High Concentrations Of Sevoflurane Research Articles

The effects of sevoflurane on cerebral blood flow autoregulation in rats.

In this study, we investigated the effect of sevoflurane on cerebral blood flow (CBF) autoregulation in rats. Twenty-four male Sprague-Dawley rats were randomly assigned to receive one of the following anesthetic treatments. In Group 1 (n = 8, control) anesthesia was maintained using fentanyl (25 microg x kg(-1) x h(-1)) and N2O/O2 (fraction of inspired oxygen 0.33). In Group 2 (n = 8) and Group 3 (n = 8), anesthesia was maintained using 2% sevoflurane (1 minimum alveolar anesthetic concentration [MAC]) and 2 MAC sevoflurane (4 vol%) in O2/air (fraction of inspired oxygen 0.33), respectively. Cortical CBF autoregulation was measured during graded hemorrhage within the mean arterial pressure (MAP) range of 100-30 mm Hg using laser Doppler flowmetry. CBF was constant with fentanyl/ N2O (Group 1) and 1 MAC sevoflurane (Group 2) within the MAP range of 100-40 mm Hg. In Group 3 (2 MAC sevoflurane), CBF decreased as a linear function of hemorrhagic hypotension. These results indicate that CBF autoregulation was intact during 1 MAC sevoflurane. In contrast, CBF autoregulation was impaired with 2 MAC sevoflurane. This is probably related to a reduction of baseline cerebrovascular tone with higher concentrations of sevoflurane, which results in a decreased capacity of autoregulatory cerebrovascular dilation during hemorrhage. The purpose of the present study was to investigate the effect of sevoflurane on cerebral blood flow autoregulation in rats. Cerebral blood flow autoregulation was intact with 1 minimum alveolar anesthetic concentration sevoflurane but was impaired with 2 minimum alveolar anesthetic concentration sevoflurane.

The Effects of Sevoflurane on Cerebral Blood Flow Autoregulation in Rats

In this study, we investigated the effect of sevoflurane on cerebral blood flow (CBF) autoregulation in rats. Twenty-four male Sprague-Dawley rats were randomly assigned to receive one of the following anesthetic treatments. In Group 1 (n = 8, control) anesthesia was maintained using fentanyl (25 microg x kg(-1) x h(-1)) and N2O/O2 (fraction of inspired oxygen 0.33). In Group 2 (n = 8) and Group 3 (n = 8), anesthesia was maintained using 2% sevoflurane (1 minimum alveolar anesthetic concentration [MAC]) and 2 MAC sevoflurane (4 vol%) in O2/air (fraction of inspired oxygen 0.33), respectively. Cortical CBF autoregulation was measured during graded hemorrhage within the mean arterial pressure (MAP) range of 100-30 mm Hg using laser Doppler flowmetry. CBF was constant with fentanyl/ N2O (Group 1) and 1 MAC sevoflurane (Group 2) within the MAP range of 100-40 mm Hg. In Group 3 (2 MAC sevoflurane), CBF decreased as a linear function of hemorrhagic hypotension. These results indicate that CBF autoregulation was intact during 1 MAC sevoflurane. In contrast, CBF autoregulation was impaired with 2 MAC sevoflurane. This is probably related to a reduction of baseline cerebrovascular tone with higher concentrations of sevoflurane, which results in a decreased capacity of autoregulatory cerebrovascular dilation during hemorrhage.The purpose of the present study was to investigate the effect of sevoflurane on cerebral blood flow autoregulation in rats. Cerebral blood flow autoregulation was intact with 1 minimum alveolar anesthetic concentration sevoflurane but was impaired with 2 minimum alveolar anesthetic concentration sevoflurane.

Leucocyte distribution during sevoflurane anaesthesia

We have examined if sevoflurane anaesthesia per se modified the number of circulating leucocytes in humans. Fifty-nine patients undergoing elective surgery were anaesthetized with sevoflurane in oxygen. The inhaled concentration was increased gradually to 5% and maintained for 20 min. Arterial blood samples were obtained before induction of anaesthesia and at 20 min. While the total number of leucocytes remained constant, circulating neutrophils decreased (mean 3370 (SD 1030) mm-3 to 3170 (940) mm-3; P < 0.01) and lymphocytes increased (1870 (520) mm-3 to 2040 (580) mm-3; P < 0.01). We conclude that high concentrations of sevoflurane modified the distribution of leucocytes in anaesthetized patients.

Absence of biochemical evidence for renal and hepatic dysfunction after 8 hours of 1.25 minimum alveolar concentration sevoflurane anesthesia in volunteers.

Sevoflurane is degraded by carbon dioxide absorbents to a difluorovinyl ether (compound A) that can cause renal and hepatic injury in rats. The present study applied sensitive markers of renal and hepatic function to determine the safety of prolonged (8 h), high concentration (3% end-tidal) sevoflurane anesthesia in human volunteers. Thirteen healthy male volunteers provided informed consent to undergo 8 h of 1.25 minimum alveolar concentration sevoflurane anesthesia delivered with a fresh gas flow of 2 l/min. Glucose, protein, albumin, N-acetyl-beta-D-glucosaminidase (NAG), and alpha- and pi-glutathione-S-transferase (GST) levels were analyzed in urine collected at 24 h before and for 3 days after sevoflurane anesthesia. Daily blood samples were analyzed for creatinine, blood urea nitrogen (BUN), alanine aminotransferase, alkaline phosphatase, and bilirubin concentrations. Circuit compound A and plasma fluoride concentrations were measured. During anesthesia, average and maximum inspired compound A concentrations were 27 +/- 7 and 34 +/- 6 (mean +/- SD) and median mean blood pressure, esophageal temperature, and end-tidal carbon dioxide levels were 63 mmHg, 36.8 degrees C, and 32 mmHg, respectively. The average serum inorganic fluoride concentration 2 h after anesthesia was 66.2 +/- 14.7 microM. Results of tests of hepatic function and renal function (BUN, creatinine concentration) were unchanged after anesthesia. Glucose, protein, albumin, and NAG excretion were not significantly increased after anesthesia. Urine concentrations of alpha-GST and pi-GST were increased on day 1 after anesthesia and alpha-GST was increased on day 2 after anesthesia but returned to normal afterward. Prolonged (8 h), high concentration (3%) sevoflurane anesthesia administered to volunteers in a fresh gas flow of 2 l/min does not result in clinically significant changes in biochemical markers of renal or hepatic dysfunction.

Isoflurane and sevoflurane interact with the nicotinic acetylcholine receptor channels in micromolar concentrations.

This study was performed to elucidate and compare the effects of sevoflurane and of isoflurane on the nicotinic acetylcholine receptor of mouse myotubes. The experiments were done with special reference to anesthetic concentrations considerably less than those used for clinical anesthesia. The patch-clamp technique was used to record acetylcholine-activated currents from the embryonic type of the nicotinic acetylcholine receptor in the outside-out mode. A piezo-driven liquid filament switch was used for the ultrafast application of acetylcholine alone or in combination with isoflurane or sevoflurane. In addition, the patches were preexposed to either anesthetic, preceding the activation with acetylcholine. The current elicited by acetylcholine was reduced reversibly and in a concentration-dependent manner by both anesthetics, which were equally effective. Preexposure of the patches to isoflurane or sevoflurane showed an additional inhibition that was present at micromolar concentrations. The time courses of current decay could be fitted by single exponentials for isoflurane. At higher concentrations of sevoflurane, the current decay became biexponential. In contrast to isoflurane, sevoflurane increased the time constants of desensitization when applied in low concentrations. At the nicotinic acetylcholine receptor, isoflurane and sevoflurane act primarily through the same mechanisms: Both affect the open and the closed state of the channels in concentrations equal to and less than those encountered clinically. The kinetics of desensitization, however, are altered in a different manner. Thus there may be several different sites of interaction.

A comparison of vital capacity breath and tidal breathing techniques for induction of anaesthesia with high sevoflurane concentrations in nitrous oxide and oxygen

Vital capacity breath and tidal breathing techniques were compared for induction of anaesthesia with 7.5% sevoflurane in nitrous oxide, and oxygen. Thirty five subjects were randomly assigned to a vital capacity breath group (19) or to a tidal breathing group (16). The mean time for induction was faster with vital capacity breath (41 s) than with tidal breathing (52 s, p < 0.05). Some involuntary movements were seen in the tidal breathing group but none in the vital capacity breath group. Coughing was seen in a quarter of the subjects in the tidal breathing group and in one subject of the vital capacity breath group. The vital capacity group showed excellent characteristics: rapid, and pleasant induction without premedication. We conclude that the vital capacity breath technique is necessary for the inhalation induction of anaesthesia; it provides enough overpressure to allow the subject to pass reliably and rapidly through the initial stages of excitement.

Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations.

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a Paco2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a Paco2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when Paco2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a Paco2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane. The hypocapnia-induced abnormality during exposure to 2 MAC of either agent was due to decreased CBF associated with low perfusion pressure, indicating that there was no direct effect of these anesthetics on cerebral energy metabolism.

Brain energy metabolism and blood flow during sevoflurane and halothane anesthesia: effects of hypocapnia and blood pressure fluctuations.

The effects of halothane and sevoflurane on cat brain energy metabolism and regional cerebral blood flow (rCBF) were evaluated during normo- and hypocapnia. Brain energy status was evaluated with phosphorous nuclear magnetic resonance spectroscopy (31P-MRS) and rCBF was measured by the hydrogen clearance method. A high concentration of halothane (3 MAC) impaired brain energy metabolism, while even a higher concentration of sevoflurane (4 MAC) had no untoward effect on brain energy metabolism. At 3 MAC of halothane, there were measurable decreases in brain phosphocreatine (69% of the control) and increases in brain inorganic phosphate (about 250% of control Pi), even though CBF was about 70% of the control value. During hypocapnia, the phosphocreatine levels began to decrease at a PaCO2 of 2.7 kPa with 2 MAC of sevoflurane (90% of the control), and at a PaCO2 of 4.0 kPa with 2 MAC of halothane (92% of the control). rCBF had decreased to less than 50% of the control value when PaCO2 was < or = 2.7 kPa with 2 MAC of sevoflurane and < or = 4.0 kPa with 2 MAC of halothane. Abnormal brain energy metabolism was only observed when rCBF was decreased to less than half of the control (non-anesthetized and normocapnic) value. Following administration of a vasopressor, metaraminol, the abnormal brain energy metabolism induced by 2 MAC of halothane at a PaCO2 of 1.33 kPa was normalized in parallel with the improved rCBF values. We conclude that hyperventilation and fluctuating blood pressure contribute to the occurrence of abnormal brain energy metabolism during halothane and sevoflurane anesthesia. This is more pronounced with halothane than with sevoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of sevoflurane on lidocaine-induced convulsions.

The influence of sevoflurane on lidocaine-induced convulsions was studied in cats. The convulsive threshold (mean +/- SD) was 41.4 +/- 6.5 mg. l(-1) with lidocaine infusion (6 mg.kg(-1).min(-1)), increasing significantly to 66.6 +/- 10.9 mg. l(-1) when the end-tidal concentration of sevoflurane was 0.8%. However, the threshold (61.6 +/- 8.7 mg. l(-1)) during 1.6% sevoflurane was not significant from that during 0.8% sevoflurane, indicating a celling effect. There was no significant difference in the convulsive threshold between sevoflurane and enflurane. The rise in blood pressure became less marked when higher concentrations of sevoflurane or enflurane were administered and the blood pressure at convulsions decreased significantly in 1.6% sevoflurane, and in 0.8% and 1.6% enflurane. However, there was no significant difference in the lidocaine concentrations measured when the systolic blood pressure became 70 mmHg. Apamin, a selective blocker of calcium-dependent potassium channels, was administered intracerebroventricularly in rats anesthetized with 0.8% sevoflurane to investigate the mechanism of the anticonvulsive effects. Apamin (10 ng) had a tendency to decrease the convulsive threshold (21.6 +/- 2.2 to 19.9 +/- 2.5 mg. l(-1)) but this was not statistically significant. It is suggested that sevoflurane reduces the convulsive effect of lidocaine toxicity but carries some risk due to circulatory depression.