The effects of prolonged low-flow sevoflurane anesthesia on renal and hepatic function.

UNLABELLED: We assessed the effects of prolonged low-flow sevoflurane anesthesia on renal and hepatic functions by comparing high-flow sevoflurane with low-flow isoflurane anesthesia. Thirty patients scheduled for surgery of > or =10 h in duration randomly received either low-flow (1 L/min) sevoflurane anesthesia (n = 10), high-flow (6-10 L/min) sevoflurane anesthesia (n = 10), or low-flow (1 L/min) isoflurane anesthesia (n = 10). We measured the circuit concentrations of Compound A and serum fluoride. Renal function was assessed by blood urea nitrogen, serum creatinine, creatinine clearance, and urinary excretion of glucose, albumin, protein, and N:-acetyl-beta-D-glucosaminidase. The hepatic function was assessed by serum aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, and total bilirubin. Compound A exposure was 277 +/- 120 (135-478) ppm-h (mean +/- SD [range]) in the low-flow sevoflurane anesthesia. The maximum concentration of serum fluoride was 53.6 +/- 5.3 (43.4-59.3) micromol/L for the low-flow sevoflurane anesthesia, 47.1 +/- 21.2 (21.4-82.3) micromol/L for the high-flow sevoflurane anesthesia, and 7.4 +/- 3.2 (3.2-14.0) micromol/L for the low-flow isoflurane anesthesia. Blood urea nitrogen and serum creatinine were within the normal range, and creatinine clearance did not decrease throughout the study period in any group. Urinary excretion of glucose, albumin, protein, and N:-acetyl-beta-D-glucosaminidase increased after anesthesia in all groups, but no significant differences were seen among the three groups at any time point after anesthesia. Lactate dehydrogenase and alkaline phosphatase on postanesthesia Day 1 were higher in the high-flow sevoflurane group than in the low-flow sevoflurane group. However, there were no significant differences in any other hepatic function tests among the groups. We conclude that prolonged low-flow sevoflurane anesthesia has the same effect on renal and hepatic functions as high-flow sevoflurane and low-flow isoflurane anesthesia. IMPLICATIONS: During low-flow sevoflurane anesthesia, intake of Compound A reached 277 +/- 120 ppm-h, but the effect on the kidney and the liver was the same in high-flow sevoflurane and low-flow isoflurane anesthesia.

[Anesthetic management of a patient with hepatocellular carcinoma with tumor thrombus extending into the right atrium].

A 58 year-old male was scheduled for surgery of his hepatic cancer. Tumor invaded to the right atrium through the inferior vena cava. The operative method of removing the tumor in the right atrium was scheduled under extracorporeal circulation after the left lobe hepatectomy. Since there was a tumor in the right atrium, central venous pressure monitoring could not be reliable. Transesophageal echocardiography (TEE) was employed in order to detect the part of the tumor flowing into the pulmonary artery or occluding the tricuspid valve. Due to massive blood loss during hepatectomy, the capacity in the right atrium decreased and the tumor was often about to engage the tricuspid valve. After the rapid fluid therapy, the right atrium capacity increased preventing the engagement of the tumor. TEE was useful not only to observe the movement of the tumor in the right atrium but also to monitor the circulating blood volume.

Sevoflurane requirements for tracheal intubation with and without fentanyl.

We studied 80 healthy ASA 1 patients (aged 20-52 yr) to determine if fentanyl affects sevoflurane requirements for achieving 50% probability of no movement in response to laryngoscopy and tracheal intubation (MAC-TI). Patients were allocated randomly to one of four fentanyl dose groups (0, 1, 2 and 4 micrograms kg-1). Patients in each group received sevoflurane at a pre-selected end-tidal concentration according to an 'up-down' technique. After steady state sevoflurane concentration had been maintained for at least 10 min, fentanyl was administered i.v. Tracheal intubation was performed 4 min after administration of fentanyl, and patients were assessed as moving or not moving. Heart rate (HR) and mean arterial pressure (MAP) were recorded before induction of anaesthesia, just before administration of fentanyl, just before laryngoscopy for intubation, and after intubation. The MAC-TI of sevoflurane was 3.55% (95% confidence intervals 3.32-3.78%), and this was reduced markedly to 2.07%, 1.45% and 1.37% by addition of fentanyl 1, 2 and 4 micrograms kg-1, with no significant difference in the reduction between 2 and 4 micrograms kg-1, showing a ceiling effect. Fentanyl attenuated haemodynamic responses (HR and MAP) to tracheal intubation in a dose-dependent manner, even with decreasing concomitant sevoflurane concentration. Fentanyl 4 micrograms kg-1 suppressed the changes in HR and MAP more effectively than fentanyl 1 or 2 micrograms kg-1 at sevoflurane concentrations close to MAC-TI.

The effects of sevoflurane on recovery of brain energy metabolism after cerebral ischemia in the rat: a comparison with isoflurane and halothane.

UNLABELLED: Isoflurane is an appropriate anesthetic for neuroanesthesia. We evaluated whether the effect of sevoflurane is similar to that of isoflurane or halothane on brain energy metabolism after cerebral ischemia followed by reperfusion using 31P-magnetic resonance spectroscopy. Wistar rats (n = 21) were divided into three groups: isoflurane-, sevoflurane-, or halothane-treated. After anesthesia induction and surgical preparation, each anesthetic concentration was adjusted to 1 minimum alveolar anesthetic concentration. Cerebral ischemia was induced with bilateral carotid occlusion and reduction of mean arterial blood pressure to 30-40 mm Hg by blood withdrawal. Magnetic resonance measurements were performed during ischemia and for 120 min of reperfusion. Intracellular pH in the isoflurane-treated, sevoflurane-treated, and halothane-treated groups decreased to 6.180 +/- 0.149, 6.125 +/- 0.134, and 6.027 +/- 0.157, respectively, at the end of ischemia. There were no differences in the change of phosphorous compounds and intracellular pH between the isoflurane-treated and the sevoflurane-treated groups during ischemia and reperfusion. However, in the halothane-treated group, we observed a significant delay in the recovery of adenosine triphosphate and intracellular pH (0.038 +/- 0.013 pH unit/min compared with 0.064 +/- 0.011 in the isoflurane-treated group and 0.058 +/- 0.008 in the sevoflurane-treated group) until 24 min of reperfusion (P < 0.05). We conclude that sevoflurane has effects similar to isoflurane on brain energy metabolism during and after cerebral ischemia. IMPLICATIONS: It is important to know whether anesthetics adversely effect brain metabolism during ischemia and reperfusion. A new anesthetic, sevoflurane, affected the brain in a manner similar to isoflurane, which has been used for many years as an anesthetic.

Partly exhausted soda lime or soda lime with water added, inhibits the increase in compound A concentration in the circle system during low-flow sevoflurane anaesthesia.

We performed low-flow sevoflurane anaesthesia at a flow rate of 1 litre min-1 in three groups (n = 8 each) using 600 g of fresh soda lime (control group), 600 g of soda lime with 60 ml of water added (water group) or 600 g of soda lime saturated with carbon dioxide, that is partly exhausted soda lime (carbon dioxide group). Degradation products in the system were measured hourly. Inspired and end-tidal carbon dioxide and sevoflurane concentrations, carbon dioxide and temperature of the soda lime were monitored. CF2 = C(CF3)-O-CH2F (compound A) was the only sevoflurane degradation product detected. The mean maximum concentration of compound A was significantly higher in the control group (mean 16.0 (SD 5.0) ppm) than in the water (1.4 (1.0) ppm) or carbon dioxide (4.0 (1.8) ppm) group, and the maximum temperature of the soda lime was significantly lower in the carbon dioxide group (30.7 (3.5) degrees C) than in the control (43.4 (1.8) degrees C) or water (40.8 (1.8) degrees C) group (P < 0.05). The use of partly exhausted soda lime or soda lime with water added reduced compound A concentrations in the system during low-flow sevoflurane anaesthesia.

[The plasma concentration of buprenorphine during its continuous epidural infusion after catheterization at different vertebral levels].

We investigated 27 patients undergoing elective surgery under epidural anesthesia. The plasma concentration of buprenorphine during its continuous epidural administration was measured by the radioimmunoassay method. We also performed a retrospective study on supplemental analgesics necessary for 48 hours after surgeries. The plasma concentration of buprenorphine was found to be stable at 300 pg.ml-1 during its continuous epidural infusion. The frequencies of administration of supplemental analgesics were 3.3 times with catheterization at upper thoracic vertebral level, 2. 1 times at lower thoracic vertebral level and 1.7 time at upper lumbar vertebral level. We conclude that analgesia with the continuous epidural administration of buprenorphine is satisfactory at low plasma concentration and is superior, considering the necessity of supplemental analgesics to other methods of systemic administration. It is estimated that the epidural distribution volume at lower thoracic and upper lumbar vertebral level is twice the volume at upper thoracic level from plasma buprenorphine concentration.