Assessment of the sedative effects of dexmedetomidine and propofol treatment in patients undergoing mechanical ventilation in the ICU and relationship between treatment and occurrence of ventilator-associated pneumonia and detection of pathogenic bacteria.

The present study aimed to investigate the sedative effects of dexmedetomidine combined with propofol in patients undergoing mechanical ventilation in the intensive care unit (ICU), and to reveal the risk factors of ventilator-associated pneumonia (VAP). A retrospective analysis of 322 patients who had been subject to mechanical ventilation in the ICU ward was performed. Subjects were divided into two groups: A group treated with dexmedetomidine and propofol (combined group) and a group treated with dexmedetomidine alone (monotherapy group). Clinical data, sedative effects, the number of VAP patients and the distribution of VAP pathogens were assessed. Multivariate analysis and receiver operating characteristic (ROC) curves were used to predict VAP. Significant differences in the sedative effects between the two groups were observed (P<0.001). The incidence of VAP was significantly higher in the monotherapy group compared with the combined group (P<0.05). Multivariate logistic regression analysis demonstrated that age, acute physiology chronic health evaluation score, consciousness, invasive operations, recovery time, extubation time and sedation regimen were independent risk factors for VAP in the ICU during mechanical ventilation. ROC curves indicated that the areas under the curve for age, acute physiology chronic health score, consciousness, invasive operations, recovery time, extubation time and sedation regimen were 0.934, 0.870, 0.632, 0.677, 0.865, 0.950 and 0.603, respectively. In summary, dexmedetomidine combined with propofol can shorten the recovery and extubation times of mechanical ventilation patients in the ICU. Different sedation schemes are also independent risk factors for VAP during mechanical ventilation in the ICU.

Glucagon-like peptide-1 protects against cardiac microvascular endothelial cells injured by high glucose.

OBJECTIVE: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose. METHODS: CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis. RESULTS: High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (P<0.05). CONCLUSIONS: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.