In neuroscience, numerous experimental procedures in animal models require surgical interventions, such as the implantation of recording electrodes or cannulas before main experiments. These surgeries can take several hours and should rely on principles that are common in the field of research and medicine. Considering the characteristics of the avian respiratory physiology, the development of a safe and replicable protocol for birds is necessary to minimize side effects of anesthetic agents, circumvent technical limitations due to the insufficient availability of patient monitoring, and to maintain stable intraoperative anesthesia. Through the consistent and responsible implementation of the three R principle of animal welfare in science (\"Replace, Reduce, Refine\"), we aimed to optimize experimental methods to minimize the burden on pigeons (Columba livia) during surgical procedures. Here, surgeries were conducted under balanced anesthesia and perioperative monitoring of heart rate, oxygen saturation, body temperature, and the reflex state. The protocol we developed is based on the combination of injectable and inhalative anesthetic drugs [ketamine, xylazine, and isoflurane, supported by the application of an opiate for analgesia (e.g., butorphanol, buprenorphine)]. The combination of ketamine and xylazine with a pain killer is established in veterinary medicine across a vast variety of species. Practicability was verified by survival of the animals, fast and smooth recovery quantified by clinical examination, sufficiency, and stability of anesthesia. Independent of painful stimuli like incision or drilling, or duration of surgery, vital parameters were within known physiological ranges for pigeons. Our approach provides a safe and conservative protocol for surgeries of extended duration for scientific applications as well as for veterinary medicine in pigeons which can be adapted to other bird species.

Scale-free statistics of coordinated neuronal activity, suggesting a universal operating mechanism across spatio-temporal scales, have been proposed as a necessary condition of healthy resting-state brain activity. Recent studies have focused on anesthetic agents to induce distinct neural states in which consciousness is altered to understand the importance of critical dynamics. However, variation in experimental techniques, species, and anesthetics, have made comparisons across studies difficult. Here we conduct a survey of several common anesthetics (isoflurane, pentobarbital, ketamine) at multiple dosages, using calcium wide-field optical imaging of the mouse cortex. We show that while low-dose anesthesia largely preserves scale-free statistics, surgical plane anesthesia induces multiple dynamical modes, most of which do not maintain critical avalanche dynamics. Our findings indicate multiple pathways away from default critical dynamics associated with quiet wakefulness, not only reflecting differences between these common anesthetics but also showing significant variations in individual responses. This is suggestive of a non-trivial relationship between criticality and the underlying state of the subject.

OBJECTIVE: To compare the effects of propofol, ketamine-propofol and isoflurane, at similar anesthetic depth, on cardiopulmonary variables in unpremedictated chickens.
METHODS: Prospective, randomized, crossover experimental trial.
METHODS: A total of 10 male Leghorn domestic chickens, aged 3 months and body mass 1.4-2.0 kg.
METHODS: Birds were randomly assigned to each of three anesthetic protocols, 7 days apart: intravenous propofol, intravenous ketamine-propofol or isoflurane. Anesthesia was induced (indicated by loss of righting reflex and tracheal intubation) and maintained with propofol (10 mg kg-1 minute-1, then 1.1 mg kg-1 minute-1), ketamine-propofol (5 mg mL-1 ketamine and 5 mg mL-1 propofol combined; 10 mg kg-1 minute-1, then 1.1 mg kg-1 minute-1) or isoflurane [5% vaporizer setting initially, then end-tidal concentration (Fe\'Iso) of 2%] for 65 minutes. Anesthesia was maintained at a similar anesthetic depth based upon positive or negative responses to toe pinch. Heart rate (HR), respiratory rate (fR), noninvasive arterial blood pressure and arterial blood gases were measured during anesthesia. Propofol or ketamine-propofol infusion rates and Fe\'Iso required to prevent movement in response to a noxious stimulus and recovery times were recorded.
RESULTS: Anesthesia induction dose was 9.0 ± 0.8 (mean ± SD) and 12.2 ± 0.3 mg kg-1 for propofol and ketamine-propofol, respectively. Propofol and ketamine-propofol infusion rates and Fe\'Iso required to prevent movement in response to the noxious stimulus were 0.88 ± 0.14 mg kg-1 minute-1, 0.92 ± 0.14 mg kg-1 minute-1 and 1.45 ± 0.28%, respectively. Cardiopulmonary variables remained clinically acceptable, but ketamine-propofol was associated with a significantly higher HR (p = 0.0001) and lower fR (p = 0.0001). Time to extubation did not differ among treatments.
CONCLUSIONS: Cardiovascular and respiratory variables were maintained within normal ranges in all treatments. Coadministration of ketamine with propofol significantly reduced the induction and maintenance dose of propofol.

OBJECTIVE: The mechanism underlying the reversible unconsciousness induced by general anesthetics (GA) remains unclear. Recent studies revealed the critical roles of myelin and oligodendrocytes (OLs) in higher functions of the brain. However, it is unknown whether myelin actively participates in the regulation of GA. The aim of this study is to investigate the roles and possible mechanisms of myelin in the regulation of consciousness alterations induced by isoflurane anesthesia.
METHODS: First, demyelination models for the entire brain and specific neural nuclei were established to investigate the potential role of myelination in the regulation of GA, as well as its possible regional specificity. c-Fos staining was then performed on the demyelinated nuclei to verify the impact of myelin loss on neuronal activity. Finally, the activity of neurons during isoflurane anesthesia in demyelinated mice was recorded by optical fiber photometric calcium signal. The related behavioral indicators and EEG were recorded and analyzed.
RESULTS: A prolonged emergence time was observed from isoflurane anesthesia in demyelinated mice, which suggested the involvement of myelin in regulating GA. The demyelination in distinct nuclei by LPC further clarified the region-specific roles of isoflurane anesthesia regulation by myelin. The effect of demyelination on isoflurane anesthesia in the certain nucleus was consistent with that in neurons towards isoflurane anesthesia. Finally, we found that the mechanism of myelin in the modulation of isoflurane anesthesia is possibly through the regulation of neuronal activity.
CONCLUSIONS: In brief, myelin in the distinct neural nucleus plays an essential role in regulating the process of isoflurane anesthesia. The possible mechanism of myelin in the regulation of isoflurane anesthesia is neuronal activity modification by myelin integrity during GA. Our findings enhanced the comprehension of myelin function, and offered a fresh perspective for investigating the neural mechanisms of GA.

General anesthesia can impact a patient\'s memory and cognition by influencing hippocampal function. The CA1 and dentate gyrus (DG), serving as the primary efferent and gateway of the hippocampal trisynaptic circuit facilitating cognitive learning and memory functions, exhibit significant differences in cellular composition, molecular makeup, and responses to various stimuli. However, the effects of isoflurane-induced general anesthesia on CA1 and DG neuronal activity in mice are not well understood. In this study, utilizing electrophysiological recordings, we examined neuronal population dynamics and single-unit activity (SUA) of CA1 and DG in freely behaving mice during natural sleep and general anesthesia. Our findings reveal that isoflurane anesthesia shifts local field potential (LFP) to delta frequency and reduces the firing rate of SUA in both CA1 and DG, compared to wakefulness. Additionally, the firing rates of DG neurons are significantly lower than CA1 neurons during isoflurane anesthesia, and the recovery of theta power is slower in DG than in CA1 during the transition from anesthesia to wakefulness, indicating a stronger and more prolonged impact of isoflurane anesthesia on DG. This work presents a suitable approach for studying brain activities during general anesthesia and provides evidence for distinct effects of isoflurane anesthesia on hippocampal subregions.

Inhalational anaesthetic agents are routinely used in veterinary anaesthesia practices, yet their consumption contributes significantly to greenhouse gas emissions and environmental impact. We conducted a 55-day observational study at a veterinary teaching hospital in Switzerland, monitoring isoflurane and sevoflurane consumption across small, equine and farm animal clinics and analysed the resulting environmental impact. Results revealed that in total, 9.36 L of isoflurane and 1.27 L of sevoflurane were used to anaesthetise 409 animals across 1,489 h. Consumption rates varied among species, with small and farm animals ranging between 8.7 and 13 mL/h, while equine anaesthesia exhibited a higher rate, 41.2 mL/h. Corresponding to 7.36 tonnes of carbon dioxide equivalent in total environmental emissions or between 2.4 and 31.3 kg of carbon dioxide equivalent per hour. Comparison to human anaesthesia settings showed comparable consumption rates to small animals, suggesting shared environmental implications, albeit on a smaller scale. This research highlights the importance of continued evaluation of veterinary anaesthesia practices to balance patient safety with environmental stewardship; potential mitigation strategies are explored and discussed.

BACKGROUND: Postoperative nausea, vomiting, and cough are the most common adverse effects of general anesthesia resulting in high discomfort to the patient resulting in uneasiness during the recovery period. This study aimed to compare the influence of intraoperative use of sevoflurane and isoflurane on postoperative nausea, vomiting, and cough.
METHODS: After approval from the institutional ethical committee, this quantitative observational institutional study was conducted on all patients aged between 18 and 65 years undergoing surgery under general anesthesia at KMC Hospital, Mangalore. Patients were allocated into the sevoflurane group or isoflurane group.
RESULTS: All demographic parameters such as age, sex, American Society of Anesthesiologists physical status, and duration were comparable (P > 0.05). The sevoflurane group had higher number of patients (11 [14.86%]) with postoperative nausea at 0 h as compared isoflurane group (7 [9.45%]). Two patients in the isoflurane group reported postoperative vomiting at 0 h, whereas no patient in the sevoflurane group reported vomiting. For cough, a statistically significant correlation was seen between the two groups (P = 0.000) with majority of patients in the isoflurane group, i.e., 50 (67.6%) patients reporting cough at 0 h while only 15 (20.3%) reported cough in the sevoflurane group.
CONCLUSIONS: Sevoflurane was found to be better than isoflurane in terms of postoperative nausea vomiting and cough immediately after emergence in our study. Isoflurane cause the emergence of cough whereas no significant difference in nausea and vomiting was observed in both groups.
Résumé Introduction:Les nausées, vomissements et toux postopératoires sont les effets indésirables les plus courants de l’anesthésie générale, entraînant un inconfort élevé pour le patient, entraînant un malaise pendant la période de récupération. Cette étude visait à comparer l’influence del’utilisation peropératoire du sévoflurane et de l’isoflurane sur les nausées, vomissements et toux postopératoires.Méthode:Après approbation du comité d’éthique institutionnel, cette étude institutionnelle observationnelle quantitative a été menée sur tous les patients âgés de 18 à 65 ans subissant une intervention chirurgicale sous anesthésie générale à l’hôpital KMC de Mangalore. Les patients ont été répartis dans le groupe sévoflurane ou le groupe isoflurane.Résultats:Tous les paramètres démographiques comme l’âge, le sexe, l’ASA PS et la durée étaient comparables. ( P > 0,05) Le groupe sévoflurane avait un nombre plus élevé de patients [11 (14,86 %)] présentant des nausées postopératoires à 0 heure par rapport au groupe isoflurane [7 (9,45 %)]. 2 patients du groupe Isoflurane ont signalé des vomissements postopératoires à 0 heure alors qu’aucun patient du groupe Sévoflurane n’a signalé de vomissements. Pour la toux, une corrélation statistiquement significative a été observée entre les deux groupes ( P = 0,000) avec une majorité de patients dansle groupe isoflurane, c’est-à-dire 50 (67,6 %) patients signalant une toux à 0 heure, alors que seulement 15 (20,3 %) ont signalé une toux dans le groupe sévoflurane.Conclusion:Le sévoflurane s’est révélé meilleur que l’isoflurane en termes de nausées, vomissements et toux postopératoires immédiatement après l’émergence dans notre étude. L’isoflurane provoque une toux d’émergence alors qu’aucune différence significative en termes de nausées et de vomissements n’a été observée dans les deux groupes.

BACKGROUND: Reversible loss of consciousness is the primary therapeutic endpoint of general anesthesia; however, the drug-invariant mechanisms underlying anesthetic-induced unconsciousness are still unclear. This study aimed to investigate the static, dynamic, topological and organizational changes in functional brain network induced by five clinically-used general anesthetics in the rat brain.
METHODS: Male Sprague-Dawley rats (n = 57) were randomly allocated to received propofol, isoflurane, ketamine, dexmedetomidine, or combined isoflurane plus dexmedetomidine anesthesia. Resting-state functional magnetic resonance images were acquired under general anesthesia and analyzed for changes in dynamic functional brain networks compared to the awake state.
RESULTS: Different general anesthetics induced distinct patterns of functional connectivity inhibition within brain-wide networks, resulting in multi-level network reorganization primarily by impairing the functional connectivity of cortico-subcortical networks as well as by reducing information transmission capacity, intrinsic connectivity, and network architecture stability of subcortical regions. Conversely, functional connectivity and topological properties were preserved within cortico-cortical networks, albeit with fewer dynamic fluctuations under general anesthesia.
CONCLUSIONS: Our findings highlighted the effects of different general anesthetics on functional brain network reorganization, which might shed light on the drug-invariant mechanism of anesthetic-induced unconsciousness.

Isoflurane is one of the most commonly used anaesthetic agents in surgery procedures. During the past decades, isoflurane has been found to cause impairment in neurological capabilities in new-borns and elderly patients. Luteolin is a flavonoid that has been documented to possess a neuroprotective effect. Here we investigated the putative neuroprotective effects of luteolin on isoflurane-induced neurotoxicity in mouse hippocampal neuronal HT22 cells and explored the potential mechanisms. We demonstrated that luteolin improved mitochondrial dysfunction and reduced oxidative stress and apoptosis in isoflurane-treated HT22 cells, and thus inhibiting the isoflurane-induced neuronal injury. Further investigations showed that isoflurane exposure caused miR-214 downregulation, which could be mitigated by treatment with luteolin. Knockdown of miR-214 attenuated the neuroprotection of luteolin on isoflurane-induced neuronal injury. More importantly, luteolin inhibited isoflurane-caused regulation of the PTEN/Akt pathway, while miR-214 knockdown altered the regulatory effect of luteolin on the PTEN/Akt pathway. Furthermore, the effects of miR-214 knockdown on the neuroprotection of luteolin could also be prevented by knockdown of PTEN, implying that the neuroprotective effect of luteolin was mediated by miR-214/PTEN/Akt signaling pathway. These findings provided evidence for the potential application of luteolin in preventing isoflurane-induced neurotoxicity.

Research has revealed that prolonged or repeated exposure to isoflurane, a common general anesthetic, can lead to cognitive and behavioral deficiencies, particularly in early life. The brain contains a wealth of LanCL1, an antioxidant enzyme that is thought to mitigate oxidative stress. Nevertheless, its precise function in mammals remains uncertain. This study uncovered a decrease in the expression of LanCL1 due to prolonged isoflurane anesthesia, accompanied by anesthesia-induced neurotoxicity in vivo and in vitro. To better understand LanCL1\'s essential function, LanCL1 overexpressing adenoviruses were employed to increase LanCL1 levels. The outcomes were analyzed using western blot and immunofluorescence methods. According to the findings, extended exposure to isoflurane anesthesia may lead to developmental neurotoxicity in vivo and in vitro. The anesthesia-induced neurotoxicity was concomitant with a reduction in LanCL1 expression. Moreover, the study revealed that overexpression of LanCL1 can mitigate the neurotoxic effects of isoflurane anesthesia, resulting in improved synaptic growth, less reactive oxygen species enhanced cell viability and rescued memory deficits in the developing brain. In conclusion, prolonged anesthesia-induced LanCL1 deficiency could be responsible for neurotoxicity and subsequent cognitive impairments in the developing brain. Additional LanCL1 counteracts this neurotoxic effect and protects neurons from long-term isoflurane anesthesia.