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Volatile anesthetic agents are increasingly widely used for critical care sedation. There are concerns that sevoflurane presents a risk of renal injury when used in this role. RCTs comparing the use of critical care sevoflurane sedation with any control in humans were systematically identified using MEDLINE, Cochrane CENTRAL, web of Science, and CINAHL (until May 2022), if they presented comparative data on renal function or serum inorganic fluoride levels. Pooled SMDs (95% CI) were calculated where possible after assessment of quality with GRADE and risk of bias with ROB-2. Eight studies analyzing 793 patients were included. The median duration of use of critical care sevoflurane sedation was 4.8 [IQR 3.5–9.2] hours; however, most trials also included a period of prior intraoperative use. No significant difference was found in serum creatinine at 1 day (SMD 0.05, 95% CI − 0.12 to 0.21), 48 h (SMD = − 0.04; 95% Cl − 0.25 to 0.17), 72 h (SMD = − 0.15; 95% CI − 0.45 to 0.15), and at discharge (SMD = − 0.1; 95% CI − 0.3 to 0.13) between the sevoflurane group and the control groups. Creatinine clearance was measured in two studies at 48 h with no significant difference (SMD = − 0.13; 95% Cl − 0.38 to 0.11). Levels of serum inorganic fluoride were significantly elevated in patients where sevoflurane was used. Sevoflurane was not associated with renal failure when used for critical care sedation of fewer than 72-h duration, despite the elevation of serum fluoride. Longer-term studies are currently inadequate, including in patients with compromised renal function, to further evaluate the role of sevoflurane in this setting. Trial registration PROSPERO (CRD42022333099) [ABSTRACT FROM AUTHOR]

Objective: This study explored the effects of sevoflurane exposure during different stages of pregnancy on the brain development of offspring. Methods: Thirty-six pregnant SD rats were randomly divided into 4 groups: control, sevoflurane exposure in early (S1) pregnancy, sevoflurane exposure in middle (S2) pregnancy, and sevoflurane exposure in late (S3) pregnancy. After natural birth, the learning and memory capacity of offspring rats was analyzed using the Morris water maze experiment. The hippocampi of offspring rats were collected. The levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the hippocampus were measured by ELISA. Additionally, the Nissl bodies in the hippocampus were analyzed using Nissl staining. Immunohistochemistry was used to examine the expression of BDNF and CPEB2 in the hippocampus of offspring. Proteins related to the NR4A1/NF-κB pathway were analyzed using western blotting. Results: The memory and learning capacity of offspring rats was significantly reduced in the S1 and S2 groups compared to the control group (p < 0.05), while there was no obvious difference between the control and S3 groups (p > 0.05). The level of IL-1β was significantly increased (p < 0.05) in the S1 group compared with the control group. Sevoflurane anesthesia received in early and middle pregnancy could significantly affect the formation of Nissl bodies in the hippocampi of offspring rats. In addition, the expression of BDNF and CPEB2 in the hippocampi of offspring rats was greatly decreased in the S1 group compared with the control group (p < 0.05). The expression of NR4A1 in the hippocampi of rat offspring was significantly decreased in the S1 and S2 groups compared with the control group (p < 0.05). The expression of proteins related to the NF-κB pathway was increased in the S1 group compared to the control group (p < 0.05). Conclusions: The neurotoxic effect of maternal sevoflurane anesthesia on the brain development of offspring is higher when the exposure occurs in early pregnancy than in late pregnancy, and its mechanism might involve the NR4A1/NF-κB pathway to increase the secretion of inflammatory cytokines. [ABSTRACT FROM AUTHOR]

A large number of studies during the past two decades have demonstrated the efficacy and safety of sevoflurane across patient populations. Clinical researchers have also investigated the effects of sevoflurane, its hemodynamic characteristics, its potential protective effects on several organ systems, and the incidence of delirium and cognitive deficiency. This review examines the clinical profiles of sevoflurane and other anesthetic agents, and focuses upon emerging topics such as organ protection, postoperative cognitive deficiency and delirium, and novel ways to improve postanesthesia outcomes. [ABSTRACT FROM AUTHOR]

Purpose: Sevoflurane is known to prolong the QT interval. This study aimed to determine the effect of the interaction between intravenous anesthetics and sevoflurane on the QT interval. Methods: The study included 48 patients who underwent lumbar spine surgery. Patients received 3 μg/kg fentanyl and were then randomly allocated to either Group T, in which they received 5 mg/kg thiamylal, or Group P, in which they received 1.5 mg/kg propofol, at 2 min after administration of fentanyl injection for anesthetic induction. Vecuronium (1.5 mg/kg) and sevoflurane (3 % inhaled concentration) were administered immediately after loss of consciousness and tracheal intubation was performed 3 min after vecuronium injection. Heart rate (HR), mean arterial pressure (MAP), bispectral index score (BIS), and the heart rate-corrected QT (QTc) interval on a 12-lead electrocardiogram were recorded immediately before fentanyl administration (T1), 2 min after fentanyl injection (T2), immediately before intubation (T3), and 2 min after intubation (T4). Results: There were no significant differences between the two groups in baseline patient characteristics. BIS and MAP significantly decreased after anesthesia induction in both groups. At T3, MAP in Group T was higher than in Group P, while HR had reduced in both groups. The QTc interval was prolonged after anesthesia induction in Group T, but did not change at any time point in Group P. The QTc interval after anesthesia induction in Group T was longer than in Group P. Conclusion: We concluded that an injection of propofol could counteract QTc interval prolongation associated with sevoflurane anesthesia induction. [ABSTRACT FROM AUTHOR]

Purpose: Sevoflurane is the most widely used volatile anesthetic of general anesthesia. In children and neonates, it is commonly used alone or in combination with thiopental or propofol. A few recent studies reported that sevoflurane induced neuronal death in the developing rodent brain. We measured the neurotoxicity of these anesthetics at clinical doses, alone and in combination, in the developing mouse brain. Methods: Seven-day-old C57BL/6 mice were randomly assigned to 6 treatment groups. Three groups were exposed to 3 % sevoflurane for 6 h after injection of saline, thiopental (5 mg/kg), or propofol (10 mg/kg), whereas three groups were exposed to room air for 6 h after injection of equal doses of saline, thiopental, or propofol. Apoptosis in the hippocampal CA1 region (CA1) and retrosplenial cortex (RC) was assessed using caspase-3 immunostaining. Results: Sevoflurane alone caused significantly higher apoptosis in the CA1 compared with saline plus air ( P = 0.04). Sevoflurane in combination with propofol resulted in significantly greater numbers of apoptotic neurons than sevoflurane alone in both the CA1 and the RC ( P = 0.04). However, there was no significant difference in apoptotic neuron density in both the regions between the groups treated with sevoflurane alone and in combination with thiopental ( P = 0.683). Conclusion: Sevoflurane alone can induce neuronal apoptosis, and this effect is enhanced by propofol. Thiopental did not exacerbate the neurotoxicity of sevoflurane. There is the possibility that the combination of sevoflurane and propofol is a more harmful anesthetic technique than sevoflurane alone in pediatric patients. [ABSTRACT FROM AUTHOR]

Purpose: We compared the recovery profile of propofol and sevoflurane when used for maintenance of anesthesia in elective day care operative procedures. Methods: One hundred ASA physical status I and II patients, aged between 18 and 50 years, were randomly assigned to receive either propofol-nitrous oxide or sevoflurane-nitrous oxide maintenance of anesthesia. Early and intermediate recovery in terms of cognitive and ambulatory functions was recorded. Psychomotor testing, in the form of Trieger dot test and digit symbol substitution test, were performed before surgery and in the post-anesthesia care unit at 15 min, 30 min, 1 h, 2 h, and 4 h following nitrous oxide switch-off to evaluate intermediate recovery. Results: There were no significant differences in recovery of early cognitive functions between the two groups, except that patients in the sevoflurane group were more responsive at around 10 min following nitrous oxide switch-off and 'recalled address' earlier than patients in the propofol group. There was no significant difference in between the two groups with regard to 'home-readiness.' Conclusions: Recovery from sevoflurane anesthesia, especially with regard to cognitive functions, may be slightly faster than from propofol, but the difference is not sufficiently significant to affect the time to 'home-readiness' in patients undergoing day care surgery. [ABSTRACT FROM AUTHOR]

Purpose: It is unclear whether volatile general anesthetics have sustained adverse effects on the immature brains of children. We performed a self-controlled study to evaluate the effects of strabismus surgery under sevoflurane-based general anesthesia on the cognitive function of pediatric patients. Methods: The study included 100 children of ages 4 to 7 years old scheduled to undergo strabismus correction under sevoflurane-based general anesthesia. Cognitive function was tested 1 day before the operation (T1), 1 month after the operation (T2), and 6 months after the operation by the Wechsler Preschool and Primary Scale of Intelligence (WPPSI) (Third Edition) method, which consists of 150 items. The scores at T1 were compared with scores at T2 and T3. Results: Seventy-two children completed the three tests. At T1, they were 66.1 ± 7.7 months old and had a mean body weight of 21.6 ± 4.0 kg. The mean anesthesia time was 67.3 ± 9.8 min. The mean interval between T1 and T2 was 25.4 ± 6.8 days, and that between T1 and T3 was 182.1 ± 27.7 days. No statistically significant decrease in WPPSI scores was observed between T1 and T2, or between T1 and T3. Conclusion: These findings from our self-controlled study show that sevoflurane-based general anesthesia does not have significantly adverse effects on the cognitive function of 4- to 7-year-old children at 1 month and 6 months after strabismus surgery. Additional studies with a larger sample size are needed. [ABSTRACT FROM AUTHOR]

The aim of this study was to compare the vascular reactivities of canine mesenteric arteries and veins to sevoflurane and to elucidate the underlying mechanism that is responsible for sevoflurane-induced hypotension. Vascular rings of canine mesenteric arteries and veins were suspended in organ baths, and the effect of 2.3% and 4.6% sevoflurane on the contractile responses to transmural electrical stimulation (ES) and to norepinephrine (NE) were determined by recording isometric tension changes. The rings were contracted to a stable tension by the addition of NE and then exposed to increasing concentrations of sevoflurane (0%–5.1%). Sevoflurane attenuated the contractile responses to transmural ES in veins but not in arteries. The concentration responses to NE were not affected by sevoflurane in arteries or in veins. At stable precontraction induced by NE, when sevoflurane was placed in the bathing medium, arteries with intact endothelium had significant contraction at 1.7% and 3.4% sevoflurane, followed by relaxation at 5.1%. On the contrary, sevoflurane produced dose-dependent relaxation in endothelium-denuded arteries and endothelium-intact veins It is suggested that the relaxation of the veins by sevoflurane may be due to the inhibition of NE release from sympathetic nerve endings and to the direct inhibition of the contractile mechanisms of vascular smooth muscle. In arteries, sevoflurane causes endothelium-dependent vasocontraction, probably by inhibiting the release of basal endothelium-derived relaxing factor (EDRF). [ABSTRACT FROM AUTHOR]

The effects of sevoflurane and halothane on the effective refractory period (ERP) and ventricular activation were examined in a canine myocardial infarction model. Sevoflurane (1 MAC) reduced the heart rate and prolonged ERP in both normal and infarcted zones. A prolongation of ERP with sevoflurane was observed also during atrial pacing at a fixed rate, but the effect was less than during sinus rhythm. Sevoflurane either further delayed or blocked the delayed activation entirely in the infarcted zones with only slight effects on the activation of the normal zones. Halothane (1 MAC) prolonged ERP during sinus rhythm and atrial pacing, but to a lesser extent during the latter. Halothane also depressed ventricular activation in the infarcted zone during atrial pacing. In conclusion, sevoflurane as well as halothane selectively depresed the delayed activation and the prolongation of ERP in myocardial infarction, which may inhibit ventricular arrhythmias in myocardial infarction. [ABSTRACT FROM AUTHOR]

We evaluated the neuromuscular effects of pipecuronium during anesthesia with equipotent concentrations of either sevoflurane, isoflurane or enflurane. Twenty-seven patients scheduled for minor elective otolaryngeal or plastic surgery were studied and randomly assigned to 3 groups, one group per anesthetic agent. Anesthesia was induced with thiamylal 5 mg·kg and the trachea was intubated with succinylcholine 1 mg·kg, then anesthesia was maintained with 60% nitrous oxide in oxygen and sevolfurane, isoflurane or enflurane, depending on the group. Neuromuscular blocking effects were monitored by recording the electromyographic activity of the adductor pollicis muscle from supramaximal stimulation of the ulnar nerve at 10-s intervals. Pipecuronium 40 μg·kg was administered when electromyographic activity had reached a stable state, 30 min after succinylcholine administration. The maximum effect (% block of control) and clinical duration (time to 25% recovery) of pipecuronium were 99.1±1.4% and 63.7±14.7 min (mean \+-S.D.) for sevoflurane, 99.0\+-2.0% and 60.9\+-20.5 min for isoflurane, and 98.0\+-2.5% and 62.8\+-28.7 min for enflurane, respectively. There were no significant differences in these values between the anesthetics. Cardiovascular stimulant effects were not observed in any of the groups. We conclude that the effect of pipecuronium under seveflurane anesthesia is similar to that under isoflurane and enflurane anesthesia. [ABSTRACT FROM AUTHOR]

The cardiovascular effects of sevoflurane were studied and compared with those of halothane in 30 healthy patients. The patients were assigned to receive 1 MAC sevoflurane (n=10), 2 MAC sevoflurane (n=10) or 1 MAC halothane (n=10) in NO 2 l·min and O 4 l·min. The changes in left ventricular diastolic and systolic dimension (Dd and Ds), fractional shortening (FS), mean velocity of circumferential fiber shortening (mVcf), left ventricular diastolic and systolic volume (Vd and Vs), stroke volume (SV), ejection fraction (EF) and cardiac index (CI) were evaluated by echocardiography. Sevoflurane produced significant dose-dependent decreases in FS, mVcf, EF and SV, but no significant changes in Dd and Vd. Therefore, the decrease in SV was due mainly to the increase in left ventricular residual volume (Vs). One MAC halothane produced a more significant decrease in FS, mVcf, EF and SV, when compared to values obtained at 1 MAC sevoflourane ( P<0.01). CI was more significantly decreased with 1 MAC halothane than with 1 MAC and 2 MAC sevoflurane ( P<0.01). This was brought about by a slight decrease in HR with halothane and a slight increase in HR with sevoflurane, in addition to a smaller decrease in SV with sevoflurane than with halothane. This study suggests that sevoflurane may better preserve cardiac function as a pump in healthy patients, when compared to halothane. [ABSTRACT FROM AUTHOR]

Sevoflurane anesthesia was given to sixteen women who had been scheduled for elective cesarean section. The maternal systolic blood pressure significantly decreased during the anesthesia induction. Both the anesthesia induction and emergence were smooth and rapid. These findings were supported partially by the pharmacokinetic analysis of sevoflurane concentration in the maternal artery and expired gas mixture. Spontaneous uterine contractions were good in 12 patients, fair in two and poor in two. The measured blood loss was 752±257 ml including amniotic fluid. No blood transfusion was given to any patient. The median value of the Apgar score at one minute was seven (range three to nine). No neonate was intubated for resuscitation. No abnormal maternal laboratory data were found, including liver and kidney function tests and blood cell counts one week after the operation. No adverse effect of sevoflurane on the neonate was found one week after the delivery and three months after the discharge. [ABSTRACT FROM AUTHOR]

In experiments on isolated rat heart lung preparation, the effects of sevoflurane on myocardial metabolism during postischemic reperfusion were evaluated with intramyocardial high energy phosphates, lactate and glycogen. Hearts were perfused for 10 min initially and made globally ischemic for 8 min. Afterwards, they were reperfused for 12 min. Sevoflurane was administered from 5 min after the start of perfusion to the end of reperfusion. There was no significant difference in myocardial lactate levels between the sevoflurane (S) and control groups. However, the myocardial ATP level in Group S was significantly higher than that in control (17.45±1.51 vs 15.50±0.87: P<0.01). The administration of sevoflurane to the isolated rat heart during pre- and post-ischemia enhanced metabolic recovery in the postischemic state. [ABSTRACT FROM AUTHOR]

The effects of 2.5% and 5% of sevoflurane anesthesia on hemodynamics and myocardial metabolism were studied in pentobarbital-pancuronium anesthetized dogs. The interaction between nicardipine and 2.5% sevoflurane was also examined. Sevoflurane produced dose-dependent ( P<0.05 to P<0.01) decreases in systolic arterial pressure (SAP), heart rate (HR), cardiac index (CI), left ventricular minute work index (LVMWI), maximum rate of rise of left ventricular pressure (LV dP/dt), the time constant of fall in isovolumic left ventricular pressure (T) and systemic vascular resistance (SVR), whereas stroke volume index (SVI) and left ventricular end-diastolic pressure (LVEDP) remained unchanged. Central venous pressure (CVP) was significantly ( P<0.05) increased at 5%. Myocardial oxygen consumption $$M\dot V_{O_2 } $$ , and myocardial lactate extraction ratio (ML ext) were decreased in a dose-dependent manner ( P<0.05). Myocardial oxygen extraction ratio (M ext) was significantly ( P<0.01) decreased at 5%. The ratio of the left ventricular minute work index to myocardial oxygen consumption $$LVMWI/M\dot V_{O_2 } $$ , i.e., left ventricular efficiency was significantly decreased only at 5% ( P<0.05). Coronary sinus blood flow (CSBF) was significantly ( P<0.05) decreased only at 2.5% sevoflurane and coronary vascular resistance (CVR) was significantly ( P<0.01) decreased only at 5% sevoflurane. The ratio of CSBF to CO (CSBF/CO) showed a tendency to increase as sevoflurane concentrations were increased. Nicardipine (0.01 mg·kg) administered intravenously under 2.5% sevoflurane caused significant ( P<0.05 to P<0.01) decreases in SAP, HR, LV dP/dt, SVR, and CVR, and increases in CVP, SVI, CI, and CSBF ( P<0.05 to P<0.01). CSBF/CO remained unchanged. $$M\dot V_{O_2 } $$ , M ext, and ML ext were significantly ( P<0.05 to P<0.01) decreased. $$LVMWI/M\dot V_{O_2 } $$ showed a tendency to increase. It is concluded that sevoflurane causes a rapidly and easily controlled cardiovascular depression and may not have unfavorable effects on coronary circulation and myocardial metabolism. Nicardipine exerts a synergistic myocardial depressant effect on sevoflurane, in terms of both cardiovascular dynamics and myocardial metabolism. [ABSTRACT FROM AUTHOR]