Background: Endotracheal intubation (ETI) is a life-saving procedure taught to medical students. We examined the influence of the order of teaching ETI through direct laryngoscopy (DL) and video laryngoscopy (VL) on learning by measuring the intubation time and learning curve of trainees, in order to explore ways to improve ETI performance. Methods: Twenty trainees were randomly divided into 2 groups. In the DL-first group, trainees used DL to perform ETI 10 times and then used VL 10 times, while the order was reversed in the VL-first group. Intubation time, number of intubation attempts, the Cormack-Lehane (CL) classification, and adverse events were recorded. The primary outcome was the cumulative summation (CUSUM). The CUSUM equation is defined as , where c t is the cumulative sum. Results: ETI was attempted on 400 patients. The difference in the mean times for the first 10 intubations between the 2 groups was not significant ( P > .05). Mean intubation time for second series in the DL-first group was significantly shorter than that of the first series ( P < .05), while there were no differences between the 2 series in the VL-first group ( P > .05). The mean intubation time in the second series of the DL-first group was shorter than for the first series of the VL-first group ( P < .05), while the mean intubation time of the first series by the DL-first group did not differ from the second series by the VL-first group ( P > .05). Eighteen attempts were required to achieve an 80% intubation success rate for the DL-first group, while more than 20 attempts were required for the trainees in the VL-first group. Conclusion: We consider that teaching trainees DL for tracheal intubation first. Clinical trial number: ChiCTR-OOR-16008364.
Aims: Dexmedetomidine (Dex) as a highly selective α2-adrenoceptor agonist, was widely used anesthetic in perioperative settings, whether Dex induces cardiac hypertrophy during perioperative administration is unknown. Methods: The effects of Dex on cardiac hypertrophy were explored using the transverse aortic constriction model and neonatal rat cardiomyocytes. Results: We reported that Dex induces cardiomyocyte hypertrophy with activated ERK, AKT, PKC and inactivated AMPK in both wild-type mice and primary cultured rat cardiomyocytes. Additionally, pre-administration of Dex protects against transverse aortic constriction induced-heart failure in mice. We found that Dex up-regulates the activation of ERK, AKT, and PKC via suppression of AMPK activation in rat cardiomyocytes. However, suppression of mitochondrial coupling efficiency and membrane potential by FCCP blocks Dex induced AMPK inactivation as well as ERK, AKT, and PKC activation. All of these effects are blocked by the α2-adrenoceptor antagonist atipamezole. Conclusion: The present study demonstrates Dex preconditioning induces cardiac hypertrophy that protects against heart failure through mitochondria-AMPK pathway in perioperative settings.
Sepsis is a global disease burden, and approximately 40% of cases develop acute lung injury (ALI). Bone marrow mesenchymal stromal cells (BMSCs) and their exosomes are widely used in treating a variety of diseases including sepsis. As an acute phase protein, serum amyloid A1 (SAA1) regulates inflammation and immunity. However, the role of SAA1 in BMSCs-exosomes in septic lung injury remains to be elucidated. Exosomes derived from serum and BMSCs were isolated by ultracentrifugation. SAA1 was silenced or overexpressed in mouse BMSCs using lentiviral plasmids, containing either SAA1-targeting short interfering RNAs or SAA1 cDNA. Sepsis was induced by cecal ligation and puncture (CLP). LPS was used to induce ALI in mice. Mouse alveolar macrophages were isolated by flow cytometry. Levels of SAA1, endotoxin, TNF-α, and IL-6 were measured using commercial kits. LPS internalization was monitored by immunostaining. RT-qPCR or immunoblots were performed to test gene and protein expressions. Serum exosomes of patients with sepsis-induced lung injury had significantly higher levels of SAA1, endotoxin, TNF-α, and IL-6. Overexpression of SAA1 in BMSCs inhibited CLP-or LPS-induced lung injury and decreased CLP-or LPS-induced endotoxin, TNF-α, and IL-6 levels. Administration of the SAA1 blocking peptide was found to partially inhibit SAA1-induced LPS internalization by mouse alveolar macrophages and reverse the protective effect of SAA1. In conclusion, BMSCs inhibit sepsis-induced lung injury through exosomal SAA1. These results highlight the importance of BMSCs, exosomes, and SAA1, which may provide novel directions for the treatment of septic lung injury.
Purpose: Multiple studies have demonstrated an obesity paradox such that obese septic patients have a lower mortality rate and a relatively favorable prognosis. However, less is known on the association between abdominal obesity and short-term mortality in patients with sepsis. We conducted this study to determine whether the obesity-related survival benefit remains among abdominal obese patients.Methods: A retrospective cohort study was conducted using data derived from the Medical Information Mart for Intensive Care IV database. Septic patients (≥18 years) with or without abdominal obesity of first intensive care units (ICU) admission in the database were enrolled. The primary outcome was mortality within 28 days of ICU admission and multivariable logistic regression analyses were employed to assess any association between abdominal obesity and the outcome variable.Results: A total of 21534 patients were enrolled finally, the crude 28-day mortality benefit after ICU admission was not observed in patients with abdominal obesity (15.8% vs. 15.3%, p=0.32). In the extended multivariable logistic models, the odds ratio (OR) of abdominal obesity was significantly inversed after incorporating metabolic variables into the logistic model (OR range 1.094-2.872, p = 0.02). The subgroup analysis showed interaction effects in impaired fasting blood glucose/diabetes and metabolic syndrome subgroups (P = 0.001 and <0.001, respectively). In the subgroups of blood pressure, high-density lipoprotein cholesterol, and triglyceride level, no interaction was detected in the association between abdominal obesity and mortality. After propensity score matching, 6523 pairs of patients were selected. The mortality significantly higher in the abdominal obesity group (17.0% vs. 14.8%, p = 0.015). Notably, the non-abdominal obese patients were weaned off vasopressors and mechanical ventilation more quickly than those in the abdominal obesity group (vasopressor‑free days on day 28 of 27.0 vs. 26.8, p < 0.001; ventilation-free days on day 28 of 26.7 vs. 25.6, p < 0.001).Conclusion: Abdominal obesity was associated with increased risk of adjusted sepsis-related mortality within 28 days after ICU admission and was partially mediated through metabolic syndrome components.
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