ventricular Pressure