ABSTRACT
Objective To investigate the clinical distribution and antibiotics resistance of nosocomial infection caused pathogenic bacteria in patients after cardiac surgery.Methods Clinical data from 612 patients after cardiac surgery under microbiologically documented nosocomial infection was retrospectively analyzed from January 2007 to December 2012.Identification on related bacterial was performed in an automatic ATB Expression system while antimicrobial susceptibility was tested by Kirby-Bauer method.Results were analyzed by WHONET5.4.Results There were 697 strains of clinical pathogenic bacilli isolates identified and 421 (60.4％) of them were isolated from sputum while 185 (26.5％) were from blood.Acinetobacter spp.(124 strains,17.8％),Pseudomonas aeruginosa (85 strains,12.2％) and Klebsiella pneumoniae (50 strains,7.2％) were the predominant Gramnegative bacilli while S.epidermidis (75 strains,10.8％) was the predominant Gram-positive cocci.The predominant eumycete was Candida albicaas (43 strains,6.2％).Results from the susceptibility test showed that carbopenems,cefoperazone/sulbactam and piperacillin/tazobactam were the most active antibiotics.The detection of meticillin-resistant Staphylococcus (MRS) were 82.9％ in S aureus and 95.9％ in coagulase negative Staphylococcus.There was no Staphylococcus strains resistant to vancomycin found.Conclusion Non-fermenting Gram-negative bacilli and Staphylococcus appeared the important pathogens in patients after cardiac surgery.Drug resistance to antibiotics was quite common.Prevention on nosocomial infection and rational use of antibiotics remained very important in reducing the amount of drug resistant strains.
ABSTRACT
<p><b>BACKGROUND</b>The loss of cardiac myocytes is one of the mechanisms involved in acute myocardial infarction (AMI)-related heart failure. Autophagy is a common biological process in eukaryote cells. The relationship between cardiac myocyte loss and autophagy after AMI is still unclear. Carvedilol, a non-selective alpha1- and beta-receptor blocker, also suppresses cardiac myocyte necrosis and apoptosis induced by ischemia. However, the association between the therapeutic effects of carvedilol and autophagy is still not well understood. The aim of the present study was to establish a rat model of AMI and observe changes in autophagy in different zones of the myocardium and the effects of carvedilol on autophagy in AMI rats.</p><p><b>METHODS</b>The animals were randomly assigned to a sham group, an AMI group, a chloroquine intervention group and a carvedilol group. The AMI rat model was established by ligating the left anterior descending coronary artery. The hearts were harvested at 40 minutes, 2 hours, 24 hours and 2 weeks after ligation in the AMI group, at 40 minutes in the chloroquine intervention group and at 2 weeks in other groups. Presence of autophagic vacuoles (AV) in the myocytes was observed by electron microscopy. The expression of autophagy-, anti-apoptotic- and apoptotic-related proteins, MAPLC-3, Beclin-1, Bcl-xl and Bax, were detected by immunohistochemical staining and Western blotting.</p><p><b>RESULTS</b>AVs were not observed in necrotic regions of the myocardium 40 minutes after ligation of the coronary artery. A large number of AVs were found in the region bordering the infarction. Compared with the infarction region and the normal region, the formation of AV was significantly increased in the region bordering the infarction (P < 0.05). The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the region bordering the infarction. Meanwhile, the expression of apoptotic-related proteins was significantly increased in the infarction region. In the chloroquine intervention group, a large number of initiated AVs (AVis) were found in the necrotic myocardial region. At 2 weeks after AMI, AVs were frequently observed in myocardial cells in the AMI group, the carvedilol group and the sham group, and the number of AVs was significantly increased in the carvedilol group compared with both the AMI group and the sham group (P < 0.05). The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the carvedilol group compared with that in the AMI group, and the positive expression located in the infarction region and the region bordering the infarction.</p><p><b>CONCLUSIONS</b>AMI induces the formation of AV in the myocardium. The expression of anti-apoptosis-related proteins increases in response to upregulation of autophagy. Carvedilol increases the formation of AVs and upregulates autophagy and anti-apoptosis of the cardiac myocytes after AMI.</p>
