ABSTRACT
BACKGROUND: Enteral nutrition has been demonstrated to reduce ventilator days and the incidence of pneumonia, but the safest route for providing enteral nutrition to mechanically ventilated patients is unclear. Our objective was to determine if there is a difference between the incidences of microaspiration of gastric secretions in patients fed via a nasogastric tube vs a postpyloric tube while undergoing rotational therapy for acute respiratory distress syndrome (ARDS). MATERIALS AND METHODS: Institutional review board approval was obtained for this prospective, randomized study. Patients were randomized to gastric or postpyloric enteral feedings. Daily tracheal secretion samples were collected, and we used an immunoassay to detect pepsin. Using the data for aspiration and tube type, a univariate unadjusted odds ratio was calculated to assess the risk of aspiration between the 2 tube types. An independent samples t test was used to analyze the hypothesis that microaspiration significantly affects lung recovery from ARDS. RESULTS: Of the 20 study patients, 9 (45%) received nasogastric feeds and 11 (55%) received postpyloric feeds. Western blot analysis for the presence of pepsin in each tracheal aspirate revealed microaspiration in 2 nasogastric (22%) and 2 (18%) postpyloric patients. The nasogastric tube provided a protective effect for aspirating with an odds ratio of .778 (95% confidence interval, .09-6.98). An independent samples t test was used and showed no significant change in PaO(2):FiO(2) ratio in the aspirating vs nonaspirating group (P = .552). CONCLUSION: The results of this study indicate that enteral nutrition should not be delayed or stopped to position the tube in patients with ARDS on rotational therapy.
Subject(s)
Enteral Nutrition/methods , Intubation, Gastrointestinal/adverse effects , Respiratory Aspiration/prevention & control , Respiratory Distress Syndrome/therapy , Adult , Aged , Female , Humans , Immunoassay , Incidence , Intubation, Gastrointestinal/methods , Length of Stay , Male , Middle Aged , Odds Ratio , Pepsin A/analysis , Pilot Projects , Prospective Studies , Respiratory Aspiration/etiology , Respiratory Distress Syndrome/complications , Risk Factors , Trachea/metabolismABSTRACT
Invasion of bladder epithelial cells by uropathogenic Escherichia coli (UPEC) contributes to antibiotic-resistant and recurrent urinary tract infections (UTIs), but this process is incompletely understood. In this paper, we provide evidence that the large guanosine triphosphatase dynamin2 and its partner, endothelial nitric oxide (NO) synthase (NOS [eNOS]), mediate bacterial entry. Overexpression of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted reduction of endogenous dynamin2 or eNOS expression with ribonucleic acid interference impairs, bacterial invasion. Exposure of mouse bladder to small molecule NOS inhibitors abrogates infection of the uroepithelium by E. coli, and, concordantly, bacteria more efficiently invade uroepithelia isolated from wild-type compared with eNOS(-/-) mice. E. coli internalization promotes rapid phosphorylation of host cell eNOS and NO generation, and dynamin2 S-nitrosylation, a posttranslational modification required for the bacterial entry, also increases during E. coli invasion. These findings suggest that UPEC escape urinary flushing and immune cell surveillance by means of eNOS-dependent dynamin2 S-nitrosylation and invasion of host cells to cause recurrent UTIs.
