Background Cardiac surgery is associated with a high risk of cardiovascular and other complications that translate into increased mortality and healthcare costs. This retrospective study was designed to determine whether the perioperative use of dexmedetomidine could reduce the incidence of complications and mortality following cardiac surgery. Methods and Results 1,134 patients who underwent CABG and CABG plus valvular and/or other procedures were included. 568 received intravenous dexmedetomidine infusion and 566 did not. Data were adjusted with propensity scores and multivariate logistic regression was used. The primary outcomes measured included mortality and postoperative major adverse cardiocerebral events (MACE: stroke, coma, perioperative myocardial infarction, heart block or cardiac arrest). Secondary outcomes included renal failure, sepsis, delirium, postoperative ventilation hours, length of hospital stay and 30-day readmission. Dexmedetomidine use significantly reduced postoperative in-hospital [1.23% vs. 4.59%; adjusted odds ratio (OR), 0.34; 95% confidence intervals (CI), 0.192 to 0.614; P < 0.0001], 30-day (1.76% vs. 5.12%; adjusted OR, 0.39; 95% CI, 0.226 to 0.655; P <0.0001) and 1-year (3.17% vs. 7.95%; adjusted OR, 0.47; 95% CI, 0.312 to 0.701; P = 0.0002) mortalities. Perioperative dexmedetomidine therapy also reduced the risk of overall complications (47.18 vs. 54.06%; adjusted OR, 0.80, 95% CI, 0.68 to 0.96; p= 0.0136) and delirium (5.46% vs. 7.42%; adjusted OR, 0.53; 95% CI, 0.37 to 0.75; p=0.0030). Conclusions Perioperative dexmedetomidine use was associated with a decrease in postoperative mortality up to one year and decreased incidence of postoperative complications and delirium in patients undergoing cardiac surgery.

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BackgroundAt present, sevoflurane inhalation anesthesia used on infants is well-known. But long-time exposure to inhalation anesthetic could cause neurologic disorder, especially nerve degeneration in infant and developing brain. The central nervous system degeneration of infants could affect the memory and cognitive function. γ-Aminobutyric acid (GABA) is a known inhibitory neurotransmitter in central nervous system. Inhalation anesthetic sevoflurane may activate GABAA receptor to inhibit central nervous system, leading to apoptosis of neural degeneration, cognitive dysfunction in the critical period of brain development.MethodsNeural stem cells were derived from Wistar embryos, cultured in vitro. Third generation of neural stem cells were randomly divided into four groups according to cultured suspension: Sevoflurane group (Group S), GABAA receptor antagonists, Bicuculline group (Group B), Sevoflurane + GABAA receptor antagonists, Bicuculline group (Group S + B), dimethyl sulphoxide (DMSO) group (Group D). Group B and Group D did not receive sevoflurane preconditioning. Group S and Group S + B were pretreated with 1 minimum alveolar concentration (MAC) sevoflurane for 0 h, 3 h, 6 h, and 12 h. Group S + B and Group B were pretreated with bicuculline (10 uM). Group D was treated with DMSO (10 uL/mL). After treatments above, all groups were cultured for 48 h. Then we measured the cells viability by Cell Counting Kit (CCK-8) assay, cytotoxicity by Lactate Dehydrogenase (LDH) assay, apoptosis ratio with Annexin V/propidium iodide (PI) staining by flow cytometry, and the expression of GABAAR, anti-apoptotic protein Bcl-2, pro-apoptotic protein Bax and Caspase-3 by western blotting.ResultsAfter exposing to sevoflurane for 0 h, 3 h, 6 h, and 12 h with 1MAC, we found that cell viability obviously decreased and cytotoxicity increased in time-dependent way. And Annexin V/PI staining indicated increased apoptosis ratio by flow cytometry. The protein level of GABAA receptor, pro-apoptotic protein Bax and apoptosis protein Caspase-3 increased; while anti-apoptotic protein Bcl-2 decreased. And bicuculline could reverse all detrimental results caused by sevoflurane.ConclusionSevoflurane can inhibit the central nervous system by activating GABAA, resulting in apoptosis of neural stem cells, thus leading to the NSCs degeneration.

Purpose: For the topical anesthetic, transcriptional transactivator peptide (TAT) modified lidocaine (LID) loaded nanostructured lipid carriers (TAT-NLCs-LID) were prepared and then used for improving transdermal delivery of local anesthetic drug. Methods: In this study, TAT was conjugated with Distearoyl phosphatidylethanolamine-(polyethylene glycol) 2000 -maleimide (DSPE-PEG 2000 -Mal) to obtain TAT-PEG 2000 -DSPE. TAT-NLCs-LID were successfully prepared and characterized by determination of their particle size, morphology, drug encapsulation efficiency and in vitro drug release behavior. The skin permeation of LID-LNPs was examined using a Franz diffusion cell mounted with depilated mouse skin in vitro and in vivo anesthesia effect was evaluated on mice. Results:The results showed that TAT-NLCs-LID have substantially small mean diameter (157.9 nm) and high encapsulation efficiency (81.8%). From the in vitro skin permeation results, transdermal flux of TAT-NLCs-LID was about several times higher than that of LID solution and NLCs-LID. In vivo anesthesia effect evaluation illustrated that TAT-NLCs-LID can enhance the transdermal delivery of LID by reducing the pain threshold in mice. Conclusion: These results indicate that the novel TAT containing drug delivery system is very useful for overcoming the barrier function of the skin and could deliver anesthetic through the skin. TAT-NLCs-LID could function as promising topical anesthetic system.