Sevoflurane For Induction Of Anesthesia Research Articles

A hypothalamus-lateral periaqueductal gray GABAergic neural projection facilitates arousal following sevoflurane anesthesia in mice.

The lateral hypothalamus (LHA) is an evolutionarily conserved structure that regulates basic functions of an organism, particularly wakefulness. To clarify the function of LHAGABA neurons and their projections on regulating general anesthesia is crucial for understanding the excitatory and inhibitory effects of anesthetics on the brain. The aim of the present study is to investigate whether LHAGABA neurons play either an inhibitory or a facilitatory role in sevoflurane-induced anesthetic arousal regulation. We used fiber photometry and immunofluorescence staining to monitor changes in neuronal activity during sevoflurane anesthesia. Opto-/chemogenetic modulations were employed to study the effect of neurocircuit modulations during the anesthesia. Anterograde tracing was used to identify a GABAergic projection from the LHA to a periaqueductal gray (PAG) subregion. c-Fos staining showed that LHAGABA activity was inhibited by induction of sevoflurane anesthesia. Anterograde tracing revealed that LHAGABA neurons project to multiple arousal-associated brain areas, with the lateral periaqueductal gray (LPAG) being one of the dense projection areas. Optogenetic experiments showed that activation of LHAGABA neurons and their downstream target LPAG reduced the burst suppression ratio (BSR) during continuous sevoflurane anesthesia. Chemogenetic experiments showed that activation of LHAGABA and its projection to LPAG neurons prolonged the anesthetic induction time and promoted wakefulness. In summary, we show that an inhibitory projection from LHAGABA to LPAGGABA neurons promotes arousal from sevoflurane-induced loss of consciousness, suggesting a complex control of wakefulness through intimate interactions between long-range connections.

The Effect of Different Propofol-Ketamine Combinations on Emergence Delirium in Children Undergoing Adenoidectomy and Tonsillectomy Surgery

PurposeEmergence delirium (ED) after sevoflurane anesthesia remains a serious issue in children. We aimed to compare different ratios of propofol-ketamine combinations to determine a better option for preventing ED. DesignA prospective, randomized clinical trial. MethodsIn this study, 112 children aged between 3 and 12 years who underwent adenoidectomy and tonsillectomy were recruited. Propofol 1 mg kg−1 + ketamine 1 mg kg−1 (1:1 ratio), propofol 1.5 mg kg−1 + ketamine 0.75 mg kg−1 (2:1 ratio), propofol 2 mg kg−1 + ketamine 0.66 mg kg−1 (3:1 ratio), and propofol 3 mg kg−1 were applied at induction of anesthesia for Groups I, II, III, and IV, respectively. Fentanyl 1 mcg kg−1 and rocuronium 0.6 mg kg−1 were applied at induction, and anesthesia was maintained with sevoflurane and O2/N2O mixture for all participants. Intravenous morphine 0.1 mg kg−1 was applied for postoperative analgesia in the last 10 minutes of surgery. ED was defined as a Watcha score of ≥3. Demographics, hemodynamics, extubation time, Watcha scores, the Face, Legs, Activity, Cry, and Consolability scores, length of stay in the postanesthesia care unit (PACU), rescue analgesic requirement, and postoperative complications were recorded. FindingsED was significantly higher at 10 and 20 minutes in Group IV. Eighteen children experienced ED in PACU, (3, 2, 2, and 11 children in Groups I, II, III, and IV, respectively). Face, Legs, Activity, Cry, and Consolability scores were significantly different at all times. Rescue analgesics were required by 3 children (10.7%) in Group I, 2 (7.1%) in Group II, 2 (7.1%) in Group III, and 10 (35.7%) in Group IV (P = .012). The PACU stay was 21.9 ± 6.4 in Group I, 18.7 ± 6.3 in Group II, 16.7 ± 5.8 in Group III, and 17.4 ± 5.8 in Group IV. Nystagmus was observed in three children in Group I. ConclusionsTo addition of ketamine to propofol during the induction of sevoflurane anesthesia can reduce the ED and analgesic requirements in children. A propofol-to-ketamine ratio of 3:1 provided better postoperative recovery with less pain and ED, without prolonging the PACU length of stay.

Activation of glutamatergic neurones in the pedunculopontine tegmental nucleus promotes cortical activation and behavioural emergence from sevoflurane-induced unconsciousness in mice

BackgroundThe neural mechanisms underlying sevoflurane-induced loss of consciousness and recovery of consciousness after anaesthesia remain unknown. We investigated whether glutamatergic pedunculopontine tegmental nucleus (PPT) neurones are involved in the regulation of states of consciousness under sevoflurane anaesthesia. MethodsIn vivo fibre photometry combined with electroencephalography (EEG)/electromyography recording was used to record changes in the activity of glutamatergic PPT neurones under sevoflurane anaesthesia. Chemogenetic and cortical EEG recordings were used to explore their roles in the induction of and emergence from sevoflurane anaesthesia. Optogenetic methods combined with EEG recordings were used to explore the roles of glutamatergic PPT neurones and of the PPT-ventral tegmental area pathway in maintenance of anaesthesia. ResultsThe population activity of glutamatergic PPT neurones was reduced before sevoflurane-induced loss of righting reflex and gradually recovered after return of righting reflex. Chemogenetic inhibition of glutamatergic PPT neurones accelerated induction of anaesthesia (hM4Di-CNO vs mCherry-CNO, 76 [17] vs 121 [27] s, P<0.0001) and delayed emergence from sevoflurane anaesthesia (278 [98] vs 145 [53] s, P<0.0001) but increased sevoflurane sensitivity. Optogenetic stimulation of glutamatergic PPT neurons or of the PPT-ventral tegmental area pathway promoted cortical activation and behavioural emergence during steady-state sevoflurane anaesthesia, reduced the depth of anaesthesia, and caused cortical arousal during sevoflurane-induced EEG burst suppression. ConclusionsGlutamatergic PPT neurones regulate induction and emergence of sevoflurane anaesthesia.

Medial Septal Glutamatergic Neurons Modulate States of Consciousness during Sevoflurane Anesthesia in Mice.

Multiple neural structures involved in maintaining wakefulness have been found to promote arousal from general anesthesia. The medial septum is a critical region that modulates arousal behavior. This study hypothesized that glutamatergic neurons in the medial septum play a crucial role in regulating states of consciousness during sevoflurane general anesthesia. Adult male mice were used in this study. The effects of sevoflurane anesthesia on neuronal activity were determined by fiber photometry. Lesions and chemogenetic manipulations were used to study the effects of the altered activity of medial septal glutamatergic neurons on anesthesia induction, emergence, and sensitivity to sevoflurane. Optogenetic stimulation was used to observe the role of acute activation of medial septal glutamatergic neurons on cortical activity and behavioural changes during sevoflurane-induced continuous steady-state of general anesthesia and burst suppression state. We found that medial septal glutamatergic neuronal activity decreased during sevoflurane anesthesia induction and recovered in the early period of emergence. Chemogenetic activation of medial septal glutamatergic neurons prolonged the induction time (mean ± SD, hM3Dq-Clozapine N-oxide vs. hM3Dq-Saline, 297.5 ± 60.1 s vs. 229.4 ± 29.9 s, P < 0.001, n = 11) and decreased the emergence time (53.2 ± 11.8 s vs. 77.5 ± 33.5 s, P = 0.025, n = 11). Lesions or chemogenetic inhibition of these neurons produced the opposite effects. During steady-state of general anesthesia and deep anesthesia-induced burst suppression state, acute optogenetic activation of medial septal glutamatergic neurons induced cortical activation and behavioural emergence. Our findings reveal that activation of medial septal glutamatergic neurons has arousal-promoting effects during sevoflurane anesthesia in male mice. The activation of these neurons prolongs the induction and accelerates the emergence of anesthesia.

COMPARISON OF INDUCTION OF GENERAL ANESTHESIA WITH PROPOFOL AND SEVOFLURANE FOREASE OF I GEL INSERTION: A RANDOMISED CONTROLLED TRIAL

Objectives: The aim of this study is to compare the conditions for supraglottic airway device (I Gel) insertion following induction of anesthesia with inhalation of Sevoflurane or intravenous induction with propofol in patients undergoing short surgery (&lt;3 h) and comparison the loss of eye reflex, Hemodynamic parameters, Jaw opening, Ease of insertion, coughing, gagging, laryngeal spasm are taken into consideration. Methods: It is randomized control trial was conducted in the Department of Anaesthesia at Command Hospital (Air Force) Bengaluru after obtaining permission from the Institutional Ethical Committee. A total of 140 patients included in the study with written consent, during the 18-month period between May 2020 and November 2021. Patients were randomized into one of the two groups as group P: Propofol and group S: Sevoflurane for induction of anesthesia. Both groups receive IV Lignocaine (2 mL of 1%) before induction of anesthesia. The grading condition for insertion between the groups were noted and compared using appropriate statistical tool using SPSS v21 operating on windows 10. Results: There was no significant difference in the mean age of patients between propofol group and sevoflurane group. Overall propofol group had the better performance compared to the sevoflurane group. There was higher incidence of repeat administration in the sevoflurane group (2.9%) compared to propofol group (1.4%), which was statistically insignificant. Conclusion: The present study found comparable results for supraglottic airway device (I Gel) following induction of anesthesia with inhalation of Sevoflurane or intravenous induction with Propofol.

Dopamine D1-receptor-expressing pathway from the nucleus accumbens to ventral pallidum-mediated sevoflurane anesthesia in mice.

General anesthesia has long been used in clinical practice, but its precise pharmacological effects on neural circuits are not fully understood. Recent investigations suggest that the sleep-wake system may play a role in the reversible loss of consciousness induced by general anesthetics. Studies in mice have shown that microinjection of dopamine receptor 1 (D1R) agonists into the nucleus accumbens (NAc) promotes recovery from isoflurane anesthesia, while microinjection of D1R antagonists has the opposite effect. Furthermore, during the induction and maintenance of sevoflurane anesthesia, there is a significant decrease in extracellular dopamine levels in the NAc, which subsequently increases during the recovery period. These findings suggest the involvement of the NAc in the regulation of general anesthesia. However, the specific role of D1R-expressing neurons in the NAc during general anesthesia and the downstream effect pathways are still not well understood. In order to analyze the impact of sevoflurane anesthesia on NAcD1R neurons and the NAcD1R -VP pathway, this study employed calcium fiber photometry to investigate alterations in the fluorescence intensity of calcium signals in dopamine D1-receptor-expressing neurons located in the nucleus accumbens (NAcD1R neurons) and the NAcD1R -VP pathway during sevoflurane anesthesia. Subsequently, optogenetic techniques were utilized to activate or inhibit NAcD1R neurons and their synaptic terminals in the ventral pallidum (VP), aiming to elucidate the role of NAcD1R neurons and the NAcD1R -VP pathway in sevoflurane anesthesia. These experiments were supplemented with electroencephalogram (EEG) recordings and behavioral tests. Lastly, a genetically-encoded fluorescent sensor was employed to observe changes in extracellular GABA neurotransmitters in the VP during sevoflurane anesthesia. Our findings revealed that sevoflurane administration led to the inhibition of NAcD1R neuron population activity, as well as their connections within the ventral pallidum (VP). We also observed a reversible reduction in extracellular GABA levels in the VP during both the induction and emergence phases of sevoflurane anesthesia. Additionally, the optogenetic activation of NAcD1R neurons and their synaptic terminals in the VP resulted in a promotion of wakefulness during sevoflurane anesthesia, accompanied by a decrease in EEG slow wave activity and burst suppression rate. Conversely, the optogenetic inhibition of the NAcD1R -VP pathway exerted opposite effects. The NAcD1R -VP pathway serves as a crucial downstream pathway of NAcD1R neurons, playing a significant role in regulating arousal during sevoflurane anesthesia. Importantly, this pathway appears to be associated with the release of GABA neurotransmitters from VP cells.

Glutamatergic neurons of piriform cortex delay induction of inhalational general anesthesia

Since their clinical application in the 1840s, the greatest mystery surrounding general anesthesia (GA) is how different kinds of general anesthetics cause reversible unconsciousness, and the precise neural mechanisms underlying the processes. Over past years, although many studies revealed the roles of cortex, thalamus, brainstem, especially the sleep-wake circuits in GA-induced loss of consciousness (LOC),the full picture of the neural circuit mechanism of GA is still largely unknown. Recent studies have focused on the importance of other brain regions. Here, we report that the activity of glutamatergic (Glu) neurons in the piriform cortex (PC), a critical brain region for odor encoding, began to increase during the LOC of GA and gradually recovered after recovery of consciousness. Chemical lesions of the anterior PC (APC) neurons accelerated the induction time of isoflurane anesthesia. Chemogenetic and optogenetic activation of APCGlu neurons prolonged isoflurane and sevoflurane anesthesia induction, whereas APCGlu neuron inhibition displayed the opposite effects. Moreover, the modification of APCGlu neurons did not affect the induction or emergence time of propofol GA. In addition, odor processing may be partially involved in the induction of isoflurane and sevoflurane GA regulated by APCGlu neurons. In conclusion, our findings reveal a critical role of APCGlu neurons in inhalational GA induction.

A Review of Current Literature of Interest to the Office-Based Anesthesiologist.

A Review of Current Literature of Interest to the Office-Based Anesthesiologist.

A Neural Circuit from the Paraventricular Thalamus to the Bed Nucleus of the Stria Terminalis for the Regulation of States of Consciousness during Sevoflurane Anesthesia in Mice.

The neural circuitry underlying sevoflurane-induced modulation of consciousness is poorly understood. This study hypothesized that the paraventricular thalamus bed nucleus of the stria terminalis pathway plays an important role in regulating states of consciousness during sevoflurane anesthesia. Rabies virus-based transsynaptic tracing techniques were employed to reveal the neural pathway from the paraventricular thalamus to the bed nucleus of the stria terminalis. This study investigated the role of this pathway in sevoflurane anesthesia induction, maintenance, and emergence using chemogenetic and optogenetic methods combined with cortical electroencephalogram recordings. Both male and female mice were used in this study. Both γ-aminobutyric acid-mediated and glutamatergic neurons in the bed nucleus of the stria terminalis receive paraventricular thalamus glutamatergic projections. Chemogenetic inhibition of paraventricular thalamus glutamatergic neurons prolonged the sevoflurane anesthesia emergence time (mean ± SD, hM4D-clozapine N-oxide vs. mCherry-clozapine N-oxide, 281 ± 88 vs. 172 ± 48 s, P < 0.001, n = 24) and decreased the induction time (101 ± 32 vs. 136 ± 34 s, P = 0.002, n = 24), as well as the EC5 0 for the loss or recovery of the righting reflex under sevoflurane anesthesia (mean [95% CI] for the concentration at which 50% of the mice lost their righting reflex, 1.16 [1.12 to 1.20] vs. 1.49 [1.46 to 1.53] vol%, P < 0.001, n = 20; and for the concentration at which 50% of the mice recovered their righting reflex, 0.95 [0.86 to 1.03] vs. 1.34 [1.29 to 1.40] vol%, P < 0.001, n = 20). Similar results were observed during suppression of the paraventricular thalamus bed nucleus-stria terminalis pathway. Optogenetic activation of this pathway produced the opposite effects. Additionally, transient stimulation of this pathway efficiently induced behavioral arousal during continuous steady-state general anesthesia with sevoflurane and reduced the depth of anesthesia during sevoflurane-induced burst suppression. In mice, axonal projections from the paraventricular thalamic neurons to the bed nucleus of the stria terminalis contribute to regulating states of consciousness during sevoflurane anesthesia.

Genetic variation of rs12918566 affects GRIN2A expression and is associated with spontaneous movement response during sevoflurane anesthesia induction.

N‐methyl‐D‐aspartate (NMDA) receptors mediate excitatory neurotransmission in the nervous system and are preferentially inhibited by general anesthetics such as sevoflurane. Spontaneous movement is a common complication during sevoflurane anesthesia induction and seriously affects operations. In this study, we investigated the relationship between NMDA polymorphisms and spontaneous movement during sevoflurane induction. This prospective clinical study enrolled 393 patients undergoing sevoflurane anesthesia as part of their surgical routine. In the GRIN1, GRIN2A, and GRIN2B genes, 13 polymorphisms that form a heteromeric complex as part of the NMDA receptor were selected using Haploview and genotyped using matrix‐assisted laser desorption ionization–time of flight mass spectrometry MassARRAY. Both RNAfold and Genotype‐Tissue Expression portals were used to identify gene expression profiles. Our data showed that 35.8% of subjects exhibited spontaneous movement. The GRIN2A rs12918566 polymorphism was associated with spontaneous movement during sevoflurane induction. A logistic regression analysis of additive, dominant, and recessive models indicated a significant association (odds ratio [OR] (95% confidence limit [CI]): 0.58 (0.42–0.80), p = .00086; OR (95% CI): 0.51 (0.31–0.84), p = .0075, and OR (95% CI): 0.47 (0.27–0.81), p = .0060, respectively). After false discovery rate (FDR) correction, the additive model was still significant with a P FDR =0.010. Bioinformatics demonstrated that the rs12918566 genomic variation affected GRIN2A expression in brain tissue. We also revealed that GRIN2A rs12918566 was significantly associated with spontaneous movement during sevoflurane induction. We believe the NMDA receptor plays an important role in regulating the anesthetic effects of sevoflurane.

Arrhythmia incidence and associated factors during volatile induction of general anesthesia with sevoflurane: a retrospective analysis of 950 adult patients

BackgroundSevoflurane has been used to induce anaesthesia in adults due to its suitability for airway management and haemodynamic stability. Few studies have reported arrhythmia during volatile induction with sevoflurane in adults. Here, we investigated the incidence of arrhythmia and risk factors associated with its occurrence during sevoflurane induction of anaesthesia in adults. Patients and MethodsWe retrospectively analysed 950 adult patients who underwent elective ear nose and throat surgery with volatile induction using sevoflurane between May and December 2015. The incidence of arrhythmia and the factors associated with its development were analysed. ResultsArrhythmia was observed in 164 (17.3%) of 950 adult patients. The most frequently observed arrhythmia was sinus tachycardia (heart rate > 120 bpm) (77 patients, 47.0%). The multivariable logistic analysis showed four independent risk factors: age (odds ratio [OR] = 0.984, 95% confidence interval [CI] = 0.973−0.996, p = 0.006), coronary artery disease (OR = 3.749, 95% CI = 1.574–8.927, p = 0.003), maximal concentration (8 vol%) of sevoflurane from the start of induction (OR = 2.696, 95% CI = 1.139–6.382, p = 0.024), and maintenance of 8 vol% sevoflurane concentration after eyelash reflex loss (OR = 1.577, 95% CI = 1.083–2.296, p = 0.018). The risk of hypotension was greater in patients in whom arrhythmia occurred, although blood pressure recovered to baseline after the concentration of sevoflurane was adjusted. ConclusionsWe recommend that the sevoflurane concentration be gradually increased with continuous and vigilant electrocardiogram and blood pressure monitoring. The sevoflurane concentration should be adjusted after sufficient unconsciousness is reached.

Changes in Plasma Glial Fibrillary Acidic Protein in Children Receiving Sevoflurane Anesthesia: A Preliminary Randomized Trial.

We investigated changes in plasma glial fibrillary acidic protein concentration during sevoflurane anesthesia induction in children < 3 years old and determined the effect of co-administering dexmedetomidine. This preliminary randomized trial included 60 pediatric patients who received sevoflurane anesthesia for >3 h. Patients were assigned to dexmedetomidine or control groups at a 1:1 ratio. The primary outcome was changes in plasma glial fibrillary acidic protein concentration of dexmedetomidine and control groups over time. Fifty-five patients were included in the final analysis. The median (interquartile range (IQR)) of the plasma glial fibrillary acidic protein level was 387.7 (298.9–510.8) pg·mL−1 immediately after anesthetic induction, 302.6 (250.9–412.5) pg·mL−1 at 30 min, and 321.9 (233.8–576.2) pg·mL−1 at 180 min after the first sample. These values did not change over time (p = 0.759). However, plasma glial fibrillary acidic protein increased after 180 min of infusion of dexmedetomidine compared with values at 30 min infusion (p = 0.04, mean difference and 95% confidence interval of 221.6 and 2.2 to 441.0 pg·mL−1). In conclusion, three hours of sevoflurane anesthesia in pediatric patients < 3 years old did not provoke neuronal injury assessed by the plasma biomarker. Further studies regarding the effect of prolonged dexmedetomidine infusion on anesthetic neuronal injury are required.

Effect of dexmedetomidine on perioperative hemodynamics and organ protection in children with congenital heart disease: A randomized controlled trial.

Background:This study aimed to investigate the effects of dexmedetomidine (Dex) on hemodynamics and organ protection in congenital heart disease (CHD) children who underwent open-heart surgery under cryogenic cardiopulmonary bypass.Methods:Ninety children were randomly allocated to group C (0.9% saline 0.2 μg/kg/hour), group D1 (Dex 0.2 μg/kg/hour), and group D2 (Dex 0.4 μg/kg/hour) (n = 30 per group). All participants received fentanyl, propofol and 1% sevoflurane for anesthesia induction. Hemodynamic data were measured from T0 (before the induction) to T7 (30 minutes after extubation). The difference of arterial internal jugular vein bulbar oxygen difference and cerebral oxygen extraction ratio were calculated according to Fick formula. Enzyme-linked immunosorbent assay was performed to detect the serum myocardial, brain and kidney injury markers. The incidence of acute kidney injury (AKI) was calculated by serum creatinine level. Tracheal extubation time, postoperative pain score and emergence agitation score were also recorded.Results:Compared with group C, group D1, and D2 exhibited reduction in hemodynamic parameters, myocardial and brain injury indicators, and tracheal extubation time. There were no significant differences in blood urea nitrogen and neutrophil gelatinase-associated lipocalin or incidence of AKI among the 3 groups. Besides, the incidence of tachycardia, nausea, vomiting and moderate agitation, and the FLACC scale in group D1 and D2 were lower than those in group C. Moreover, Dex 0.4 g/kg/hour could further reduce the dosage of fentanyl and dopamine compared with Dex 0.2 g/kg/hour.Conclusions:Dex anesthesia can effectively maintain hemodynamic stability and diminish organ injuries in CHD children.

Monochromatic Blue Light Activates Suprachiasmatic Nucleus Neuronal Activity and Promotes Arousal in Mice Under Sevoflurane Anesthesia.

Background: Monochromatic blue light (MBL), with a wavelength between 400–490 nm, can regulate non-image-forming (NIF) functions of light in the central nervous system. The suprachiasmatic nucleus (SCN) in the brain is involved in the arousal-promoting response to blue light in mice. Animal and human studies showed that the responsiveness of the brain to visual stimuli is partly preserved under general anesthesia. Therefore, this study aimed to investigate whether MBL promotes arousal from sevoflurane anesthesia via activation of the SCN in mice.Methods: The induction and emergence time of sevoflurane anesthesia under MBL (460 nm and 800 lux) exposure was measured. Cortical electroencephalograms (EEGs) were recorded and the burst-suppression ratio (BSR) was calculated under MBL during sevoflurane anesthesia. The EEGs and local field potential (LFP) recordings with or without locally electrolytic ablated bilateral SCN were used to further explore the role of SCN in the arousal-promoting effect of MBL under sevoflurane anesthesia. Immunofluorescent staining of c-Fos was conducted to reveal the possible downstream mechanism of SCN activation.Results: Unlike the lack of effect on the induction time, MBL shortened the emergence time and the EEG recordings showed cortical arousal during the recovery period. MBL resulted in a significant decrease in BSR and a marked increase in EEG power at all frequency bands except for the spindle band during 2.5% sevoflurane anesthesia. MBL exposure under sevoflurane anesthesia enhances the neuronal activity of the SCN. These responses to MBL were abolished in SCN lesioned (SCNx) mice. MBL evoked a high level of c-Fos expression in the prefrontal cortex (PFC) and lateral hypothalamus (LH) compared to polychromatic white light (PWL) under sevoflurane anesthesia, while it exerted no effect on c-Fos expression in the ventrolateral preoptic area (VLPO) and locus coeruleus (LC) c-Fos expression.Conclusions: MBL promotes behavioral and electroencephalographic arousal from sevoflurane anesthesia via the activation of the SCN and its associated downstream wake-related nuclei. The clinical implications of this study warrant further study.

Circadian differences in emergence from volatile anaesthesia in mice: involvement of the locus coeruleus noradrenergic system

BackgroundCircadian differences in the induction, maintenance, or emergence from volatile anaesthesia have not been well studied. MethodsThe minimal alveolar concentration (MAC) for preventing movement in response to a painful stimulus, MAC for loss of righting reflex (MACLORR), and MAC for recovery of righting reflex (MACRORR) in C57BL/6J male mice with isoflurane or sevoflurane exposure were measured during either the light or dark phase. Time to onset of loss of righting reflex (TimeLORR) and recovery of righting reflex (TimeRORR) upon exposure to 1 MAC of isoflurane or sevoflurane were determined. EEG was also monitored in the light and dark phase under isoflurane or sevoflurane exposure. The noradrenergic toxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) was used to deplete noradrenergic neurones in the locus coeruleus to explore the impact of norepinephrine on these measurements. ResultsMACLORR, TimeLORR, and MAC did not show light- or dark-phase-dependent variations for either isoflurane or sevoflurane exposure. However, MACRORR was higher and TimeRORR was shorter in the dark phase than in the light phase for both isoflurane and sevoflurane exposure. The EEG delta wave power was higher but theta wave power was lower in the light phase than that in the dark phase during the rest state and emergence of anaesthesia. These light- and dark-phase-dependent changes in emergence were abolished in DSP-4-treated mice. ConclusionOur data show that circadian differences exist during emergence but not during induction or maintenance of sevoflurane or isoflurane anaesthesia. The locus coeruleus noradrenergic system may contribute to these differences.

Hemodynamic Stability, Patient Acceptance and Cost of Intravenous Propofol and Inhalational Sevoflurane for Induction of Anaesthesia: A Prospective, Randomized Comparative Study.

IntroductionThe effects of an anesthetic agent on the hemodynamic stability are of prime importance in patients with compromised hemodynamics. Although comparative studies of sevoflurane and propofol are reported, most of these are aimed to assess maintenance and early postoperative recovery. There are very few studies on hemodynamic changes occurring with these two agents. This study compares the hemodynamic stability, patient acceptance, and cost of intravenous (IV) propofol versus inhalational (IH) sevoflurane for the induction of anesthesia.MethodsThis prospective, randomized comparative study was conducted among 80 patients with American Society of Anaesthesiologists (ASA) grade-I requiring general anesthesia (GA) for elective surgical procedures. The study was approved by the institutional ethics committee and was conducted as per the principles of the Declaration of Helsinki and Good Clinical Practice (GCP) guidelines. Enrolled patients were randomized to receive either intravenous (IV) propofol 2 mg/kg (n=40) or gradual inhalational (IH) induction with sevoflurane (n=40). All patients were maintained with sevoflurane 2% in 67% nitrous oxide (N2O) and O2. Hemodynamic parameters like pulse rate and mean arterial pressure (MAP) were monitored every minute up to five minutes. Patients' acceptance was assessed on a 10-item questionnaire, and the cost of anesthesia was assessed based on the anesthetic requirement. The hemodynamic parameters were compared between the two groups using two-way repeat-measures ANOVA. The incidence of hypotension was compared using Fischer’s test. ResultsThe two groups were similar at baseline with respect to the demography and other baseline characteristics. There was greater (p<0.05) fall in MAP with propofol induction (28.48%) compared to sevoflurane (14.61%). Greater reduction in pulse rate (p<0.05) with sevoflurane (9.18) induction was observed compared to propofol (5.28). Patient acceptance for both drugs was similar (p>0.05). Although sevoflurane was unpleasant, propofol injection was painful. Ninety percent of patients preferred propofol for repeat anesthesia as against 85% of patients with sevoflurane. Considering the quantity of anesthetic consumed and the unit cost, propofol was more costly as compared to sevoflurane.ConclusionSevoflurane maintains better hemodynamic stability compared to propofol, and patient acceptance of both drugs is similar. Induction with sevoflurane was found to be cheaper as compared to propofol induction.

Effects of intravenous and mask induction on post-operative emergence delirium in pediatric patients undergoing tonsillectomy with or without adenoidectomy

Emergence delirium occurs in children during recovery from general anesthesia. The aim of the study was to examine the effects of mask and intravenous sevoflurane anesthesia induction on emergence delirium in children undergoing tonsillectomy with or without adenoidectomy. This single-blinded, prospective, randomized clinical trial was conducted in the operating room and the post-operative recovery area at a university hospital. Sixty-seven children (aged 3-12years) were randomly assigned to receive either mask induction (group M) or intravenous induction (group IV). Vascular access was provided in group M after 8% sevoflurane and 60% nitrous oxide in oxygen were given through a mask. In the IV cohort, an intravenous cannula was inserted prior to induction. The incidence of emergence delirium was assessed using the Pediatric Anesthesia Emergence Delirium (PAED) scale after arrival in the post-anesthesia care unit. Post-operative pain was assessed using the Face, Legs, Activity, Cry, and Consolability (FLACC) scale. PAED scores were significantly higher in group M at 5min (group M = 12.2 ± 4.215, group IV = 9.1 ± 4.0; mean difference = 3.094, 95% CI [1.108; 5.081]; P = 0.003), at 15min (group M = 8.0 ± 2.6, group IV = 5.1 ± 2.3; mean difference = 2.942, 95% CI [1.586-4.301]; P < 0.001), and at 30min (group M = 5.1 ± 2.8, group IV = 2.5 ± 1.8; mean difference = 2.620, 95% CI [1.457; 3.783]; P < 0.001) than in group IV. The FLACC scale scores were similar between the two groups. Mask induction for pediatric patients undergoing tonsillectomy with or without adenoidectomy increased Pediatric Anesthesia Emergence Delirium scores more than intravenous induction. NCT03252405.

Comparison of the Effects of Propofol and Sevoflurane on QT Interval in Pediatrics Undergoing Cochlear Implantation: A Randomized Clinical Trial Study.

BackgroundChildren with sensorineural hearing loss are at risk of cardiac electrophysiologic abnormalities. Inhalational Sevoflurane induction in these children can cause QT prolongation.ObjectivesIn order to evaluate the safety of inhalational induction of anesthesia with sevoflurane in children with sensorineural hearing loss, who are candidates for cochlear implant, its electrophysiologic effects was compared with intravenous induction of anesthesia with propofol.MethodsIn this double-blind randomized clinical trial, 61 children aged between one and eighteen years old, who were candidates for cochlear implantation, were randomly allocated to groups receiving anesthesia with sevoflurane (n = 32) or propofol (n = 29) for induction of anesthesia. Two 12-leads ECG were taken from all of patients before and after induction and QTc, Tp-e interval, and JTc were measured and compared.ResultsTwo cases, who had pre-induction QTc longer than 500 ms were excluded from the study. Patients had similar age (102.58 ± 87 versus 101.46 ± 67 months, P = 0.95) and gender (males: 48.3% versus 56.3%, P = 0.53) distribution. The researchers observed significant post induction difference in QTc values between these groups (propofol 422.5 ± 40, sevoflurane 445.0 ± 29, P = 0.016). There was no significant difference in the percent QTc and Tp-e changes in propofol and sevoflurane groups. Greater percentage of patients with increased Tp-e interval (> 100 ms) in the sevoflurane group than the propofol group was also seen. There was no significant long QTc difference (QTc > 500 ms or more than 60 ms increase from baseline) after induction of anesthesia in the sevoflurane group compared to the propofol group (15.6% versus 13.8%, P = 0.84).ConclusionsAfter electrophysiological evaluations in children with sensorineural hearing loss, in patients whose pre-induction QTc is not longer than 500 ms, propofol seems safer than inhalational sevoflurane for induction of anesthesia.

A Comparison of Bispectral Index and Entropy During Sevoflurane Anesthesia Induction in Children with and without Diplegic Cerebral Palsy.

Background: This study compared the correlation of bispectral index (BIS) or entropy with different sevoflurane concentrations between children with and without cerebral palsy (CP) during induction. Methods: For eighty-two children (40 CP and 42 non-CP children), anesthesia was induced with sevoflurane. BIS and entropy (response entropy and state entropy (RE and SE)) were recorded before and after the induction of anesthesia at end-tidal sevoflurane concentrations of 1–3 vol%. The sedation status was assessed using an Observer’s Assessment of Alertness/Sedation scale. The ability to predict awareness was estimated using the area under the receiver-operator characteristic curve (AUC) analysis. Results: RE, SE and BIS values decreased continuously over the observed concentration range of sevoflurane in both groups. The SE values while awake and the RE, SE, BIS values at 3 vol% sevoflurane were lower in children with CP than in those without CP. The AUC of the BIS was significantly better than RE or SE in children without CP. The AUC of the BIS was not significantly higher than that of the RE or SE in children with CP. Conclusion: BIS seems better correlated than entropy with the clinical state of loss of response in children without CP, but not in those with CP.

Comparison by Real-Time Hemodynamic and Cardiac Efficiency Monitoring of Sufentanil-Midazolam and Sevoflurane for Anesthesia Induction in Children Undergoing Cardiac Surgery: A Prospective Randomized Study

Background Intravenous sufentanil-midazolam and inhalational sevoflurane are widely used for anesthetic induction in children undergoing cardiac surgery. However, knowledge about their effects on hemodynamics and cardiac efficiency remains limited due largely to the lack of direct monitoring method. We used minimally invasive technique pressure recording analytical method (PRAM) to directly monitor hemodynamics and cardiac efficiency and compared the effects of the two anesthetic regimens in children undergoing ventricular septal defect repair. Methods Forty-Four children (2.3±0.9 years) were randomly divided into two groups to receive either intravenous sufentanil (1 μg/kg) and midazolam (0.2 mg/kg) (Group SM) or 2.0 minimal alveolar concentration (MAC) sevoflurane (Group S) to complete induction after sedation was obtained with 2.0 MAC sevoflurane. Systemic hemodynamic data recorded by PRAM included heart rate (HR), systolic (SBP) and mean (MBP) blood pressure, stroke volume index (SVI), cardiac index (CI), systemic vascular resistance index (SVRI), the maximal slope of systolic upstroke (dp/dtmax) and cardiac cycle efficiency (CCE) after sedation obtained, 1, 2, 5 min after induction achieved, 1, 2, 5 and 10 min after intubation. Results HR, SVRI showed a decrease in Group SM but an increase in Group S (Ptime*group<0.0001) in the study period. SVI and CCE showed an increase in Group SM but a decrease in Group S (Ptime*group<0.0001). SBP, MBP and CI were related to time after polynomial transformation, and showed an increase after intubation in Group SM but a decrease in Group S (Ptime2*group<0.0001). Conclusion PRAM provides meaningful and direct monitoring of hemodynamics and cardiac efficiency during the dynamic period of anesthetic induction in children undergoing cardiac surgery. As compared to inhalational sevoflurane, intravenous sufentanil-midazolam exerts more favorable effects on systemic hemodynamics and cardiac efficiency during anesthetic induction in this group of patients.