暂无摘要。

UNASSIGNED: In patients undergoing cancer surgery, it is ambiguous whether propofol-based total intravenous anesthesia (TIVA) elicits a significantly higher overall survival rate than volatile anesthetics (VA). Consequently, evaluating the impact of TIVA and VA on long-term oncological outcomes is crucial.
UNASSIGNED: This study compared TIVA versus VA for cancer surgery patients and investigated the potential correlation between anesthetics and their long-term surgical outcomes.
UNASSIGNED: A comprehensive search of Medline, EMBASE, Scopus, and Cochrane Library identified English-language peer-reviewed journal papers. The statistical measurements of hazard ratio (HR) and 95% CI were calculated. We assessed heterogeneity using Cochrane Q and I2 statistics and the appropriate p-value. The analysis used RevMan 5.3.
UNASSIGNED: The meta-analysis included 10 studies with 14036 cancer patients, 6264 of whom received TIVA and 7777 VA. In this study, we examined the long-term oncological outcomes of cancer surgery patients with TIVA and VA. Our data show that the TIVA group had a considerably higher overall survival rate (HR = 0.49, 95% CI: 0.30-0.80) and recurrence-free survival rate (HR = 0.56, 95% CI: 0.32-0.97). Each outcome was statistically significant (p < 0.05).
UNASSIGNED: The present study concludes that TIVA is a more effective anesthetic agent than VA in obtaining better long-term oncological outcomes in cancer patients after surgery as it provides a higher overall survival rate, a higher recurrence-free survival rate and fewer post-operative pathological findings in patients who have undergone surgery for cancer as compared to VA.

The extensive use of inhalational anesthetics contributes to both indoor and outdoor (environmental) pollution. The influence of genetic susceptibility on DNA damage and oxidative stress and the possible modulation of gene expression have not yet been investigated upon occupational exposure to waste anesthetic gases (WAGs). This study assessed 8-oxoguanine DNA glycosylase 1 (OGG1) and superoxide dismutase 2 (SOD2) gene expression, which are related to oxidized DNA repair and antioxidant capacity, respectively, and the influence of their polymorphisms (OGG1 rs1052133 and SOD2 rs4880) in 100 professionals highly exposed to WAGs and 93 unexposed volunteers (control group). Additionally, X-ray repair cross complementing 1 (XRCC1 rs25487 and rs1799782) and ataxia telangiectasia mutated (ATM rs600931) gene polymorphisms as well as genetic instability (micronucleus-MN and nuclear bud-NBUD) and oxidative stress (malondialdehyde-MDA and ferric reducing antioxidant power-FRAP) biomarkers were assessed in the groups (control and exposed) and in the subgroups of the exposed group according to job occupation (anesthesiologists versus surgeons/technicians). Except for the ATM TT controls (associated with increased FRAP), there were no influences of OGG1, XRCC1, ATM, and SOD2 polymorphisms on MN, NBUD, MDA, and FRAP values in exposed or control subjects. No significant difference in the expression of either gene evaluated (OGG1 and SOD2) was found between the exposed and control groups. Increased OGG1 expression was observed among OGG1 -/Cys individuals only in the control group. Among the exposed group, anesthesiologists had a greater duration of WAG exposure (both h/week and years) than surgeons/technicians, which was associated with increased MDA and decreased antioxidant capacity (FRAP) and SOD2 expression (redox status). Higher expression of OGG1 was found in -/Cys surgeons/technicians than in anesthesiologists with the same genotype. Increased antioxidant capacity was noted in the surgeons/technicians carrying the ATM T allele and in those carrying XRCC1 -/Gln. Increased MN was influenced by OGG1 -/Cys in surgeons/technicians. Anesthesiologists with ATM CC exhibited increased MN, and those carrying the C allele (CC/CT genotype) exhibited increased NBUD. SOD2 polymorphism did not seem to be relevant for WAG exposure. These findings contribute to advancing the knowledge on genetic susceptibility/gene expression/genetic instability/oxidative stress, including differences in job occupation considering the workload, in response to occupational exposure to WAGs.

Sevoflurane has become an important volatile anesthetic in clinic and has been widely studied in recent years. Numerous studies have demonstrated the efficacy of sevoflurane in safeguarding against brain damage across various domains. For example, it has played a neuroprotective role in subarachnoid hemorrhage (SAH), traumatic brain injury, and ischemia/reperfusion injury. The ensuing critique will focus on the significance of sevoflurane in experimental SAH and shed light on the underlying mechanisms. The findings of the current investigation demonstrate that sevoflurane possesses neuroprotective capabilities and clarify that it effectively attenuates secondary damage resulting from SAH through anti-inflammatory and anti-apoptotic pathways. More specifically, sevoflurane is observed to mitigate arterial vasospasm, diminish microvascular thrombosis, and alleviate cerebral edema. In light of these discoveries, we maintain that sevoflurane exhibits significant promise in the management of SAH, and it merits additional investigation to facilitate its prompt clinical implementation. Therefore, a thorough understanding of the neuroprotective properties of sevoflurane is beneficial to exploring novel therapeutic solutions for SAH and providing clinicians with alternative treatment modalities.

We investigated the effects of sevoflurane exposure on the expression of matrix metalloproteinase (MMP), expression and ablation of natural killer group 2, member D (NKG2D) ligands (UL16-binding proteins 1-3 and major histocompatibility complex class I chain-related molecules A/B), and natural killer (NK) cell-mediated cytotoxicity in breast cancer cells.
Three human breast cancer cell lines (MCF-7, MDA-MB-453, and HCC-70) were incubated with 0 (control), 600 (S6), or 1200 μM (S12) sevoflurane for 4 h. The gene expression of NKG2D ligands and their protein expression on cancer cell surfaces were measured using multiplex polymerase chain reaction (PCR) and flow cytometry, respectively. Protein expression of MMP-1 and -2 and the concentration of soluble NKG2D ligands were analyzed using western blotting and enzyme-linked immunosorbent assays, respectively.
Sevoflurane downregulated the mRNA and protein expression of the NKG2D ligand in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells but did not affect the expression of MMP-1 or -2 or the concentration of soluble NKG2D ligands in the MCF-7, MDA-MB-453, and HCC-70 cells. Sevoflurane attenuated NK cell-mediated cancer cell lysis in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells (P = 0.040, P = 0.040, and P = 0.040, respectively).
Our results demonstrate that sevoflurane exposure attenuates NK cell-mediated cytotoxicity in breast cancer cells in a dose-dependent manner. This could be attributed to a sevoflurane-induced decrease in the transcription of NKG2D ligands rather than sevoflurane-induced changes in MMP expression and their proteolytic activity.

Evaluation of the possible toxic effects of occupational exposure to anesthetics is of great importance, and the literature is limited in assessing the possible association between occupational exposure to anesthetics and oxidative stress and genetic damage. To contribute to the gap of knowledge in relation to cause-effect, this cohort study was the first to monitor exposure assessment and to evaluate oxidative stress, DNA damage, and gene expression (OGG1, NRF2, HO-1, and TP53) in young adult physicians occupationally exposed to the most modern halogenated anesthetics (currently the commonly used inhalational anesthetics worldwide) in addition to nitrous oxide gas during the medical residency period. Therefore, the physicians were evaluated before the beginning of the medical residency (before the exposure to anesthetics-baseline), during (1 1/2 year) and at the end (2 1/2 years) of the medical residency. Anesthetic air monitoring was performed in operating rooms without adequate ventilation/scavenging systems, and biological samples were analyzed for lipid peroxidation, protein carbonyl content, primary and oxidative DNA damage, antioxidant enzymes and plasma antioxidant capacity, and expression of some key genes. The results showed induction of lipid peroxidation, DNA damage, glutathione peroxidase activity, and NRF2 and OGG1 expression up to the end of medical residency. Plasma antioxidant capacity progressively increased throughout medical residency; oxidative DNA damage levels started to increase during medical residency and were higher at the end of residency than at baseline. Protein carbonyls increased during but not at the end of medical residency compared to baseline. The antioxidant enzyme superoxide dismutase activity remained lower than baseline during and at the end of medical residency, and HO-1 (related to antioxidant defense) expression was downregulated at the end of medical residency. Additionally, anesthetic concentrations were above international recommendations. In conclusion, high concentrations of anesthetic in the workplace induce oxidative stress, gene expression modulation, and genotoxicity in physicians during their specialization period.

Many factors affect the prognosis of patients undergoing tumor surgery, and anesthesia is one of the potential influencing factors. In general anesthesia, inhalation anesthesia is widely used in the clinic because of its strong curative effect and high controllability. However, the effect of inhalation anesthetics on the tumor is still controversial. More and more research has proved that inhalation anesthetics can intervene in local recurrence and distant metastasis of tumor by acting on tumor biological behavior, immune response, and gene regulation. In this paper, we reviewed the research progress of diverse inhalation anesthetics promoting or inhibiting cancer in the critical events of tumor recurrence and metastasis, and compared the effects of inhalation anesthetics on patients\' prognosis in clinical studies, to provide theoretical reference for anesthesia management of patients undergoing tumor surgery.

OBJECTIVE: Myocardial ischemia reperfusion injury (IRI) occurs occasionally in the process of ischemic heart disease. Sevoflurane preconditioning has an effect on attenuating IRI. Preserving the structural and functional integrity of mitochondria is the key to reduce myocardial IRI. Silent information regulator 3 (SIRT3), a class of nicotinamide adenine dinucleotide (NAD+) dependent deacetylases, is an important signal-regulating molecule in mitochondria. This study aims to explore the role of mitochondrial NAD+-SIRT3 pathway in attenuating myocardial IRI in rats by sevoflurane preconditioning.
METHODS: A total of 60 male Sprague Dawley (SD) rats were randomly divided into 5 groups (n=12): A sham group (Sham group), an ischemia reperfusion group (IR group), a sevoflurane preconditioning group (Sev group, inhaled 2.5% sevoflurane for 30 min), a sevoflurane preconditioning+SIRT3 inhibitor 3-TYP group (Sev+3-TYP group, inhaled 2.5% sevoflurane for 30 min and received 5 mg/kg 3-TYP), and a 3-TYP group (5 mg/kg 3-TYP). Except for the Sham group, the IR model in the other 4 groups was established by ligating the left anterior descending coronary artery. The size of myocardial infarction was determined by double staining. Serum cardiac troponin I (cTnI) level was measured. The contents of NAD+ and ATP, the activities of mitochondrial complexes I, II, and IV, the content of MDA, the activity of SOD, and the changes of mitochondrial permeability were measured. The protein expression levels of SIRT3, SOD2, catalase (CAT), and voltage dependent anion channel 1 (VDAC1) were detected by Western blotting. The ultrastructure of myocardium was observed under transmission electron microscope. MAP and HR were recorded immediately before ischemia (T0), 30 min after ischemia (T1), 30 min after reperfusion (T2), 60 min after reperfusion (T3), and 120 min after reperfusion (T4).
RESULTS: After ischemia reperfusion, the content of NAD+ in cardiac tissues and the expression level of SIRT3 protein were decreased (both P<0.01), and an obvious myocardial injury occurred, including the increase of myocardial infarction size and serum cTnI level (both P<0.01). Correspondingly, the mitochondria also showed obvious damage on energy metabolism, antioxidant function, and structural integrity, which was manifested as: the activities of mitochondrial complexes I, II, and IV, ATP content, protein expression levels of SOD2 and CAT were decreased, while MDA content, VDAC1 protein expression level and mitochondrial permeability were increased (all P<0.01). Compared with the IR group, the content of NAD+ in cardiac tissues and the expression level of SIRT3 protein were increased in the Sev group (both P<0.01); the size of myocardial infarction and the level of serum cTnI were decreased in the Sev group (both P<0.01); the activities of mitochondrial complexes I, II, and IV, ATP content, protein expression levels of SOD2 and CAT were increased, while MDA content, VDAC1 protein expression level, and mitochondrial permeability were decreased in the Sev group (all P<0.01). Compared with the Sev group, the content of NAD+ in cardiac tissues and the expression level of SIRT3 protein were decreased in the Sev+3-TYP group (both P<0.01); the size of myocardial infarction and the level of serum cTnI were increased in the Sev+3-TYP group (both P<0.01); the activities of mitochondrial complexes I, II, and IV, ATP content, protein expression levels of SOD2 and CAT were decreased, while MDA content, VDAC1 protein expression level, and mitochondrial permeability were increased in the Sev+3-TYP group (all P<0.01).
CONCLUSIONS: Sevoflurane preconditioning attenuates myocardial IRI through activating the mitochondrial NAD+-SIRT3 pathway to preserve the mitochondrial function.
目的: 缺血再灌注损伤(ischemia reperfusion injury，IRI)常发生于缺血性心脏疾病。七氟醚预处理有减轻心肌IRI的作用。保存线粒体结构和功能的完整是减轻心肌IRI的关键，线粒体内重要的信号调节分子沉默信息调节因子3(silent information regulator 3，SIRT3)是一类依赖于烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide，NAD+)的去乙酰化酶。本研究旨在探讨NAD+-SIRT3通路在七氟醚预处理减轻大鼠心肌IRI中的作用。方法: 将60只健康成年雄性SD大鼠随机分为5组(n=12)：假手术组(Sham组)、缺血再灌注组(IR组)、七氟醚预处理组(Sev组，给予2.5%七氟醚吸入30 min)、七氟醚预处理+SIRT3抑制剂3-TYP干预组(Sev+3-TYP组，给予尾静脉注射5 mg/kg 3-TYP和2.5%七氟醚吸入30 min)、3-TYP干预组(3-TYP组，给予尾静脉注射5 mg/kg 3-TYP)。Sham组只开胸不结扎，其他4组采用结扎冠状动脉左前降支的方法建立缺血再灌注模型。采用双重染色法测定心肌梗死面积。测定血清大鼠肌钙蛋白I(cardiac troponin I，cTnI)水平。测定心肌组织中NAD+、ATP、MDA含量，线粒体复合体Ⅰ、II、IV及SOD的活性，线粒体通透性的改变。采用蛋白质印迹法检测心肌组织中SIRT3、SOD2、过氧化氢酶(catalase，CAT)和电压依赖性阴离子通道1(voltage dependent anion channel 1，VDAC1)的蛋白质表达水平。在透射电子显微镜下观察心肌超微结构。记录缺血前即刻(T0)、缺血30 min(T1)、再灌注30 min(T2)、再灌注60 min(T3)和再灌注120 min(T4)时的HR和MAP。结果: 缺血再灌注后，心肌组织中NAD+含量减少，SIRT3蛋白质表达水平降低(均P<0.01)，同时出现明显的心肌损伤，包括心肌梗死面积增加，血清cTnI水平升高(均P<0.01)。相应地，线粒体也出现明显的能量代谢、抗氧化功能和结构完整性的受损，表现为：线粒体复合体I、II、IV活性，ATP含量，SOD2和CAT蛋白质表达水平下降，而MDA含量、VDAC1蛋白质表达水平和线粒体通透性增加(均P<0.01)。与IR组比较，Sev组心肌组织中NAD+含量增加，SIRT3蛋白质表达水平升高(均P<0.01)；心肌梗死面积缩小，血清cTnI水平降低(均P<0.01)；线粒体复合体I、II、IV活性，ATP含量，SOD2和CAT蛋白质表达水平升高，而MDA含量、VDAC1蛋白质表达水平和线粒体通透性降低(均P<0.01)。与Sev组比较，Sev+3-TYP组心肌组织中NAD+含量减少，SIRT3蛋白质表达水平降低(均P<0.01)；心肌梗死面积增加，血清cTnI水平升高(均P<0.01)；线粒体复合体I、II、IV活性，ATP含量，SOD2和CAT蛋白质表达水平下降，而MDA含量、VDAC1蛋白质表达水平和线粒体通透性增加(均P<0.01)。结论: 七氟醚预处理通过激活线粒体NAD+-SIRT3通路，保存线粒体功能，从而减轻心肌IRI。.

暂无摘要。

The aim of this work is to analyze the health hazards of enflurane exposure and to analyze the occupational exposure limits (OEL). The method of obtaining evidence based on a review of online databases of scientific journals was used. Enflurane is an inhalation anesthetic. Malignant hyperthermia, seizures, arrhythmias, respiratory depression and hypotension have been observed in patients. Occupational exposure to enflurane may occur in healthcare professionals. The target organ for enflurane is the central nervous system with a critical consequence of deterioration in psychomotor performance. In studies on volunteers recruited from the medical staff of operating rooms exposed to enflurane, a significant deterioration in the results of the Simple Reaction Time Test was shown. World experts\' groups assume that the LOAEC (lowest observed adverse effect concentration) value for the deterioration of psychomotor test results is 5-10% of the MAC value (minimal anesthetic concentration), i.e., 6342-12 684 mg/m3. Assessment of the nephrotoxic potential of enflurane has shown that it is unlikely to occur because biotransformation of enflurane in humans results in a low peak serum fluoride concentration of 15 μmol/l. Early reports about liver damage in patients were not be supported. Occupational exposure epidemiological studies have raised concerns about the effects of anesthetic gas mixtures on the abortion rate or on fetal development and birth defects in children, but none of these studies specifically determined the type and concentration of anesthetic gases used. The carcinogenicity and mutagenicity studies were negative. Occupational exposure to enflurane is not monitored in Poland, as no standard value has been established for it in the air of the working environment. It is necessary to quickly introduce this anesthetic along with the applicable limit value to the OEL list. Med Pr. 2022;73(1):51-69.
Ponieważ przeprowadzono niewiele badań dotyczących wpływu zawodowego narażenia na enfluran na stan zdrowia, celem pracy była analiza zagrożeń zdrowotnych wynikających z narażenia na tę substancję oraz analiza jej dopuszczalnych stężeń w środowisku pracy. Zastosowano metodę zbierania dowodów na podstawie przeglądu internetowych baz danych czasopism naukowych. Enfluran należy do wziewnych środków ogólnie znieczulających. Obserwowano, że u pacjentów powodował on złośliwą hipertermię, napady padaczkowe, zaburzenia rytmu serca, depresję ośrodka oddechowego i niedociśnienie tętnicze. Nieliczne dane wskazują na możliwość uszkodzenia wątroby czy niewydolności nerek na skutek narkozy. Narażenie zawodowe na enfluran może występować u pracowników opieki medycznej. Narządem docelowym dla enfluranu jest ośrodkowy układ nerwowy, a skutkiem krytycznym pogorszenie sprawności psychomotorycznej. W badaniach z udziałem ochotników rekrutowanych spośród personelu medycznego sal operacyjnych narażonego na enfluran wykazano istotne pogorszenie wyników w Teście czasu reakcji prostej. Grupy eksperckie na świecie za najniższy poziom działania szkodliwego (lowest observed adverse effect concentration – LOAEC) dla pogorszenia wyników testów psychomotorycznych przyjmują stężenie na poziomie 5–10% minimalnego stężenia w powietrzu pęcherzyków płucnych w trakcie znieczulania (minimal anesthetic concentration – MAC), tj. 6342–12 684 mg/m3. Ocena potencjalnego działania nefrotoksycznego enfluranu wykazała, że jest ono mało prawdopodobne, gdyż biotransformacja enfluranu u ludzi skutkuje niskim szczytowym stężeniem fluorku w surowicy, średnio 15 μmol/l. Wczesne doniesienia przypisujące uszkodzenie wątroby u pacjentów nie zostały potwierdzone. Badania epidemiologiczne dotyczące narażenia zawodowego wzbudziły obawy co do wpływu mieszanin gazów znieczulających na częstość poronień, rozwój płodu i wady wrodzone u dzieci, jednak w żadnym z tych badań nie określono szczegółowo rodzaju i stężenia stosowanych gazów znieczulających. W badaniu rakotwórczości i mutagenności uzyskano wyniki negatywne. W Polsce nie monitoruje się narażenia zawodowego na enfluran, ponieważ nie ustalono dla niego wartości normatywnej w powietrzu środowiska pracy. Konieczne jest szybkie wprowadzenie tego anestetyku wraz z obowiązującą wartością dopuszczalną do wykazu NDS (najwyższe dopuszczalne stężenie). Med. Pr. 2022;73(1):51–69.