MicroRNA expression in the hippocampal CA1 region under deep hypothermic circulatory arrest.

Using deep hypothermic circulatory arrest, thoracic aorta diseases and complex heart diseases can be subjected to corrective procedures. However, mechanisms underlying brain protection during deep hypothermic circulatory arrest are unclear. After piglet models underwent 60 minutes of deep hypothermic circulatory arrest at 14°C, expression of microRNAs (miRNAs) was analyzed in the hippocampus by microarray. Subsequently, TargetScan 6.2, RNA22 v2.0, miRWalk 2.0, and miRanda were used to predict potential targets, and gene ontology enrichment analysis was carried out to identify functional pathways involved. Quantitative reverse transcription-polymerase chain reaction was conducted to verify miRNA changes. Deep hypothermic circulatory arrest altered the expression of 35 miRNAs. Twenty-two miRNAs were significantly downregulated and thirteen miRNAs were significantly upregulated in the hippocampus after deep hypothermic circulatory arrest. Six out of eight targets among the differentially expressed miRNAs were enriched for neuronal projection (cyclin dependent kinase, CDK16 and SLC1A2), central nervous system development (FOXO3, TYRO3, and SLC1A2), ion transmembrane transporter activity (ATP2B2 and SLC1A2), and interleukin-6 receptor binding (IL6R) - these are the key functional pathways involved in cerebral protection during deep hypothermic circulatory arrest. Quantitative reverse transcription-polymerase chain reaction confirmed the results of microarray analysis. Our experimental results illustrate a new role for transcriptional regulation in deep hypothermic circulatory arrest, and provide significant insight for the development of miRNAs to treat brain injuries. All procedures were approved by the Animal Care Committee of Xuanwu Hospital, Capital Medical University, China on March 1, 2017 (approval No. XW-INI-AD2017-0112).

[Reasonable anesthetic management for correction of Ebstein's anomaly].

OBJECTIVE: To summarize the experience in anesthetic management for correction of Ebstein's anomaly. METHODS: A total of 79 patients with Ebstein's anomaly who underwent surgical repair in our hospital during the time from March 2004 to September 2010 were retrospectively summarized for their anesthetic management. Anesthesia was done for the patients undergoing correction of Ebstein's anomaly. The adults patients were premedicated with intramuscular morphine 0.2 mg/kg and diazepam 0.05 mg/kg. The children patients were premedicated with intramuscular ketamine 5 - 8 mg/kg and atropine 0.05 - 0.20 mg. General anesthesia was induced with midazolam 0.1 - 0.2 mg/kg, etomidate 0.2 - 0.3 mg/kg, sulfentanil 1.0 - 1.5 µg/kg, pipecuronium or vecuronium 0.1 - 0.2 mg/kg, and maintained with isoflurane inhalation and intermittent iv. midazolam and sulfentanil. RESULTS: Anesthetic course was smooth. The symptom in all cases was improved significantly after operation. No patients died during perioperative period. CONCLUSION: The key points for the anesthetic management of Ebstein's anomaly include precise preoperative evaluation, steady hemodynamic, proper maintenance of suitable pulmonary vascular resistance and cardiac function.