Effects of Rapid Increases of Desflurane and Sevoflurane to Concentrations of 1.5 MAC on Systemic Vascular Resistance and Catecholamine Response during Cardiopulmonary Bypass

Background: Airway irritation was hypothesized to trigger the transient cardiovascular stimulation associated with desflurane. The authors administered desflurane during cardiopulmonary bypass (CPB), thus avoiding airway contact, and compared the effects of rapid increases of desflurane to 1.5 MAC on systemic vascular resistance index (SVRI) and catecholamine response to those of 1.5 MAC sevoflurane.

Methods: Forty-eight patients, undergoing elective coronary bypass surgery, were randomly allocated to receive either desflurane or sevoflurane during hypothermic (32-33 [degree sign] Celsius) nonpulsatile CPB at exhaust gas concentrations of 1.5 MAC for 15 min. SVRI was calculated at baseline, 1, 2, 3, 4, 5, 7, 9, 12, and 15 min after starting volatile anesthetics' delivery. Plasma catecholamine concentrations were determined in 12 desflurane-treated patients and 12 sevoflurane-treated patients at baseline, 5, and 15 min.

Results: The time-course of Delta SVRI, (changes in SVRI from baseline), from baseline to 5 min was significantly different between desflurane- and sevoflurane-treated patients, whereas there was no difference from 7 to 15 min. In the desflurane group, SVRI from 1 to 7 min remained unchanged to baseline level, thereafter declining to significantly lower values at 9, 12, and 15 min compared with values from 0 to 5 min, whereas sevoflurane produced an immediate and significant reduction in SVRI. With desflurane, catecholamine concentrations remained unchanged to baseline level at 5 and 15 min; with sevoflurane, they decreased with time.     

Systemic and regional hemodynamics of isoflurane and sevoflurane in rats.

The authors studied the effects of sevoflurane and isoflurane on systemic hemodynamics and regional blood flow distribution (microsphere technique) in 15 rats during general anesthesia with intravenous chloralose and controlled ventilation. Inhaled anesthetics were applied to reduce mean arterial blood pressure (MAP) to 70 mm Hg (1.66 vol% sevoflurane and 0.96 vol% isoflurane) and 50 mm Hg (MAP 50; 3.95 vol% sevoflurane and 2.43 vol% isoflurane). Control recordings were obtained with intravenous chloralose only. At a MAP of 70 mm Hg, both anesthetics reduced heart rate, cardiac output, and systemic vascular resistance to a similar degree. Isoflurane decreased systemic vascular resistance markedly at a MAP of 50 mm Hg and thereby maintained cardiac output at higher levels than sevoflurane. The left ventricular rate-pressure product decreased comparably with both anesthetics. Cerebral blood flow increased dose-dependently with both inhaled anesthetics but to a greater degree with isoflurane. Total hepatic blood flow remained unchanged from control at a MAP of 70 mm Hg but decreased at a MAP of 50 mm Hg. This was due to reductions of hepatic arterial and portal venous tributaries. Renal blood flow was reduced with only the high concentrations of the anesthetics. Myocardial blood flow was reduced at all concentrations of volatile anesthetic; however, the decrease was less with isoflurane. This would indicate a more pronounced coronary vasodilation by isoflurane as the rate-pressure product, as a measure of the actual left ventricular oxygen demand, decreased by comparable degrees with both anesthetics. Our results indicate that sevoflurane and isoflurane (each approximately 0.7 MAC) have no dissimilar systemic and regional hemodynamic effects at a MAP of 70 mm Hg in this animal model. At higher concentrations (approximately 1.7 MAC), cerebral blood flow was more with isoflurane than with sevoflurane and was associated with a more pronounced vasodilation in the myocardium.     

The influence of isoflurane on the vascular reflex response to lung inflation in dogs.

Positive pressure ventilation can affect hemodynamic stability by neuroreflex-mediated activity. Inhalational anesthesia is known to attenuate the arterial baroreflex function; however, little information is known about the effect of volatile anesthetics on the lung inflation reflex. The influence of isoflurane on static lung inflation reflex-induced changes in venous capacitance and systemic resistance was investigated in dogs. After controlling carotid sinus pressure at 50 mmHg and initiating total cardiopulmonary bypass, the lungs were inflated to tracheal pressures of 10 and 20 mmHg. The systemic vascular resistance index (SVRI) decreased by 0.04 +/- 0.03 and 0.13 +/- 0.03 mmHg.kg.min.ml-1 during tracheal inflation pressures of 10 and 20 mmHg, respectively. There as an accompanying change in systemic vascular capacitance index (SVCI) by 1.0 +/- 0.65 and 3.3 +/- 0.82 ml.kg-1 during tracheal inflation pressures of 10 and 20 mmHg. The addition of isoflurane decreased the reflex vascular response to lung inflation in a dose-dependent manner. A concentration of 1 MAC isoflurane administered via the cardiopulmonary bypass machine attenuated the change in SVRI to tracheal inflation pressures of 10 and 20 mmHg by 75% and 67%, respectively. Isoflurane at 1 MAC also reduced the reflex capacitance response to tracheal pressures of 10 and 20 mmHg by 36% each. Lung inflation-induced changes in SVRI and SVCI were abolished at isoflurane concentrations of 2 MAC. We conclude that under the conditions of this study, 1 MAC isoflurane was shown to attenuate lung reflex-induced changes in SVRI and SVCI and that at higher isoflurane concentrations (2 MAC) these reflex-induced changes were not seen.     

Relationship between minimum alveolar concentration and electroencephalographic bispectral index as well as spectral edge frequency 95 during isoflurane/epidural or sevoflurane/epidural anesthesia]

To investigate the relationship between minimum alveolar concentration (MAC) and electroencephalographic variables, we measured the bispectral index (BIS) and the spectral edge frequency 95 (SEF 95) in 17 patients undergoing elective surgery during isoflurane/epidural (n = 8) or sevoflurane/epidural (n = 9) anesthesia. Patients received 2.0 MAC end-tidal concentrations of isoflurane or sevoflurane, and the BIS and the SEF 95 were recorded after 15 min of an unchanged end-tidal concentration. The concentration of the inhalational agent was decreased to 1.2 MAC, and measurements were repeated again. During isoflurane anesthesia, the BIS increased significantly (3.6 +/- 3.9 at 2.0 MAC, 43.5 +/- 9.2 at 1.2 MAC [mean +/- SD]). In contrast, the BIS did not change significantly during sevoflurane anesthesia (35.3 +/- 8.4 at 2.0 MAC, 42.8 +/- 6.1 at 1.2 MAC). There were significant differences in the BIS and the SEF 95 at 2.0 MAC between isoflurane and sevoflurane groups. In contrast, the BIS and the SEF 95 showed no difference at 1.2 MAC between the groups. These findings suggest that different inhalational anesthetics may have different effects on the BIS and the SEF 95.     

Recovery from sevoflurane and isoflurane anaesthesia after outpatient gynaecological laparoscopy

As the low blood solubility (blood gas partition coefficient 0.69) of sevoflurane suggests a rapid emergence from anaesthesia, recovery from sevoflurane anaesthesia was compared to isoflurane in outpatient gynaecological laparoscopy. Fifty ASA I or II, consenting women participated in a randomised, controlled and single blind study. The patients received, after induction of anaesthesia with propofol, either sevoflurane or isoflurane, both with 67% nitrous oxide in oxygen, for maintenance of anaesthesia. The study drug was administered at 1 MAC (end tidal concentration 0.6% for sevoflurane and 0.5% for isoflurane) but adjusted in 0.5 MAC steps, if clinically indicated. Before the end of surgery the end tidal concentration of the study drug was reduced to 0.5 MAC. Recovery assessments were made from the time anaesthetic gases were discontinued. The subjects were able to open eyes in 2.3 (0.8–7.0) min and 4.1 (2.0–6.8) min, orientate in 2.8 (1.0–6.8) min and 4.7 (2.2–8.3) min and follow orders in 2.6 (0.7–6.8) min and 4.3 (1.2–7.3) min, in the sevoflurane and isoflurane groups, respectively ( P <0.05) [median (range)]. Walking was achieved in 72 (24–464) min and 66 (35—134) min, tolerance of oral fluids in 37 (15–88) min and 35 (45–161) min and voiding in 262 (96–459) min and 217 (52–591) min in the sevoflurane and isoflurane groups, respectively (NS). Overall home readiness was achieved in 281 (96–708) min after sevoflurane group and 242 (96–591) min after isoflurane (NS). Postoperative nausea and vomiting was common in both groups (55% for sevoflurane and 45% for isoflurane) and contributed to three subjects in the sevoflurane group and four in the isoflurane group being admitted to hospital.     

Intravenous dexmedetomidine inhibits cerebrovascular dilation induced by isoflurane and sevoflurane in dogs.

Our aim in this study, performed using a closed cranial window preparation, was to investigate the effect of systemic pretreatment with dexmedetomidine on cerebrovascular response to isoflurane or sevoflurane. After instrumentation under pentobarbital anesthesia, 48 dogs were assigned to one of two groups: the isoflurane group or the sevoflurane group (n = 24 each). Twenty-four dogs received saline (n = 6) or one of three different doses of dexmedetomidine (0.5, 1.0, or 2.0 micrograms/kg) (n = 6 each) i.v. Animals were then exposed to three different minimum alveolar anesthetic concentrations (MACs; 0.5, 1.0, and 1.5) of either isoflurane or sevoflurane. Cerebrovascular diameters were measured at each stage. Pretreatment with dexmedetomidine decreased pial vessel diameters. Both isoflurane and sevoflurane significantly dilated both arterioles and venules in a concentration-dependent manner. Isoflurane- and sevoflurane-induced dilation of cerebral arterioles was significantly attenuated in the presence of dexmedetomidine. The dexmedetomidine-induced attenuation of the vascular responses was not dependent on the dose of dexmedetomidine and was not different between isoflurane and sevoflurane. The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane could be attenuated by the systemic administration of dexmedetomidine, and this interaction between dexmedetomidine and volatile anesthetics showed no evidence of dose-dependency. Implications: The systemic administration of dexmedetomidine attenuates the dilation of cerebral vessels induced by isoflurane and sevoflurane in pentobarbital-anesthetized dogs. This interaction was not dependent on the clinical (0.5-2.0 micrograms/kg) dose of dexmedetomidine and was not different between isoflurane and sevoflurane anesthesia.     

Comparison of isoflurane and halothane when used to control intraoperative hypertension in patients undergoing coronary artery bypass surgery

The hemodynamic effects of isoflurane and halothane when used to control intraoperative hypertension were evaluated in 20 patients undergoing coronary artery bypass grafting. The patients were anesthetized with flunitrazepam, fentanyl, pancuronium, and N2O-O2. Control measurements were made after skin incision. When mean arterial pressure increased to 110 mm Hg due to sternal spread or surgical manipulation of the aorta, isoflurane or halothane were used to return arterial pressure to control levels. Using a non-rebreathing system, inspired isoflurane concentrations of 1.5-2.0 vol% or halothane concentrations of 1.0-1.5 vol% were necessary. Measurements were repeated during the hypertensive episode and after treatment with isoflurane or halothane while surgical stimulation continued. Both inhalation anesthetics decreased arterial pressure to baseline values within 5-10 min. The lowering of arterial pressure with halothane was not accompanied by significant decreases in the elevated systemic vascular resistance and pulmonary capillary wedge pressure. Cardiac index and stroke volume index decreased markedly when halothane was used (18% and 25%, respectively). In contrast, isoflurane significantly decreased systemic vascular resistance (42%). This reduction of left ventricular afterload was associated with an increase in cardiac index (22%) and a decrease in left ventricular filling pressure. Heart rate did not change significantly. These findings indicate that isoflurane is superior to halothane for controlling intraoperative hypertension during coronary artery bypass surgery.     

Comparison of recovery after intermediate duration of anaesthesia with sevoflurane and isoflurane

BACKGROUND: The purpose of this study was to compare recovery from anaesthesia after sevoflurane and isoflurane were administered to children for more than 90 min. METHODS: After parental informed consent and ethical committee approval, children aged between 2 months and 6 years, ASA I or II, were randomly allocated to sevoflurane (n=20) or isoflurane (n=20) groups. Halogenated agents were discontinued following skin closure and patients were ventilated mechanically with 100% oxygen until minimum alveolar concentration (MAC) values awake were obtained (endtidal concentrations 0.6 MAC for sevoflurane and 0.4 MAC for isoflurane). Effective perioperative analgesia was provided by a caudal block. RESULTS: The mean (+/- SD) duration of anaesthesia was 132 +/- 38 min and 139 +/- 49 min for sevoflurane and isoflurane, respectively. Early recovery occurred sooner in the isoflurane group (time to extubation was 16 +/- 7 min and 11 +/- 5 min, P<0.01; Aldrete's score at 0 min was 5.5 +/- 1.5 and 7.4 +/- 1.8, P<0.001, respectively). But the time to be fit for discharge from recovery room was similar at 136 +/- 18 min and 140 +/- 20 min, respectively. CONCLUSIONS: After intermediate duration of anaesthesia administered to children for up to 90 min, isoflurane and sevoflurane allow recovery after approximatively the same lapse of time.     

Isoflurane-induced Cerebral Hyperemia in Neuronal Nitric Oxide Synthase Gene Deficient Mice

Background: Nitric oxide (NO) has been reported to play an important role in isoflurane-induced cerebral hyperemia in vivo. In the brain, there are two constitutive isoforms of NO synthase (NOS), endothelial NOS (eNOS), and neuronal NOS (nNOS). Recently, the mutant mouse deficient in nNOS gene expression (nNOS knockout) has been developed. The present study was designed to examine the role of the two constitutive NOS isoforms in cerebral blood flow (CBF) response to isoflurane using this nNOS knockout mouse.

Methods: Regional CBF (rCBF) in the cerebral cortex was measured with laser-Doppler flowmetry in wild-type mice (129/SV or C57BL/6) and nNOS knockout mice during stepwise increases in the inspired concentration of isoflurane from 0.6 vol% to 1.2, 1.8, and 2.4 vol%. Subsequently, a NOS inhibitor, Nomega -nitro-L-arginine (L-NNA), was administered intravenously (20 mg/kg), and 45 min later, the rCBF response to isoflurane was tested again. In separate groups of wild-type mice and the knockout mice, the inactive enantiomer, Nomega -nitro-D-arginine (D-NNA) was administered intravenously in place of L-NNA. Brain NOS activity was measured with radio-labeled L-arginine to L-citrulline conversion after treatment with L-NNA and D-NNA.

Results: Isoflurane produced dose-dependent increases in rCBF by 25 +/- 3%, 74 +/- 10%, and 108 +/- 14% (SEM) in 129/SV mice and by 32 +/- 2%, 71 +/- 3%, and 96 +/- 7% in C57BL/6 mice at 1.2, 1.8, and 2.4 vol%, respectively. These increases were attenuated at every anesthetic concentration by L-NNA but not by D-NNA. Brain NOS activity was decreased by 92 +/- 2% with L-NNA compared with D-NNA. In nNOS knockout mice, isoflurane increased rCBF by 67 +/- 8%, 88 +/- 12%, and 112 +/- 18% at 1.2, 1.8, and 2.4 vol%, respectively. The increase in rCBF at 1.2 vol% was significantly greater in the nNOS knockout mice than that in the wild-type mice. Administration of L-NNA in the knockout mice attenuated the rCBF response to isoflurane at 1.2 and 1.8 vol% but had no effect on the response at 2.4 vol%.     

The comparative cardiovascular effects of sevoflurane with halothane and isoflurane

Using closed chest dogs, the cardiovascular effects of sevoflurane were compared with those of halothane and isoflurane in equipotent doses of 1.0, 1.5, 2.0, 2.5 and 3.0 MAC. They were evaluated by the changes of arterial blood pressure, central venous pressure, pulmonary artery pressure, maximum rate of left ventricular pressure rise (LV dp/dt), cardiac output and coronary sinus blood flow. The suppression of left cardiac function by sevoflurane was less than that of halothane, but was greater than that of isoflurane. Heart rate, systemic vascular resistance with sevoflurane were slightly lower than that of isoflurance. The coronary sinus blood flows with sevoflurane and isoflurane were significantly (P < 0.05 at 1.0 MAC, P < 0.005 at 2.0 MAC) higher than halothane. There was no significant difference on coronary sinus flow between sevoflurane and isoflurane. The depth of anesthesia could be quickly changed by adjustment of inspired sevoflurane concentration in comparison with the other two anesthetics.(Kazama T, Ikeda K: The comparative cardiovascular effects of sevoflurane with halothane and isoflurane. J Anesth 2: 63–68, 1988)     

Sevoflurane and isoflurane do not enhance the pre- and postischemic eicosanoid production in guinea pig hearts

Eicosanoids and volatile anesthetics can influence cardiac reperfusion injury. Accordingly, we analyzed the effects of sevoflurane and isoflurane applied in clinically relevant concentrations on the myocardial production of prostacyclin and thromboxane A2 (TxA2) and on heart function. Isolated guinea pig hearts, perfused with crystalloid buffer, performed pressure-volume work. Between two working phases, hearts were subjected to 15 min of global ischemia followed by reperfusion. The hearts received no anesthetic, 1 minimum alveolar anesthetic concentration (MAC) isoflurane (1.2 vol%), or 0.5 and 1 MAC sevoflurane (1 vol% and 2 vol%), either only preischemically or pre- and postischemically. In additional groups, cyclooxygenase function was examined by an infusion of 1 microM arachidonic acid (AA) in the absence and presence of sevoflurane. The variables measured included the myocardial production of prostacyclin, TxA2 and lactate, consumption of pyruvate, coronary perfusion pressure, and the tissue level of isoprostane 8-iso-PGF2alpha. External heart work, determined pre- and postischemically, served to assess recovery of heart function. Volatile anesthetics had no impact on postischemic recovery of myocardial function (50%-60% recovery), perfusion pressure, lactate production, or isoprostane content. Release of prostacyclin and TxA2 was increased in the early reperfusion phase 5-8- and 2-4-fold, respectively, indicating enhanced AA liberation. Isoflurane and sevoflurane did not augment the eicosanoid release. Only 2 vol% sevoflurane applied during reperfusion prevented the increased eicosanoid formation in this phase. Infusion of AA increased prostacyclin production approximately 200-fold under all conditions, decreased pyruvate consumption irreversibly, and markedly attenuated postischemic heart work (25% recovery). None of these effects were mitigated by 2 vol% sevoflurane. In conclusion, only sevoflurane at 2 vol% attenuated the increased liberation of AA during reperfusion. Decreased eicosanoid formation had no effect on myocardial recovery in our experimental setting while excess AA was deleterious. Because eicosanoids influence intravascular platelet and leukocyte adhesion and activation, sevoflurane may have effects in reperfused tissues beyond those of isoflurane. IMPLICATIONS: In an isolated guinea pig heart model, myocardial eicosanoid release was not increased by isoflurane or sevoflurane, either before or after ischemia. Sevoflurane (2 vol%) but not isoflurane attenuated the increased release of eicosanoids during reperfusion.     

Rates of awakening from anesthesia with I-653, halothane, isoflurane, and sevoflurane: a test of the effect of anesthetic concentration and duration in rats

The low blood solubility of two new inhaled anesthetics, I-653 (human blood/gas partition coefficient, 0.42) and sevoflurane (0.69), suggested that awakening from these agents should be more rapid than awakening from currently available anesthetics such as isoflurane (1.4) and halothane (2.5). This prediction proved valid in a study of these four agents in rats given 0.4, 0.8, 1.2, or 1.6 MAC for 2.0 hr or 1.6 MAC for 0.5 or 1.0 hr. At a given dose and duration, awakening was most rapid with the least soluble agent and longest with the most soluble agent. For example, recovery of muscle coordination at 1.2 MAC administered for 2 hr required 4.7 +/- 3.0 min (mean +/- SD) with I-653, 14.2 +/- 8.1 min with sevoflurane, 23.2 +/- 7.6 min with isoflurane, and 47.2 +/- 4.7 min with halothane.     

Influence of nitrous oxide on minimum alveolar concentration of sevoflurane for laryngeal mask insertion in children

BACKGROUND: Inhalational induction with sevoflurane and nitrous oxide is frequently used for Laryngeal Mask Airway (LMA; Laryngeal Mask Company, Henley-on-Thames, United Kingdom) insertion in children. The authors determined the influence of nitrous oxide on the minimum alveolar concentration (MAC) of sevoflurane for LMA insertion. METHODS: One hundred twenty unpremedicated children (age, 1-9 yr; American Society of Anesthesiologists physical status I) were randomly assigned to receive 1 of 15 end-tidal concentrations of nitrous oxide and sevoflurane for inhalational induction via a facemask: 0% nitrous oxide with 1.2, 1.4, 1.6, 1.8, or 2.0% sevoflurane; 33% nitrous oxide with 0.8, 1.0, 1.2, 1.4, or 1.6% sevoflurane; or 67% nitrous oxide with 0.4, 0.6, 0.8, 1.0, or 1.2% sevoflurane. The LMA was inserted after steady state end-tidal anesthetic concentrations had been maintained for 15 min. The response to insertion was recorded by three independent blinded observers. The interaction between nitrous oxide and sevoflurane was determined using logistic regression analysis. RESULTS: The MAC of sevoflurane for LMA insertion (95% confidence limit) was 1.57% (1.42-1.72%), and the concentration of sevoflurane required to prevent movement in 95% of children was 1.99% (1.81-2.57%). The addition of 33% and 67% nitrous oxide linearly decreased the MAC of sevoflurane for LMA insertion by 22% and 49%, respectively (P < 0.001). The interaction coefficient between nitrous oxide and sevoflurane did not differ from zero (P = 0.7843), indicating that the relation was additive. CONCLUSIONS: Nitrous oxide and sevoflurane suppress the responses to LMA insertion in a linear and additive fashion in children.     

Influence of Nitrous Oxide on Minimum Alveolar Concentration of Sevoflurane for Laryngeal Mask Insertion in Children

Background: Inhalational induction with sevoflurane and nitrous oxide is frequently used for Laryngeal Mask Airway (TM) (LMA (TM); Laryngeal Mask Company, Henley-on-Thames, United Kingdom) insertion in children. The authors determined the influence of nitrous oxide on the minimum alveolar concentration (MAC) of sevoflurane for LMA (TM) insertion.

Methods: One hundred twenty unpremedicated children (age, 1-9 yr; American Society of Anesthesiologists physical status I) were randomly assigned to receive 1 of 15 end-tidal concentrations of nitrous oxide and sevoflurane for inhalational induction via a facemask: 0% nitrous oxide with 1.2, 1.4, 1.6, 1.8, or 2.0% sevoflurane; 33% nitrous oxide with 0.8, 1.0, 1.2, 1.4, or 1.6% sevoflurane; or 67% nitrous oxide with 0.4, 0.6, 0.8, 1.0, or 1.2% sevoflurane. The LMA (TM) was inserted after steady state end-tidal anesthetic concentrations had been maintained for 15 min. The response to insertion was recorded by three independent blinded observers. The interaction between nitrous oxide and sevoflurane was determined using logistic regression analysis.

Results: The MAC of sevoflurane for LMA (TM) insertion (95% confidence limit) was 1.57% (1.42-1.72%), and the concentration of sevoflurane required to prevent movement in 95% of children was 1.99% (1.81-2.57%). The addition of 33% and 67% nitrous oxide linearly decreased the MAC of sevoflurane for LMA (TM) insertion by 22% and 49%, respectively (P < 0.001). The interaction coefficient between nitrous oxide and sevoflurane did not differ from zero (P = 0.7843), indicating that the relation was additive.     

The effect of desflurane and sevoflurane on cerebral oximetry under steady-state conditions

We studied the effect of sevoflurane and desflurane on regional cerebral oxygenation (rSO2). Twenty-two patients undergoing abdominal hysterectomy received sevoflurane and desflurane for 15 min each and 30 min apart under steady-state conditions in a randomized, crossover manner to maintain a bispectral index (BIS) of 40-50. In another 22 patients undergoing the same anesthesia and surgery BIS was maintained at 20-30. During the 15-min administration of each anesthetic at steady-state conditions rSO2, BIS, inspired and end-tidal anesthetic concentrations, end-tidal CO2, Spo2, systolic and diastolic blood pressures, and heart rate were recorded every 3 min. The rSO2 did not differ between sevoflurane and desflurane when BIS values were maintained between 40-50 or 20-30. The MAC(BIS) values required to maintain BIS at 40-50 and at 20-30 were 1.0 versus 1.2 (P = 0.004) and 1.6 versus 1.8 (P < 0.001) for desflurane and sevoflurane respectively. Higher rSO2 values were obtained by 1.6 MAC (71 +/- 13) than by 1 MAC of desflurane (66 +/- 10; P < 0.001) and by 1.8 MAC (72 +/- 11) than by 1.2 MAC of sevoflurane (66 +/- 13; P < 0.001). In conclusion, equipotent concentrations of desflurane or sevoflurane in terms of BIS are associated with similar rSO2 values, but larger anesthetic concentrations of both anesthetics increased the rSO2 values.     

七氟醚、异氟醚和地氟醚对神经外科手术患者经颅电刺激运动诱发电位的影响

目的 比较七氟醚、异氟醚和地氟醚对神经外科手术患者经颅电刺激运动诱发电位(MEPs)的影响.方法 择期行神经外科手术患者60例,年龄18～64岁,ASA分级Ⅰ或Ⅱ级.随机分为3组(n=20):七氟醚组、异氟醚组和地氟醚组.监测BIS值和经颅电刺激MEPs.调节七氟醚、异氟醚和地氟醚吸入浓度,使其呼气末浓度分别达到0.50、0.75、1.00和1.30 MAC,每一浓度均维持15 min,视为稳态呼气末浓度.于给予吸入麻醉药前(基础状态)和达到各稳态呼气末浓度(T1-4)时,记录MEPs的波幅和潜伏期以及BIS值.记录MEPs波形记录失败情况.结果 与七氟醚组和异氟醚组比较,地氟醚组T1.2时波幅和BIS值降低,T1-4时潜伏期延长(P＜0.05);七氟醚组和异氟醚组各指标比较差异无统计学意义(P＞0.05).七氟醚组、异氟醚和地氟醚组基础状态、T1、T2时的记录失败率均为0;T3时记录失败率分别为0、5%和20%,三组比较差异无统计学意义(P＞0.05);T4时记录失败率分别为5%、20%和45%,与七氟醚组和异氟醚组比较,地氟醚组记录失败率升高(P＜0.05);七氟醚组和异氟醚组比较差异无统计学意义(P＞0.05).结论 地氟醚对神经外科手术患者经颅电刺激MEPs的抑制作用强于七氟醚和异氟醚.术中行MEPs监测时,七氟醚和异氟醚适宜的呼气末浓度为1.00 MAC,地氟醚为0.75～1.00 MAC.     

Isoflurane may not influence postoperative cardiac troponin I release and clinical outcome in adult cardiac surgery

BACKGROUND AND OBJECTIVE: Isoflurane has been shown experimentally to protect the myocardium against infarction but the clinical relevance of these findings is not yet well established. We therefore evaluated the effects of isoflurane administration before cardiopulmonary bypass (CPB) on postoperative cardiac troponin I (cTnI) release and clinical outcome in a large group of adult patients scheduled for cardiac surgery. METHODS: Three hundred and fifty-nine consecutive patients were included prospectively in an open observational study and divided into two groups according to whether or not isoflurane was administered before CPB. Postoperative cTnI release, in-hospital mortality, time to discharge from hospital, time to extubation and non-fatal postoperative cardiac events (number of internal cardioversions, need for inotropic support, ischaemic events, dysrhythmias and/or conduction abnormalities) were recorded. RESULTS: Two hundred and twenty-one (62%) patients did not receive isoflurane and 138 (38%) received isoflurane (1.3% [1.0-1.8%] minimum alveolar concentration over 22 [15-331 min). Postoperative cTnI release was not significantly different between the control and isoflurane groups (5.9 [1.0-336.8] vs. 6.0 [1.5-392.0] ng mL(-1), P = 0.88). No significant differences were found in non-fatal cardiac events (63% vs. 57%, P = 0.22) and in-hospital mortality (1.8% vs. 1.4%, P = 0.79) between the control and isoflurane groups. CONCLUSIONS: No significant effect was observed on postoperative cTnI release and in-hospital outcome when isoflurane was added to standardized intravenous anaesthesia before CPB in adult patients undergoing cardiac surgery.     

Increased noradrenaline release from rat preoptic area during and after sevoflurane and isoflurane anesthesia

PURPOSE: To study the effects of sevoflurane and isoflurane on noradrenaline release from the rat preoptic area (POA). METHOD: Sixteen male Wistar rats were studied. A microdialysis probe with a 2 mm long semipermeable membrane was implanted in the POA. Dialysates were collected at intervals often minutes. After obtaining five control samples for 50 min, 30 min inhalation of 3% sevoflurane or 1.8% isoflurane was performed. After cessation of the inhalation, five more samples were obtained for 50 min as recovery phase. Noradrenaline (NA) concentration in the dialysates was measured by high pressure liquid chromatography with an electrochemical detector. RESULTS: Both sevoflurane and isoflurane caused marked increases in NA release from the rat POA (sevoflurane 233% at 20 min, isoflurane 357% at ten minutes after the start of inhalation). The marked NA releases were also observed during the emergence from sevoflurane and isoflurane anesthesia (sevoflurane 269% at 20 min, isoflurane 368% at ten minutes in the recovery phase). CONCLUSION: This study suggests that enhanced release of NA in the POA during sevoflurane and isoflurane may explain the excitatory phase observed during the peri-anesthetic period with these agents.     

静吸复合麻醉下七氟醚与异氟醚对颅内压的影响

目的:在颅内顺应性正常神经外科病人,观察1.0 MAC七氟醚与异氟醚对颅内压的影响。方法:垂体瘤或颅咽管瘤手术病人16例,随机分为两组:A组为咪唑安定 芬太尼 1.0 MAC异氟醚;B组为咪唑安定 芬太尼 1.0 MAC七氟醚。选择L_(3～4)行蛛网膜下腔穿刺。麻醉诱导采用芬太尼-咪唑安定-阿曲库铵。插管后维持稳定30分开始吸入七氟醚(或异氟醚)。分别于麻醉前、吸入麻醉药前、达预定呼气末浓度30分内观察监测指标。结果:1.0 MAC七氟醚和异氟醚均可显著降低脑灌注压,异氟醚作用较强。吸入1.0 MAC七氟醚后颅内压首先呈显著性下降,15分后回复至基础水平。吸入1.0 MAC异氟醚后颅内压无显著性变化。结论:在颅内顺应性正常患者,1.0 MAC七氟醚和异氟醚均可安全用于神经外科麻醉。     

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)