Ventilator-associated pneumonia (VAP) is one of the most prevalent and serious complications of mechanical ventilation, which is considered a common nosocomial infection in critically ill patients. There are some great options for the prevention of VAP: (i) minimize ventilator exposure; (ii) intensive oral care; (iii) aspiration of subglottic secretions; (iv) maintain optimal positioning and encourage mobility; and (v) prophylactic probiotics. Furthermore, clinical management of VAP depends on appropriate antimicrobial therapy, which needs to be selected based on individual patient factors, such as previous antibacterial therapy, history of hospitalization or mechanical ventilation, and bacterial pathogens and antibiotic resistance patterns. In fact, antibiotic resistance has exponentially increased over the last decade, and the isolation of a multidrug-resistant (MDR) pathogen has been identified as an independent predictor of inadequate initial antibiotic therapy and which is significantly associated with increased mortality. Multiple attempts were used in the treatment of VAP, such as novel antibacterial agents, inhaled antibiotics and monoclonal antibodies. In this review, we summarize the current therapeutic options for the prevention and treatment of VAP, aiming to better management of VAP in clinical practice.
Aim of Study: To Prevent the Monocrotaline induced extracellular matrix remodeling of pulmonary artery by inhibiting Ubiquitin Proteasome System in rat pulmonary artery hypertension model. Study Design: Experimental Study Place and Duration of Study: Xi’an Jiaotong University, Animal experiment center Xi’an China, from January 2016 to July 2018. Materials and Methods: Thirty-three male Sprague-Dawley rats were divided in to three groups namely control group, Monocrotaline (M.C.T) induced group and M.G-132 (a proteasome inhibitor) treated group. The pulmonary artery hypertension (P.A.H) model was established by giving intraperitoneal injection of Monocrotaline (M.C.T) furthermore the M.G-132 was given to hold back proteasome function. The right ventricular systolic pressure (R.V.S.P) and the right ventricular hypertrophy index (R.V.H.I) were used to assess the progress developing P.A.H. Vascular remodeling was determined by H&E staining and the level of ubiquitinated-PTEN protein was measured by Immunoblotting. Results: The final results revealed that the M.C.T increased R.V.S.P and R.V.H.I in rats, whereas these alterations were concealed in P.A.H induced rats which were treated by M.G-132. Also the Zymograghy results in control vs. experimental group revealed that the activity of Matrix metalloproteinase (MMP2/9) in the PAH model group was considerably elevated at (P<0.05), while treatment of M.G-132 in M.C.T-induced P.A.H-rats decreased the activity of MMP2/9 at (p<0.05). Conclusions: However, further in-depth investigations are need of a time to explore the transformations of ubiquitin proteasome & MMP activity in chronic MCT induced-pulmonary artery hypertension model. Keywords: P.A.H, Ubiquitin, Monocrotaline, Extra-cellular remodeling, M.M.P (Matrix metalloproteinases)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.