Perfusion of ischemic myocardium during anesthesia with sevoflurane

BACKGROUND: Sevoflurane produces direct vasodilation of coronary arteries in vitro and decreases coronary vascular resistance in vivo, pharmacologic properties that may contribute to the development of "coronary steal." This investigation examined the effects of sevoflurane on the distribution of regional myocardial perfusion in chronically instrumented dogs with steal-prone coronary artery anatomy. METHODS: Dogs were chronically instrumented for measurement of aortic and left ventricular pressure, diastolic coronary blood flow velocity and subendocardial segment length. After recovery from surgery, dogs underwent repetitive, brief, left anterior descending coronary artery (LAD) occlusions via an implanted hydraulic vascular occluder to enhance collateral development. A progressive left circumflex coronary artery (LCCA) stenosis was also obtained using an ameroid constrictor. After development of LCCA stenosis, the LAD was totally occluded to produce a model of multivessel coronary artery disease. Systemic hemodynamics, regional contractile function and myocardial perfusion measured with radioactive microspheres were assessed in the conscious state and during sevoflurane anesthesia at 1.0 and 1.5 MAC with and without restoration of arterial blood pressure and heart rate to conscious levels. RESULTS: Total LAD occlusion with simultaneous LCCA stenosis increased heart rate, mean arterial pressure, left ventricular systolic and end-diastolic pressures, end-diastolic segment length, and rate-pressure product in conscious dogs. Subsequent administration of sevoflurane caused dose-related decreases in arterial pressure, left ventricular systolic pressure, double product, and peak rate of increase of left ventricular pressure at 50 mmHg. Perfusion of normal myocardium was unchanged during sevoflurane anesthesia. In contrast, sevoflurane caused dose-dependent decreases in blood flow to myocardium supplied by the stenotic LCCA, which returned to control levels after restoration of heart rate and arterial pressure. No reduction in collaterally derived blood flow to the occluded region was produced by 1.0 or 1.5 MAC sevoflurane. No redistribution of blood flow away from the occluded LAD region to normal or stenotic myocardium occurred during sevoflurane anesthesia. In fact, increases in the ratio of blood flow between occluded and normal zones or occluded and stenotic zones were observed in the subepicardium during 1.5 MAC sevoflurane with maintenance of the heart rate and arterial pressure at conscious levels. CONCLUSIONS: The results demonstrate that sevoflurane does not reduce or abnormally redistribute myocardial blood flow derived from coronary collateral vessels in a chronically instrumented canine model of multivessel coronary artery obstruction.     

Repeated low-flow sevoflurane anesthesia: effects on hepatic and renal function in beagles

We studied the effects of repeated low-flow sevoflurane anesthesia for 6 hours. Five beagle dogs received 1.3 MAC (3%) sevoflurane anesthesia. Anesthesia of 6 hours was repeated on at the 7th day after the first anesthesia. Compound A gas samples were collected from the inspiratory limb during anesthesia. Concentrations of serum and renal fluoride, hepatic and renal function parameters were measured during and up to 7 days after the first and second anesthesia. The peak concentration of compound A was 23.7 +/- 3.6 ppm at 2 hours and the same level remained during the anesthesia. Plasma fluoride level exceeded 50 mmol.l-1 during anesthesia and rapidly decreased to the preanesthesia level thereafter. Serum GOT increased slightly only on the first postanesthesia day. No significant changes in other blood chemistry studies were observed. The excretion of renal tubular enzymes did not increase during and after anesthesia. Repeated low flow sevoflurane anesthesia in beagles did not affect hepatic and renal function significantly.     

The effects of sevoflurane, isoflurane, halothane, and enflurane on hemodynamic responses during an inhaled induction of anesthesia via a mask in humans

A rapid increase in isoflurane or desflurane concentration induces tachycardia and hypertension and increases-plasma catecholamine concentration. Little information is available as to whether sevoflurane, halothane, and enflurane induce similar responses during anesthesia induction via mask. Fifty ASA physical status I patients, aged 20-40 yr, and scheduled for elective minor surgery, received one of four volatile anesthetics: sevoflurane, isoflurane, halothane, or enflurane. Anesthesia was induced with thiamylal, followed by inhalation of 0.9 minimum alveolar anesthetic concentration (MAC) of the anesthetic in 100% oxygen via mask. The inspired concentration of anesthetic was increased by 0.9 MAC every 5 min to a maximum of 2.7 MAC. Heart rate (HR) and systolic blood pressure (SBP) were measured before and every minute for 15 min during anesthetic inhalation. In the sevoflurane and isoflurane groups, venous blood samples were drawn to determine the concentrations of plasma epinephrine and norepinephrine 3 min after each increase in anesthetic concentration. Sustained increments in HR were observed after increases in inspired isoflurane concentration to 1.8 MAC and 2.7 MAC (peak changes of 15 +/- 3 and 17 +/- 3 bpm, respectively). Isoflurane also increased SBP transiently after the inspired concentration was increased to 2.7 MAC (peak change of 10 +/- 4 mm Hg). Enflurane increased HR after the inspired concentration was increased to 2.7 MAC (peak change of 9 +/- 2 bpm). In contrast, changes in sevoflurane and halothane concentrations did not induce hyperdynamic responses. Plasma norepinephrine concentration in the isoflurane group was significantly higher than that in the sevoflurane group during 2.7 MAC (P = 0.022). We propose that there is a direct relationship between airway irritation of the anesthetic and immediate cardiovascular change during an inhaled induction of anesthesia.     

Preservation of the ration of cerebral blood flow/metabolic rate for oxygen during prolonged anesthesia with isoflurane, sevoflurane, and halothane in humans

BACKGROUND: In several animal studies, an increase in cerebral blood flow (CBF) produced by volatile anesthetics has been reported to resolve over time during prolonged anesthesia. It is important to investigate whether this time-dependent change of CBF takes place in humans, especially in clinical situations where surgery is ongoing under anesthesia. In this study, to evaluate the effect of prolonged exposure to volatile anesthetics (isoflurane, sevoflurane, and halothane), the CBF equivalent (CBF divided by cerebral metabolic rate for oxygen (CMRO2) was determined every 20 min during anesthesia lasting more than 4h in patients. METHODS: Twenty-four surgical patients were assigned to three groups at random to receive isoflurane, sevoflurane, or halothane (8 patients each). End-tidal concentration of the selected volatile anesthetic was maintained at 0.5 and 1.0 MAC before surgery and then 1.5 MAC for the 3 h of surgical procedure. Normothermia and normocapnia were maintained. Mean arterial blood pressure was kept above 60 mmHg, using phenylephrine infusion, if necessary. CBF equivalent was calculated every 20 min as the reciprocal of arterial-jugular venous oxygen content difference. RESULTS: CBF equivalent at 0.5 MAC of isoflurane, halothane, and sevoflurane was 21 +/- 4, 20 +/- 3, and 21 +/- 5 ml blood/ml oxygen, respectively. All three examined volatile anesthetics significantly (P<0.01) increased CBF equivalent in a dose-dependent manner (0.5, 1.0, 1.5 MAC). AT 1.5 MAC, the increase of CBF equivalent with all anesthetics was maintained increased with minimal fluctuation for 3 h. The mean value of CBF equivalent at 1.5 MAC in the isoflurane group (45 +/- 8) was significantly (P<0.01) greater than those in the halothane (32 +/- 8) and sevoflurane (31 +/- 8) groups. Electroencephalogram was found to be relatively unchanged during observation periods at 1.5 MAC. CONCLUSIONS: These results demonstrate that CBF/CMRO2 ratio is markedly increased above normal and maintained during prolonged inhalation of volatile anesthetics in humans. It is impossible to determine whether these data indicate a stable CBF or whether CBF and CMRO2 are changing in parallel during the observation period. The unchanging electroencephalographic pattern suggests that the former possibility is more likely and that the increase of CBF produced by volatile anesthetics is maintained over time without decay, which has been reported in several animal studies. It also is suggested that isoflurane possesses greater capability to maintain global CBF relative to CMRO(2) than does halothane or sevoflurane. time.)     

Immunohistochemical localization of cytosolic sialidase in the epithelium of rat cornea and conjunctiva

OBJECTIVE: To compare the hemodynamic change, course of recovery and adverse reaction in desflurane, sevoflurane and enflurane inhalation under low flow for patients undergoing selective abdominal surgery. METHODS: Following thiopental induction, 42 patients were divided into three groups: the first group received desflurane, the second sevoflurane and the third enflurane. During surgery, one of the agents around 1 minimum alveolar concentration (MAC) was used for maintenance, with fresh gas flow of 0.3-0.5 L/min for either desflurane or enflurane, and (0.8-1.0) L/min for sevoflurane. Heart rate (HR), blood pressure and end-tidal anesthetic concentration were monitored continuously. Time intervals from cutting off anesthetic to patient opening eyes, following commands, stating the time and location and recalling date of birth were all recorded. In addition, postoperative nausea or vomiting was traced. RESULTS: Desflurane caused the least cardiovascular depression. with mean arterial pressure (MAP) maintained significantly better at 10, 30 and 60 minutes of surgery and with HR stabilized right after incision as well. Its emergence was 2 times faster than sevoflurane, and 5-6 times quicker than enflurane. However, nausea or vomiting was found the lowest in patients receiving sevoflurane, though no distinct difference was shown between desflurane and enflurane. Nevertheless, patients under desflurane suffered less. CONCLUSIONS: Desflurane offers significant advantages for clinical anesthesia maintenance over sevoflurane and enflurane. It provides minimal cardiovascular depression, much quicker recovery, yet still causes some nausea during emergence.     

Effects of xenon on hemodynamic responses to skin incision in humans

BACKGROUND: The authors evaluated the hemodynamic suppressive effects of xenon in combination with sevoflurane at skin incision in patients undergoing surgery. METHODS: Forty patients were assigned randomly to receive one of the following four anesthetics: 1.3 minimum alveolar concentration (MAC) sevoflurane, 0.7 MAC xenon with 0.6 MAC sevoflurane, 1 MAC xenon with 0.3 MAC sevoflurane, or 0.7 MAC nitrous oxide with 0.6 MAC sevoflurane (n = 10 each group). Systolic blood pressure and heart rate were measured before anesthesia, before incision, and approximately 1 min after incision. RESULTS: The changes in hemodynamic variables in response to incision were less with sevoflurane in combination with xenon and nitrous oxide than with sevoflurane alone. Changes in heart rate (in beats/min) were 19+/-11 (+/- SD) for sevoflurane alone, 11+/-6 for 0.7 MAC xenon-sevoflurane, 4+/-4 for 1 MAC xenon-sevoflurane, and 8+/-7 for nitrous oxide-sevoflurane. Changes in systolic blood pressure were 35+/-18 mmHg for sevoflurane alone, 18+/-8 mmHg for 0.7 MAC xenon-sevoflurane, 16+/-7 mmHg for 1 MAC xenon-sevoflurane, and 14+/-10 mmHg for nitrous oxide-sevoflurane. CONCLUSIONS: Xenon and nitrous oxide in combination with sevoflurane can reduce hemodynamic responses to skin incision compared with sevoflurane alone. One probable explanation may be that xenon has analgesic properties similar to those of nitrous oxide, although the exact mechanism is yet to be determined.     

Absence of renal and hepatic toxicity after four hours of 1.25 minimum alveolar anesthetic concentration sevoflurane anesthesia in volunteers

Sevoflurane is degraded by CO2 absorbents to Compound A. The delivery of sevoflurane with a low fresh gas flow increases the generation of Compound A. The administration of Compound A to rats can produce injury to renal tubules that is dependent on both the dose and duration of exposure to Compound A. The present study evaluated renal and hepatic function in eight volunteers after a 1-L/min delivery of 3% (1.25 minimum alveolar anesthetic concentration) sevoflurane for 4 h. Volunteers gave their informed consent and provided 24-h urine collections before and for 3 days after sevoflurane anesthesia. Urine samples were analyzed for glucose, protein, albumin, and alpha- and pi-glutathione-S-transferase. Daily blood samples were analyzed for markers of renal and liver injury or dysfunction. Circuit Compound A and plasma fluoride concentrations were determined. During anesthesia, the average maximal inspired Compound A concentration was 39 +/- 6 (mean +/- SD). The median mean arterial pressure, esophageal temperature, and end-tidal CO2 were 62 +/- 6 mmHg, 36.5 +/- 0.3 degrees C, and 30.5 +/- 0.5 mm Hg, respectively. Two hours after anesthesia, the plasma fluoride concentration was 50 +/- 9 micromol/L. All markers of hepatic and renal function were unchanged after anesthesia (repeated-measures analysis of variance P > 0.05). Low-flow sevoflurane was not associated with renal or hepatic injury in humans based on unchanged biochemical markers of renal and liver function. IMPLICATIONS: Sevoflurane delivered in a 3% concentration with a fresh gas flow of 1 L/min for 4 h generated an average maximal Compound A concentration of 39 ppm but did not result in any significant increase in sensitive markers of renal function or injury, including urinary protein, albumin, glucose, and alpha- and pi-glutathione-S-transferase.     

Clinical sevoflurane metabolism and disposition. I. Sevoflurane and metabolite pharmacokinetics

BACKGROUND: Sevoflurane has low blood and tissue solubility and is metabolized to free fluoride and hexafluoroisopropanol (HFIP). Although sevoflurane uptake and distribution and fluoride formation have been described, the pharmacokinetics of HFIP formation and elimination are incompletely understood. This investigation comprehensively characterized the simultaneous disposition of sevoflurane, fluoride, and HFIP. METHODS: Ten patients within 30% of ideal body weight who provided institutional review board-approved informed consent received sevoflurane (2.7% end-tidal, 1.3 MAC) in oxygen for 3 h after propofol induction, after which anesthesia was maintained with propofol, fentanyl, and nitrous oxide. Sevoflurane and unconjugated and total HFIP concentrations in blood were determined during anesthesia and for 8 h thereafter. Plasma and urine fluoride and total HFIP concentrations were measured during and through 96 h after anesthetic administration. Fluoride and HFIP were quantitated using an ion-selective electrode and by gas chromatography, respectively. RESULTS: The total sevoflurane dose, calculated from the pulmonary uptake rate, was 88.8 +/- 9.1 mmol. Sevoflurane was rapidly metabolized to the primary metabolites fluoride and HFIP, which were eliminated in urine. HFIP circulated in blood primarily as a glucuronide conjugate, with unconjugated HFIP < or = 15% of total HFIP concentrations. In blood, peak unconjugated HFIP concentrations were less than 1% of peak sevoflurane concentrations. Apparent renal fluoride and HFIP clearances (mean +/- SE) were 51.8 +/- 4.5 and 52.6 +/- 6.1 ml/min, and apparent elimination half-lives were 21.4 +/- 2.8 and 20.1 +/- 2.6 h, respectively. Renal HFIP and net fluoride excretion were 4,300 +/- 540 and 3,300 +/- 540 mumol. Compared with the estimated sevoflurane uptake, 4.9 +/- 0.5% of the dose taken up was eliminated in the urine as HFIP. For fluoride, 3.7 +/- 0.4% of the sevoflurane dose taken up was eliminated in the urine, which, because a portion of fluoride is sequestered in bone, corresponded to approximately 5.6% of the sevoflurane dose metabolized to fluoride. CONCLUSIONS: Sevoflurane was rapidly metabolized to fluoride and HFIP, which was rapidly glucuronidated and eliminated in the urine. The overall extent of sevoflurane metabolism was approximately 5%.     

Preservation of hypoxic pulmonary vasoconstriction during sevoflurane and desflurane anesthesia compared to the conscious state in chronically instrumented dogs

BACKGROUND: The authors' objective was to assess the extent to which sevoflurane and desflurane anesthesia alter the magnitude of hypoxic pulmonary vasoconstriction compared with the response measured in the same animal in the conscious state. METHODS: Left pulmonary vascular pressure-flow plots were generated in seven chronically instrumented dogs by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure-left atrial pressure) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder implanted around the right main pulmonary artery. Pressure-flow plots were generated during normoxia and hypoxia on separate days in the conscious state, during sevoflurane (approximately 3.5% end-tidal), and during desflurane (approximately 10.5% end-tidal) anesthesia. Values are mean+/-SEM. RESULTS: In the conscious state, administration of the hypoxic gas mixture by conical face mask decreased (P < 0.01) systemic arterial PO2 from 94+/-2 mmHg to 50+/-1 mmHg and caused a leftward shift (P < 0.01) in the pressure-flow relationship, indicating pulmonary vasoconstriction. The magnitude of hypoxic pulmonary vasoconstriction in the conscious state was flow-dependent (P < 0.01). Neither anesthetic had an effect on the baseline pressure-flow relationship during normoxia. The magnitude of hypoxic pulmonary vasoconstriction during sevoflurane and desflurane was also flow-dependent (P < 0.01). Moreover, at any given value of flow the magnitude of hypoxic pulmonary vasoconstriction was similar during sevoflurane and desflurane compared with the conscious state. CONCLUSION: These results indicate that hypoxic pulmonary vasoconstriction is preserved during sevoflurane and desflurane anesthesia compared with the conscious state. Thus, inhibition of hypoxic pulmonary vasoconstriction is not a general characteristic of inhalational anesthetics. The flow-dependent nature of the response should be considered when assessing the effects of physiologic or pharmacologic interventions on the magnitude of hypoxic pulmonary vasoconstriction.     

Application of alpha-keto acid decarboxylases in biotransformations

BACKGROUND: Low-flow sevoflurane anesthesia is associated with increasing circuit concentrations of compound A, which is nephrotoxic in rats, but the effect of compound A and low-flow sevoflurane anesthesia on renal function in humans is unclear. The authors compared the effects of high- and low-flow sevoflurane and isoflurane anesthesia on renal function and on several possible markers of nephrotoxicity in humans. METHODS: Forty-two patients without preexisting renal disease underwent either low-flow isoflurane (1 l/min, n = 14), low-flow sevoflurane (1 l/min, n 14), or high-flow sevoflurane (6 l/min, n = 14) anesthesia for body-surface-area surgery scheduled to last at least 4 h. Twenty-four-hour urinary excretion of N-acetyl-beta-glucosaminidase (NAG), beta2-microglobulin, protein, glucose, blood urea nitrogen (BUN), and serum creatinine concentrations were measured before and after anesthesia. RESULTS: There were no differences in blood urea nitrogen, creatinine, and creatinine clearance among the three groups after anesthesia. Increased urinary N-acetyl-beta-glucosaminidase excretions were seen in the low-flow and high-flow sevoflurane groups, but not in the low-flow isoflurane group (P < 0.01). Ten patients in the low-flow sevoflurane group had 24-h urinary excretion of protein that exceeded the normal ranges after anesthesia, but only one patient in the isoflurane and none in the high-flow sevoflurane groups had this. CONCLUSIONS: Low-flow sevoflurane anesthesia was associated with mild and transient proteinuria. However, the observed proteinuria was not associated with any changes in blood urea nitrogen, creatinine, and creatinine clearance in these patients with no preexisting renal disease.     

Renal function in patients during and after hypotensive anesthesia with sevoflurane

STUDY OBJECTIVES: To evaluate renal function during and after hypotensive anesthesia with sevoflurane compared with isoflurane in the clinical setting. DESIGN: Randomized, prospective study. SETTING: Inpatient surgery at Rosai Hospital. PATIENTS: 26 ASA physical status I and II patients scheduled for orthopedic surgery. INTERVENTIONS: Patients received isoflurane, nitrous oxide (N2O), and fentanyl (Group I = isoflurane group; n = 13) or sevoflurane, N2O, and fentanyl (Group S = sevoflurane group; n = 13). Controlled hypotension was induced with either isoflurane or sevoflurane to maintain mean arterial pressure at 60 mmHg for 120 minutes. MEASUREMENTS AND MAIN RESULTS: Measurements included serum inorganic fluoride (previously speculated to influence renal function), creatinine clearance (CCr; to assess renal glomerular function), urinary N-acetyl-beta-D-glucosaminidase (NAG; to assess renal tubular function), blood urea nitrogen (BUN), and serum creatinine (as clinical renal function indices). Serum fluoride, CCr, and NAG were measured before hypotension, 60 minutes, and 120 minutes after the start of hypotension, 30 minutes after recovery of normotension, and on the first postoperative day. BUN and serum creatinine were measured preoperatively and on the third and seventh postoperative days. Minimum alveolar concentration times hour was 3.6 +/- 1.8 in Group I and 4.0 +/- 0.7 in Group S. In both groups, BUN and serum creatinine did not change, and CCr significantly decreased after the start of hypotension. In Group I, serum fluoride and NAG did not change. In Group S, serum fluoride significantly increased after the start of hypotension compared with prehypotension values and compared with Group I values. In addition, NAG significantly increased at 120 minutes after the start of hypotension and at 30 minutes after recovery of normotension, but returned to prehypotension values on the first postoperative day. CONCLUSIONS: Two hours of hypotensive anesthesia with sevoflurane under 5 L/min total gas flow in patients having no preoperative renal dysfunction transiently increased NAG, which is consistent with a temporary, reversible disturbance of renal tubular function.     

Oral clonidine premedication reduces minimum alveolar concentration of sevoflurane for tracheal intubation in children

BACKGROUND: Sevoflurane is a useful anesthetic for inhalational induction in children because of its low solubility in blood and relatively nonpungent odor. Clonidine has sedative and anxiolytic properties and reduces the requirement for inhalation agents. Nitrous oxide (N2O) also decreases the requirement of inhaled anesthetics, but the effect is variable. The minimum alveolar concentration for tracheal intubation (MAC(TI)) of sevoflurane was assessed with and without N2O and clonidine premedication. METHODS: Seventy-two patients, aged 3-11 yr, were assigned to one of six groups (n = 12 each). They received one of three preanesthetic medications (two groups for each premedication): placebo (control), 2 microg/kg oral clonidine or 4 microg/kg oral clonidine. In one group of each premedication, anesthesia was induced with sevoflurane in oxygen; in the other group, anesthesia was induced with sevoflurane in the presence of 60% N2O. Each concentration of sevoflurane at which tracheal intubation was attempted was predetermined according to Dixon's up-and-down method and held constant for at least 20 min before the trial RESULTS: The MAC(TI) of sevoflurane in the absence of N2O (mean +/- SEM) was 3.2 +/- 0.2%, 2.5 +/- 0.1%, and 1.9 +/- 0.2% in the control, 2-microg/kg clonidine, and 4-microg/kg clonidine groups, respectively. Nitrous oxide (60%) decreased the MAC(TI) of sevoflurane by 26%, 24%, and 27% in the control, 2-microg/kg clonidine, and 4-microg/kg clonidine groups. CONCLUSIONS: Oral clonidine premedication decreased the MAC(TI) of sevoflurane. Nitrous oxide also decreased the MAC(TI). The combination of clonidine and N2O lessened the MAC(TI) of sevoflurane more than did either drug alone.     

Founder effect at PGL1 in hereditary head and neck paraganglioma families from the Netherlands

After repeated exposure to inhaled anesthetics, the hepatic function and metabolism of anesthetics may change. The purpose of this study was to investigate inorganic fluoride (F-) kinetics and renal and hepatic function after repeated exposure to sevoflurane. Ten patients (aged 40-70 yr) who had received sevoflurane anesthesia with a gas flow of 6 L/min for neurosurgery twice in 30-90 days were studied. Serum and urine F- concentrations were measured up to 24 h after anesthesia. Blood urea nitrogen, serum creatinine, serum and urine beta2-microglobulin, urine N-acetyl-beta-D-glucosaminidase, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin concentrations were measured up to 7 days after anesthesia. The area under the curve (AUC) of serum and urine F- concentration and half-life of serum F concentration were calculated. Urine beta2-microglobulin, AST, and ALT increased to abnormal levels after both anesthesias, with no difference between anesthesias. No measured variables, AUC of serum and urine F- concentration, or half-life of serum F- concentration showed any differences between the first and second anesthesias. In conclusion, the second exposure to sevoflurane with a high gas flow of 6 L/min in 30-90 days did not change the hepatic and renal function or affect the metabolism of sevoflurane. Implications: We studied the changes of metabolism of sevoflurane and hepatic and renal function after repeated sevoflurane anesthesia in 30-90 days. There were changes indicative of mild liver and kidney injury after sevoflurane anesthesia, but repeated exposure to sevoflurane did not enhance these changes.     

Attentional bias in active smokers, abstinent smokers, and nonsmokers

Pure autonomic failure is characterized by orthostatic hypotension, sweating disorder, urinary incontinence, and syncope. A 64 year-old man with pure autonomia failure was scheduled for suprapubic prostatectomy. We monitoring direct arterial pressure and inserted pulmonary artery catheter prior to the induction of anesthesia. General anesthesia was induced with diazepam 10 mg, fentanyl 0.3 mg, and vecuronium 8 mg for tracheal intubation. Anesthesia was maintained with sevoflurane (0.2-1.5%), 60% nitrous oxide in oxygen supplemented with intermittent epidural anesthesia. During anesthesia, blood loss was immediately replaced with banked blood because autonomic failure could not compensate hypovolemia well. Epidural anesthesia in this patient was considered to cause less hypotension than in patients with normal autonomic function. Therefore, we think epidural anesthesia is a useful anesthesia method for patients with pure autonomic failure. The emergence from anesthesia was smooth and no complications were seen during the perioperative period.     

Alterations of normal left ventricular performance by general anesthesia

Serial invasive and noninvasive (systolic time interval) measurements of left ventricular performance were obtained in six healthy volunteers during general anesthesia employing the following sequence: thiopental induction, succinylcholine (prior to endotracheal intubation), and halothane--100 per cent oxygen at 1.25 and 1.75 MAC. Heart rate (HR), mean pulmonary arterial "wedge" pressure (PAW) and mean systemic arterial pressure (MAP) were measured continuously; cardiac index and systolic time intervals (STI's) were measured during each intervention. At both levels of halothane, MAP and stroke work index decreased (both P less than 0.02), while HR and systemic vascular resistance did not change. At 1.25 MAC halothane PAW was unchanged, but at 1.75 MAC PAW increased from 8 +/- 4 (SD) to 11 +/- 5 torr (P less than 0.02). Preload was altered at 1.25 MAC by administration of 600-1,000 ml lactated Ringer's solution; PAW increased from 9 +/- 4 to 17 +/- 3 torr (P less than 0.01). At 1.75 MAC halothane, volume expansion increased PAW in a similar manner, but the resultant ventricular function curve was depressed compared with 1.25 MAC halothane. In additon, at each level of halothane anesthesia, the ventricular function curve was depressed compared with results obtained in awake normal subjects. Afterload was altered at 1.25 MAC halothane by infusion of phenylephrine sufficient to raise MAP by 30 per cent. This intervention resulted in a greater depression of cardiac performance than that observed at 1.75 MAC halothane alone. Although alterations in STI's were directionally similar to changes observed in invasive hemodynamic measurements, STI's were sensitive to acute alternations in loading conditions. It is concluded that the levels of halothane commonly employed for general anesthesia significantly depress left ventricular performance in normal subjects, as evidenced by abnormal responses to alterations in preload and afterload, and that STI's should not be employed for routine measurement of left ventricular performance during anesthesia unless both the afterload and the preload on the myocardium are known.     

Generalised mitochondrial cytopathy is an absolute contraindication to orthotopic liver transplant in childhood

OBJECTIVE: To compare mask anesthesia induction and recovery characteristics between 2 inhalant anesthetic agents: isoflurane and sevoflurane. ANIMALS: 16 clinically normal, young adult Beagles. PROCEDURE: Using a cross-over design, dogs were randomly selected to receive sevoflurane or isoflurane via a face mask and a circle anesthetic system. Vaporizer setting concentrations were increased in stepwise, equal minimum alveolar concentrations (MAC) for each anesthetic until the vaporizer setting of 2.6% for isoflurane or 4.8% for sevoflurane (2 MAC) was reached. Concentration was kept constant until the dog had a negative tail clamp response and was intubated. End-tidal concentration was maintained at 1.8 to 2.0% or 3.3 to 3.8% for isoflurane or sevoflurane, respectively (1.4 to 1.6 MAC) for 30 minutes. Dogs were allowed to recover with only tail clamp stimulation until a positive response was obtained. Extubation was performed when a spontaneous swallow reflex was observed. Dogs were allowed to achieve sternal recumbency and stand unassisted without further stimulation. RESULTS: Sevoflurane induction resulted in shorter time to loss of palpebral reflex, negative tail clamp response, and time to tracheal intubation, and was of better quality than isoflurane induction. Both anesthetics were associated with rapid and smooth recovery. CONCLUSIONS: Sevoflurane mask induction is faster and of better quality, compared with isoflurane, in adult dogs. Recovery time and quality are comparable. CLINICAL RELEVANCE: On the basis of these results, sevoflurane is a suitable inhalant anesthetic for mask induction and recovery in adult dogs and appears to have some advantages over isoflurane, including faster and smoother mask induction.     

Effects of thiopental and sevoflurane on hemodynamics during anesthetic management of electroconvulsive therapy

The effect of thiopental and sevoflurane (1 MAC, 2 MAC) on hemodynamics was assessed in a randomized study involving 38 adult patients undergoing electroconvulsive therapy (ECT). Blood pressure, heart rate and electrocardiogram (ECG) were monitored during the ECT procedure. After oxygenation, hypnosis was induced with a bolus injection of thiopenal (TPS) 4 mg.kg-1. Muscle relaxation was achieved by succinylcholine, 1 mg.kg-1 intravenously before ECT procedure. Ventilation was assisted using a face mask with 100% oxygen (TPS group), 1.7% sevoflurane (1 MAC group) or 3.4% sevoflurane (2 MAC group), plus 50% nitrous oxide and 50% oxygen. Thereafter, an electrical stimulus was administered. A total of 150 treatment sessions were evaluated. The rate pressure product increased in every group right after ECT, but the use of sevoflurane (2 MAC) significantly diminished the response compared with sevoflurane (1 MAC) and thiopental. In the sevoflurane (2 MAC) group, no ventricular arrhythmias were observed. In general, it seems that sevoflurane (2 MAC) is as effective as thiopental and sevoflurane (1 MAC) as an induction agent for ECT.     

Normal trachea during forced expiration: dynamic CT measurements

In order to understand the mechanism of acute renal failure frequently observed in severe acute pancreatitis, renal microcirculation and renal hemodynamics were investigated during experimental acute pancreatitis in dogs induced by autologous bile and trypsin mixture into the pancreatic duct. Renal tissue blood flow (hydrogen gas clearance method), renal arterial blood flow, and cardiac output (transonic blood flow meter) were each measured for 5 h after induction of pancreatitis. The effect on renal hemodynamics of a new synthesized protease inhibitor--E-3123; 4-(2-succinimidoethylthio)phenyl-4-quanidinobenzoate methane sulfonate--intravenously infused at the rate of 3 mg/kg/h was also investigated. The mean blood pressure and pulse pressure decreased after induction of pancreatitis. Renal microcirculation and renal artery blood flow decreased during the experiment. However, in dogs with treated by E-3123, renal microcirculation was preserved during the first hour of the experiment and decreased gradually afterward, but it was significantly higher than that of the dogs without E-3123 during 3-5 h. The mean blood pressure and pulse pressure were preserved nearly at preoperative levels during the experimental period. We concluded that renal microcirculation decreased concomitantly with a deterioration of acute pancreatitis, and that the new pancreatic protease inhibitor E-3123 may have some beneficial effect to improve renal hemodynamics in the early period of acute pancreatitis.     

The effect of low-rose prostaglandin E1 on circulation, respiration and body temperature during surgical anesthesia

We investigated the effects of low-dose prostaglandin E1 (PGE1) on circulation, respiration, and body temperature during surgical anesthesia. We studied 109 adult patients undergoing upper abdominal operations under thoracic epidural combined with inhalational anesthesia. Patients were divided into 2 groups; Control group (n = 42) and PGE1 group (n = 67). In PGE1 group, PGE1 infusion was started at the rate of 0.02 microgram.kg-1.min-1 before the induction of anesthesia and was terminated at the end of surgery. There were no differences between the groups in demographic, anesthetic and surgical characteristics. After treatment with PGE1, arterial pressure decreased slightly but significantly, resulting in lower arterial pressure in PGE1 group than in control group before the induction of anesthesia. After the induction of anesthesia, however, arterial pressure decreased significantly in both groups, and the differences in arterial pressure between the groups were not observed any more during surgery. Heart rate was not different between the groups throughout the study period. Intraoperative urine output was greater in PGE1 group than in control group. PaO2/FIO2 ratio was not different between the groups both before and during anesthesia. Rectal temperature remained slightly but significantly lower in PGE1 group throughout surgery. Rectal-to-palm temperature gradient tended to be smaller in PGE1 group 1 hour after the induction of anesthesia. Low-dose PGE1 reduced arterial pressure. However, the difference in arterial pressure between the groups was so small that the difference disappeared during surgery. Meanwhile, low-dose PGE1 increased urine output, suggesting that renal blood flow was better-maintained with PGE1. In spite of several investigations reporting an unfavorable effect of PGE1 on PaO2, low dose PGE1 did not affect PaO2 in this study. Finally low-dose PGE1 reduced core temperature, though slightly, probably through redistribution of the body heat.     

Topical versus peribulbar anesthesia, without sedation, for clear corneal phacoemulsification

Electroconvulsive therapy (ECT) is an appropriate clinical model to investigate blood flow during seizures. In this study cerebral blood flow velocity (CBFV) was measured during 40 ECTs in 10 patients by means of transcranial Doppler sonography. EEG was recorded continuously. Under general anesthesia, the pre-convulsive blood flow velocity (Vmean) decreased significantly. After ECT, we measured a dramatic increase in Vmean which was significantly greater in the left MCA than in the right MCA. After termination of seizures, flow velocities returned to baseline levels. The striking increase in cerebral blood flow velocity reflects excessive cerebral metabolism during convulsive neuronal activation. The left hemisphere seems to be more sensitive to electrical stimuli as was indicated by its predominant augmentation of CBFVs.