Artesunate enhances radiosensitivity of esophageal cancer cells by inhibiting the repair of DNA damage.

Radiotherapy plays an important therapeutic role in esophageal cancer (EC). However, acquired radioresistance impairs the efficacy of radiotherapy, often leading to treatment failure. Therefore, it is important to develop novel radiosensitizers to enhance the clinical treatment of EC. The purpose of this study was to investigate the role of artesunate (ART) on radiosensitivity of human EC cell line TE-1. We found that ART inhibited the proliferation of EC cells and enhanced the radiosensitivity of TE-1 cells (SER = 1.24). In vivo tumor growth of xenografts was inhibited markedly by irradiation (IR) combined with ART, with a tumor inhibition rate of 53.76% in IR + ART group vs. 41.13% in IR-alone group. Pretreatment with ART significantly prompted cell apoptosis and reversed the IR-induced G2/M arrest. ART treatment could aggravate DNA damage of EC cells and prolong the formation of γ-H2AX foci induced by IR. ART up-regulated P21 and down-regulated the expression of cyclin D1, RAD51, RAD54, Ku70 and Ku86 protein of irradiated TE-1 cells. These findings support that ART induce radiosensitivity of TE-1 cells in vitro and in vivo, and may prove to be a promising radiosensitizer for EC treatment.

Xeroderma pigmentosum complementation group D (XPD) gene polymorphisms contribute to bladder cancer risk: a meta-analysis.

Numerous epidemiological studies have been conducted to investigate the association between Xeroderma pigmentosum complementation group D (XPD) Asp312Asn (rs1799793 G > A) and Lys751Gln (rs13181 A > C) polymorphisms and bladder cancer risk; however, the conclusions remain controversial. With this in mind, we performed this meta-analysis with 11 studies including 3,797 cases and 5,094 controls for Asp312Asn and 21 studies including 6,360 cases and 7,894 controls for Lys751Gln polymorphism. We searched available literatures from PubMed, Embase, and CBM databases. Crude odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the strength of the associations. Moreover, to validate biological plausibility of our findings, the effects of these two polymorphisms on XPD gene expression within three ethnicities was determine by gene expression analysis based on imputed genotypes from HapMap. Overall, the variant allele of Asp312Asn polymorphism was associated with an increased risk of bladder cancer (Asn/Asn vs. Asp/Asp: OR = 1.51, 95% CI = 1.19-1.91; Asp/Asn vs. Asp/Asp: OR = 1.23, 95% CI = 1.12-1.35; recessive model: OR = 1.33, 95% CI = 1.10-1.61; dominant model: OR = 1.32, 95% CI = 1.14-1.52; and allele comparing: OR = 1.26, 95% CI = 1.11-1.42). We found the Lys751Gln was associated with increased bladder cancer risk only under the recessive model (OR = 1.14, 95% CI = 1.01-1.29). Stratification analyses demonstrated an increased risk for Asians and hospital-based studies under all genetic models while only under the dominant model for Caucasians as to the Asp312Asn polymorphism and for Caucasians under the recessive model as to the Lys751Gln polymorphism. We also found the Asp312Asn polymorphism can significantly influence mRNA expression levels among Asians and Caucasians, and the Lys751Gln polymorphism has a similar effect for Caucasians. Despite some limitations, this meta-analysis suggests that polymorphisms in XPD gene may contribute to bladder cancer susceptibility. These findings need further validation by large well-designed prospective studies.

Low dose of dexamethasone combined with netupitant and palonosetron in preventing nausea and vomiting in breast cancer patients induced by anthracycline drugs.

BACKGROUND: To study the effects of various courses of dexamethasone (DEX) combined with 5-HT3 receptor antagonists (RA) and NK-1 RA in suppressing high-grade nausea and vomiting (CINV) caused by anthracycline and cyclophosphamide chemotherapy regimens (AC or EC) in breast cancer (BC) patients. PATIENTS AND METHODS: A prospective study was performed with 252 BC patients who received AC between January, 2019 and June, 2022 in our hospital. Patients were randomly separated into control Group (N = 130) who received DEX 12 mg on day 1 and 8 mg per dose on day 2-4 and observation group (N = 122) treated with DEX 5 mg per dose on days 1-4. The response was monitored. Primary study endpoint was complete resolution (CR) of patients nausea or vomiting; secondary study endpoints included acute CR and delayed CR; and complete control (CC), acute CC, delayed CC, and safety. RESULTS: All patients underwent six rounds of chemotherapy, and no difference was found in the clinical data. CR of acute/delayed phase was (94.3%/88.5%, P > 0.05), (89.3%/90.8%, P > 0.05); total CR was (80.3%/81.5%, P > 0.05); CC was (56.6%/59.2%, P > 0.05), (64.8%/67.7%, P > 0.05); total CR was (48.4%/53.1%, P > 0.05). CONCLUSIONS: The preventive antiemetic effects of NEPA, a fixed-dose combination of netupitant and palonosetron combined with DEX 5 mg per dose on days 1-4, can be similar to DEX 12 mg on day 1 and 8 mg per dose on days 2-4, low-dose hormone with better safety, which is beneficial.

CircRAD54L2 promotes triple-negative breast cancer progression by regulating the miR-888 family/PDK1 axis.

BACKGROUND: The long-term prognosis of breast cancer with metastasis remains extremely poor. Genetic alterations in tumor cells result in cellular heterogeneity, promoting cancer cells invasion and colonization in some organs during the metastatic process. CircRNAs are very promising as critical biological markers and precise diagnoses in identifying disease mechanisms and developing new methods for effective treatment. However, the role of aberrant expression of circRNAs in breast cancer progression remains largely unknown. METHODS: RNase R treatment and quantitative RT-PCR (qRT-PCR) were performed for circRNA detection. Transwell chamber assays were used to examine the chemotactic migration and invasion of breast cancer cells. RESULTS: This study identified and characterized the circRAD54L2 originating from exon 1, 2, 3, and 4 of the RAD54L2 gene. Importantly, we found that circRAD54L2, rather than RAD54L2 linear mRNA, was significantly upregulated in breast cancer cell lines. Furthermore, we found that inhibiting circRAD54L2 expression markedly reduced the invasion, metastasis, and proliferation of breast cancer cells via sponging of the miR-888 family, which downregulated the expression of pyruvate dehydrogenase kinase 1 (PDK1). CONCLUSION: Our results showed that circRAD54L2 could regulate PDK1 expression by sponging the miR-888 family competing for the ceRNA mechanism, indicating that circRAD54L2 may act as an essential upstream regulator and providing further mechanistic evidence to support the notion that circRAD54L2/miR-888s/PDK1 is a promising therapeutic target in the treatment of breast cancer.

The Pan-Cancer Crosstalk Between the EFNA Family and Tumor Microenvironment for Prognosis and Immunotherapy of Gastric Cancer.

Background: EFNA1-5 have important physiological functions in regulating tumorigenesis and metastasis. However, correlating EFNA genes in the tumor immune microenvironment (TIME), and the prognosis of patients with gastric cancer remains to be determined. Methods: Using public databases, the expression of EFNA1-5 in pan-cancer and gastric cancer was comprehensively analyzed using UCSC Xena, the Oncomine dataset and UALCAN. We further completed survival analysis by Kaplan-Meier plotter to evaluate the prognosis of the high and low expression groups of the EFNAs gene in patients with gastric cancer. The TIMER tool was used to reveal the correlation between immune cell infiltration and genes of interest. Spearman correlation was used to find an association between the EFNA genes and tumor stem cells, TIME, microsatellite instability (MSI) or tumor mutational burden (TMB). We also used cBioportal, GeneMANIA and STRINGS to explore the types of changes in these genes and the protein interactions. Finally, we described the TIME based on QUANTISEQ algorithm, predicted the relationship between the EFNA genes and half-maximal inhibitory concentration (IC50), and analyzed the relationship between the EFNA family genes and immune checkpoints. Results: The expression of EFNA1, EFNA3, EFNA4, and EFNA5 was elevated in pan-cancer. Compared with normal adjacent tissues, EFNA1, EFNA3, and EFNA4 were up-regulated in gastric cancer. In terms of the influence on the survival of patients, the expression of EFNA3 and EFNA4 were related to overall survival (OS) and disease-free survival (DFS) for patients with gastric cancer. High expression of EFNA5 often predicted poor OS and DFS. In gastric cancer, the expression of EFNA3 and EFNA4 showed a significant negative correlation with B cells. The higher the expression of EFNA5, the higher the abundance of B cells, CD4+T cells and macrophages. CD8+T cells, dendritic cells infiltration and EFNA1-4 expression were negatively correlated. The infiltration of CD4+T cells, macrophages and neutrophils was negatively correlated with the expression of EFNA1, EFNA3, and EFNA4. TMB and MSI were positively correlated with EFNA3/EFNA4 expression. In the tumor microenvironment and drug sensitivity, EFNA3/4/5 also showed a significant correlation. In addition, we explored the relationship between the EFNA family genes and the immune microenvironment (B cells, M2 macrophages, monocytes, CD8+ T cells, regulatory T cells, myeloid dendritic cells, natural killer cells, non-regulatory CD4+ T cells), immune checkpoint (PDCD1, PDCD1LG2, CD274, CTLA4), and IC50 of common chemotherapeutic drugs for gastric cancer (5-fluorouracil, cisplatin, docetaxel and gemcitabine). Conclusions: Our study provides new ideas for tumor treatment and prognosis from the perspective of TIME, and nominates EFNA1-5 to become potential therapeutic targets for gastric cancer.

Metformin reverses tamoxifen resistance through the lncRNA GAS5-medicated mTOR pathway in breast cancer.

Background: Metformin (Met) has antitumor effects on various cancers, but it is still unclear whether it exerts a reversible effect on endocrine resistance in breast cancer (BC) patients. In the present survey, metformin's effects on tamoxifen-resistant MCF cells (The cell line was established at the Michigan Cancer Foundation, hence the name MCF cell) were evaluated and the molecular mechanism was explored. Methods: We constructed a tamoxifen-resistant BC cell line MCF-7R, then applied Cell Counting Kit-8 (CCK-8), flow cytometry, and EdU assessments to determine the growth and apoptosis of MCF-7R cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to evaluate the expression level of lncRNA GAS5 and the mTOR-associated proteins. Overexpression and downregulation of lncRNA GAS5 were carried out to explore the molecular mechanism of Met. Results: The combined effect of Met and OHT (4-hydroxytamoxifen, main active metabolite of tamoxifen) was to remarkably reduce the growth and increase the apoptosis of MCF-7R cells compared with OHT alone. The levels of the mTOR, p-mTOR and p-P70S6K proteins in MCF-7R cells decreased after Met treatment, but the p-AMPK2 and PTEN proteins significantly increased. The overexpression of lncRNA GAS5 in MCF-7R cells inhibited cell growth with decreased mTOR, p-mTOR, PCNA, and Bcl-2 proteins. Metformin had no significant effect on MCF-7R cells with lncRNA GAS5 knockdown but contrarily activated p-mTOR. Conclusions: Metformin can inhibit overactivation of the mTOR signaling pathway through upregulating lncRNA GAS5 expression, thereby inhibiting the growth and inducing the apoptosis of BC cells, providing a new clinical treatment for BC.

CircKIF5B Promotes Hepatocellular Carcinoma Progression by Regulating the miR-192 Family/XIAP Axis.

Background: The long-term prognosis of HCC (hepatocellular carcinoma) with metastasis remains extremely poor. CircRNAs are promising as critical biological markers in identifying disease mechanisms and developing new effective treatments. However, the role of the aberrant expression of circRNAs in HCC progression remains largely unknown. Methods: CircKIF5B location was investigated by RNA fluorescence in situ hybridization (RNA-FISH). For circRNA determination, RNase R treatment and Real-Time Quantitative RT-PCR (qRT-PCR) were performed. Transwell chamber assays examined the chemotactic migration and invasion of liver cancer cells. Results: This study identified the circRNA circKIF5B originating from exons 1, 2, and 3 of the KIF5B gene. Importantly, we found that circKIF5B circRNA, rather than KIF5B linear mRNA, was notably upregulated in liver cancer cell lines and tissues. Moreover, we found that silencing circKIF5B markedly reduced the proliferation, invasion, and metastasis of liver cancer cells by sponging the miR-192 family, thus decreasing the expression of X-linked inhibitor of apoptosis (XIAP). Conclusion: Our data demonstrate that circKIF5B can regulate XIAP expression by sponging miR-192 and miR-215 competing for the ceRNA mechanism, indicating that circKIF5B may act as an essential upstream regulator and providing mechanistic evidence to support the view that circKIF5B/miR-192s/XIAP is a promising therapeutic target for treating liver cancer.

FH535 inhibits proliferation and migration of colorectal cancer cells by regulating CyclinA2 and Claudin1 gene expression.

Wnt signaling pathway plays a major role in the progression of colorectal cancer (CRC). Small molecules which can cut off this signal transduction can be promising anti-cancer drugs for CRC therapy. Therefore, we aimed to investigate the mechanisms of FH535, an inhibitor of the Wnt signaling pathway, on inhibiting proliferation and migration of colorectal cancer cells DLD-1 and SW620. We found that FH535 could significantly suppress the growth of DLD-1 and SW620 cells in a concentration-dependent and time-dependent manner. The results of cell cycle tests showed that FH535 could significantly induce G2/M arrest in colorectal cancer cells. Transwell and Wound-healing assays revealed that FH535 notably inhibited cell migration. Moreover, we found that FH535 down-regulated ß-catenin and CyclinA2 expressions while up-regulating Claudin-1 expression at both mRNA and protein levels, which may contribute to the FH535-induced inhibitory effect on proliferation and migration in human colorectal cancer cells. Our study revealed that FH535 inhibited proliferation and migration of colorectal cancer cells by regulating CyclinA2 and Claudin1 gene expression, which enriches regulatory network of FH535 and may contribute to being promising anti-cancer drugs for CRC therapy.

Synaptotagmin-7, a binding protein of P53, inhibits the senescence and promotes the tumorigenicity of lung cancer cells.

Lung cancer has been one of the most common malignancies in the world. Cell senescence has been recognized as the avenue to inhibit tumor progression. However, the mechanisms remain poorly understood. In the present study, we have shown that synaptotagmin-7 (SYT7) expression was up-regulated in lung cancer. SYT7 also promoted the growth and colony formation of lung cancer cells and inhibited their senescence. In a molecular mechanism study, SYT7 was shown to interact with P53 and to potentiate the interaction between P53 and MDM2. Taken together, the present study demonstrates the oncogenic roles of SYT7 in lung cancer, and suggests that SYT7 may be a good therapeutic target for lung cancer treatment.

[Concurrent standard dose of cisplatin, paclitaxel, and radiotherapy followed by surgery in treatment of thoracic esophageal carcinoma].

OBJECTIVE: To investigate the curative effect of incorporation of the regimen of standard dose of paclitaxel combined with cisplatin into concurrent radiotherapy as pre-operative treatment for patients with esophageal carcinoma. METHODS: Twenty-six patients with primary diagnosis of esophageal carcinoma, 17 in stage II and 9 in stage III, underwent conventional fractionated radiotherapy with a total dosage of 40 Gy (2 Gy per day, 5 doses per week). Paclitaxel were given intravenously at a dose of 135 mg/m(2) for 3 h on day1 and day 22. Cisplatin was given intravenously at a dose of 20 mg/m(2) on D1-D3 and D22-24. 4 - 6 weeks after the completion of chemo-radiotherapy, left thoracic incision and transhiatal esophagectomy with anastomosis in the neck was performed. The patients were followed up for 42.28 months. Kaplan-Meier method was used to analyze the overall survival (OS) and disease-free survival (DFS), and Log-rank test was performed to assess the survival rates statistical significance among groups. RESULTS: The radical resection rate was 96.15%. The pathologic response to chemoradiotherapy were grade I in 9 patients, grade II in 6 patients, and grade III in 11 patients. The pathological complete remission (PCR) rate was 42.31% (11/26). Toxicity grade 3 - 4 included leucopenia (7.69%, 2/26), thrombocytopenia (7.69%, 2/26), and radiation esophagitis (11.54%, 3/26). Surgery-related complications included anastomotic leakage (3.85%, 1/26), recurrent laryngeal nerve injury (7.69%, 2/26), and chylothorax (3.85%, 1/26). The 3- and 5-year overall survival rates were 62.96% and 54.56% respectively. The 3- and 5-year disease-free survival rates were 59.94% and 55.65% respectively. The 3-year overall survival rates of the patients with different pathologic responses were 25.40% (for those of grade I), 60% (for grade II), and 90.91% (for grade III) respectively (P < 0.05). The 5-year overall survival rates were 0 (for grade I), 60% (for grade II), and 81.82% (for grade III) respectively (P < 0.05). CONCLUSION: Preoperative chemoradiotherapy containing full dose of paclitaxel and cisplatin increases the 5-year overall survival for the patients with postoperative pathologic response grade II and above, and does not increase the treatment-related complications.

Reversible severe fatty liver induced by capecitabine: A case report.

RATIONALE: Capecitabine (CAP) is a chemotherapeutic agent used to treat breast and gastrointestinal cancers. The most common adverse reactions of CAP primarily included gastrointestinal and dermatological effects. Whereas, the CAP-induced fatty liver had never been reported. PATIENT CONCERNS: In this study, a-69-year old female presented a history of hypertension with regulated blood pressure, whereas diabetes mellitus, hyperlipidemia, and hepatitis were excluded. No alcohol,tobacco, or other drugs use was declared. DIAGNOSES: She was diagnosed as infiltrating ductal carcinoma of left breast with the hepatic and pulmonary metastasis. The dihydropyrimidine dehydrogenase (DPD) deficiency is not involved. INTERVENTIONS: She received treatment with CAP that was administered orally at a dosage of 1500mg twice daily intermittently (2weeks on/1 week off). The treatment was well-tolerated any typical adverse reactions such as diarrhea, nausea, and hand-foot syndrome (HFS) were noted. The parameters of the functional liver, the total cholesterol, and triglyceride were in normal ranges before and after therapy. After 3 cycles of the treatment, computed tomography (CT) scan revealed signs of fatty liver. After a 10-cycle course, CAP was substituted with tamoxifen because of the further aggravation of fatty liver. OUTCOMES: Several months after withdrawal, the follow-up CT scans demonstrated significant improvement of fatty liver. LESSONS: We presented a case of breast cancer with severe fatty liver as a consequence of the administration of CAP that was not involved in DPD deficiency or CAP-associated hypertriglyceridemia; these potential adverse effects of therapy with CAP should be intensely investigated.

Synergistic interaction between MEK inhibitor and gefitinib in EGFR-TKI-resistant human lung cancer cells.

With the increasing use of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKIs) in patients with advanced non-small cell lung cancer (NSCLC), acquired resistance has become a major clinical problem. A combination of different signaling pathway inhibitors is a promising strategy to overcome this. In the present study, the mitogen-activated protein kinase kinase 1/2 inhibitor, AZD6244, was used in combination with gefitinib to investigate the efficacy of this treatment in NSCLC cell lines, particularly in gefitinib-resistant cells. The EGFR-TKI-sensitive PC-9 (mutant EGFR/wild-type K-Ras) and EGFR-TKI-resistant A549 (wild-type EGFR/mutant K-Ras) human NSCLC cell lines were treated with AZD6244 alone, gefitinib alone or the combination of the two drugs, and the effects were evaluated using cell proliferation assays, with alterations in signaling pathways analyzed by western blotting. It was found that the growth inhibitory effect of combination treatment with gefitinib and AZD6244 was greater than that of gefitinib alone in the EGFR-TKI-resistant A549 cells. Treatment of A549 cells with gefitinib alone reduced the expression level of the activated form of Akt, and the combination of the two drugs showed stronger inhibition of phosphorylated-Akt and phosphorylated-extracellular signal-regulated kinases. The data showed that the combination of AZD6244 and gefitinib exhibited dose-dependent synergism in gefitinib-resistant NSCLC cells. Thus, a preclinical rationale exists for the use of AZD6244 to enhance the efficacy of gefitinib in patients with EGFR-TKI-resistant NSCLC.

Association between CYP1A1 Ile462Val Polymorphism and Oral Squamous Cell Carcinoma Susceptibility: Evidence from 13 Investigations.

CYP1A1 Ile462Val polymorphism might play a key role in pathogenesis of oral squamous cell carcinoma (OSCC). Many case-control studies have investigated the association between CYP1A1 Ile462Val polymorphism and OSCC susceptibility. However, the conclusions are inconsistent. To aim a convincible conclusion, we carried out a meta-analysis to systematically evaluate the association of CYP1A1 Ile462Val polymorphism with OSCC susceptibility. We searched Pubmed, Web of Science, Ovid and Embase databases for available publications. The odds ratio (OR) with the corresponding 95% confidence interval (95% CI) was carried out to estimate the association. A total of 13 papers including 1468 cases and 2183 controls were included, a significant increased OSCC risk was observed in recessive model (OR=1.64, 95% CI=1.08-2.49), but not other genetic models. Our results suggest that the homozygous variant of CYP1A1 Ile462Val might be a risk factor of OSCC.

Application of Narcotrend® monitor for evaluation of depth of anesthesia in infants undergoing cardiac surgery: a prospective control study.

BACKGROUND AND OBJECTIVES: To investigate the clinic effectiveness, safety and feasibility of Narcotrend® monitor for evaluation of depth of anesthesia in congenital heart disease (CHD) infants undergoing cardiac surgery. METHODS: A total of 80 infants receiving general anesthesia in selective surgery were randomly selected. Infants were assigned into two groups (n=40 per group). In the Narcotrend group, the depth of anesthesia was monitored with the Narcotrend monitor. In the standard group, the depth of anesthesia was controlled according to the experience. The mean arterial pressure (MAP) and heart rate (HR) were determined, as well as the dose of fentanyl, muscle relaxant, recovery time and extubation time were recorded. RESULTS: In both groups, vital signs were stable during the surgery. When compared with the standard group, the MAP and HR were more stable, the total dose of fentanyl and muscle relaxant were significantly reduced and the recovery time and extubation time were markedly shortened in the Narcotrend group. CONCLUSION: The application of Narcotrend monitor was beneficial to the control of the depth of anesthesia in CHD infants receiving total intravenous anesthesia, in which small amount of narcotics can achieve optimal anesthesia. Moreover, the recovery time and extubation time are reduced and the harmful consequence such as intraoperative awareness can be avoided.

Aplicação do monitor Narcotrend® para avaliar a profundidade da anestesia em crianças submetidas à cirurgia cardíaca: estudo prospectivo e controlado / Application of Narcotrend® monitor for evaluation of depth of anesthesia in infants undergoing cardiac surgery: a prospective control study / Aplicación del monitor Narcotrend® para evaluar la profundidad de la anestesia en niños sometidos a la cirugía cardíaca: estudio prospectivo y controlado

JUSTIFICATIVA E OBJETIVOS: Investigar a eficácia clínica, segurança e viabilidade do monitor Narcotrend® para avaliar a profundidade da anestesia em crianças com doença cardíaca congênita (DCC) submetidas à cirurgia cardíaca. MÉTODOS: Foram randomicamente selecionadas 80 crianças submetidas à anestesia geral em cirurgia seletiva. As crianças foram divididas em dois grupos de forma aleatória (n = 40 por grupo). No grupo Narcotrend, a profundidade da anestesia foi monitorada com o Narcotrend. No grupo padrão, a profundidade da anestesia foi controlada de acordo com a experiência clínica. A pressão arterial média (PAM) e a frequência cardíaca (FC) foram determinadas e a dose de fentanil e relaxante muscular e os tempos de recuperação e de extubação foram registrados. RESULTADOS: Em ambos os grupos, os sinais vitais apresentaram-se estáveis durante a cirurgia. No grupo Narcotrend, a PAM e a FC foram mais estáveis, a dose total de fentanil e relaxante muscular significativamente menor e os tempos de recuperação e extubação acentuadamente mais reduzidos em comparação com o grupo padrão. CONCLUSÃO: A aplicação do monitor Narcotrend para medir a profundidade da anestesia foi útil para controlar a profundidade da anestesia em crianças com DCC que receberam anestesia intravenosa total, na qual uma pequena quantidade de narcóticos pode obter a anestesia ideal. Além disso, os tempos de recuperação e extubação foram menores e os efeitos secundários, como sensibilização intraoperatória, puderam ser evitados.

BACKGROUND AND OBJECTIVES: To investigate the clinic effectiveness, safety and feasibility of Narcotrend® monitor for evaluation of depth of anesthesia in congenital heart disease (CHD) infants undergoing cardiac surgery. METHODS: A total of 80 infants receiving general anesthesia in selective surgery were randomly selected. Infants were assigned into two groups (n = 40 per group). In the Narcotrend group, the depth of anesthesia was monitored with the Narcotrend monitor. In the standard group, the depth of anesthesia was controlled according to the experience. The mean arterial pressure (MAP) and heart rate (HR) were determined, as well as the dose of fentanyl, muscle relaxant, recovery time and extubation time were recorded. RESULTS: In both groups, vital signs were stable during the surgery. When compared with the standard group, the MAP and HR were more stable, the total dose of fentanyl and muscle relaxant were significantly reduced and the recovery time and extubation time were markedly shortened in the Narcotrend group. CONCLUSION: The application of Narcotrend monitor was beneficial to the control of the depth of anesthesia in CHD infants receiving total intravenous anesthesia, in which small amount of narcotics can achieve optimal anesthesia. Moreover, the recovery time and extubation time are reduced and the harmful consequence such as intraoperative awareness can be avoided.

JUSTIFICATIVA Y OBJETIVOS: Investigar la eficacia clínica, la seguridad y la viabilidad del monitor Narcotrend® para evaluar la profundidad de la anestesia en niños con enfermedad cardíaca congénita (ECC) sometidos a la cirugía cardíaca. MÉTODOS: Un total de 80 niños sometidos a la anestesia general en cirugía selectiva fueron seleccionados aleatoriamente. Los niños fueron divididos en dos grupos de forma aleatoria (N = 40 por grupo). En el grupo Narcotrend, la profundidad de la anestesia se monitorizó con el monitor Narcotrend. En el grupo estándar, la profundidad de la anestesia fue controlada de acuerdo con la experiencia. Se midieron la presión arterial promedio (PAP) y la frecuencia cardíaca (FC). Fueron registrados también la dosis de fentanilo y de relajante muscular junto con los tiempos de recuperación y de desentubación. RESULTADOS: En los dos grupos, los signos vitales se mantuvieron estables durante la cirugía. En el grupo Narcotrend, la PAP y la FC fueron más estables, la dosis total de fentanilo y de relajante muscular significativamente menor y los tiempos de recuperación y desentubación ostensiblemente más reducidos en comparación con el grupo estándar. CONCLUSIONES: La aplicación del monitor Narcotrend para medir la profundidad de la anestesia fue útil en el control de la profundidad de la anestesia en niños con ECC que reciben anestesia intravenosa total, en donde una pequeña cantidad de narcóticos puede alcanzar la anestesia ideal. Además, los tiempos de recuperación y desentubación fueron menores, y el efecto secundario, como la sensibilización intraoperatoria, pudo ser evitado.