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Objective To investigate the bacteriological distribution of nosocomial pneumonia induced by acute stroke, and to improve the preventative and therapeutic measures. Methods The clinical data of 192 patients with nosocomial pneumonia induced by acute stroke were analyzed respectively. Results Among the 192 cases, 13 pathogenic microorganisms and 116 strains were cultivated, and the first 4 strains were Escherichia coli, Psendomonas aeruginosa, Klebsiella and Staphylococcus aurens. Gram-negative bacteria were sensitive to imipenem, and Gram-positive bacteria were sensitive to vancomycin. Conclusion The main pathogens of nosocomial pneumonia in acute stroke patients may be Escherichia coli and Pseudomonas aeruginosa. The measures improving the therapeutic outcome of acute stroke include the enhancement of nursing quality, prevention of cross infection in hospital, increasing predictability of the occurrence of pneumonia induced by acute stroke, and the control of pneumonia.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of ulinastatin on gut mucosal apoptosis and bacterium translocation in a rat model of sepsis.</p><p><b>METHODS</b>Fifty rats were randomly assigned into 4 groups, namely the control (n=5, no operation or drugs), ulinastatin pretreatment (n=15, treated with 25,000 U/kg ulinastatin 2 h before operation), ulinastatin treatment (n=15, treated with 25,000 U/kg ulinastatin 2 h after operation) and sepsis model (n=15, without drug treatment) groups. The rats in the later 3 groups were subjected to cecal ligation and puncture (CLP). At 3, 6 and 12 h after CLP, the rats were sacrificed and the ileum was removed to examine the pathology and apoptosis of the mucosa. The DNA of Bacillus coli in the whole blood was detected using PCR.</p><p><b>RESULTS</b>Sepsis caused of epithelial cell loss in the ileal villi, ulceration and blebbing of the lamina propria. Ulinastatin treatment administered before and after the operation both significantly alleviated these morphological anomalies. The sepsis rats showed significantly increased intestinal mucosal apoptotic index as compared with the other 3 groups (P<0.05). Ulinastatin pretreatment, in comparison ulinastatin treatment 12 h after CLP, significantly increased the intestinal mucosal apoptotic index (P<0.05). Bacillus coli DNA was positive in sepsis and postoperative ulinastatin treatment groups but negative in the control and pretreated groups.</p><p><b>CONCLUSION</b>Increased intestinal musocal apoptosis and gut bacterial translocation occur in rats following sepsis, and ulinastatin can effectively decrease intestinal mucosal apoptosis and inhibit bacterial translocation.</p>