PURPOSE: This study was performed to test the clinical usefulness of the glucose test strip method for early detection of pulmonary aspiration in tube fed patients. METHOD: The subjects for the study were 36 patients who were receiving enteral feedings and 39 patients who were not given enteral feedings. For the analysis, the tube fed patients were divided into two groups (clinically significant aspiration and no aspiration) according to criteria. RESULT: The mean glucose concentration of tracheal secretions from non enteral fed patients was 26.35mg/dl and were lower than those concentrations found in tube fed patients (32.75mg/dl). The mean glucose concentration of the aspiration group was 45.60mg/dl and the glucose concentration of the non aspiration group was 19.93mg/dl. The difference was statistically significant (t=2.163, p=. 038). More subjects in the no aspiration group (73%) than the aspiration group (56%) had glucose concentrations below 20mg/dl. After deleting the cases that had samples containing blood, glucose concentrations of tracheal aspirates were lower in both groups. CONCLUSION: The glucose level of the aspiration group was significantly lower than the no aspiration group and more subjects in the aspiration group had a glucose level higher than 101mg/dl. Therefore, the glucose test of tracheal secretions in tube fed patients could be a desirable test for screening for tracheal aspiration. Especially the patient who is showing repeatedly high glucose levels should not be given feedings until reassessment is completed.
Adult ; Aged ; Aged, 80 and over ; Enteral Nutrition/*adverse effects ; Female ; Glucose/*analysis ; Humans ; Intubation, Gastrointestinal/*adverse effects ; Male ; Middle Aged ; Pneumonia, Aspiration/*diagnosis ; *Reagent Strips ; Trachea/*secretion

BACKGROUND: Hypersecretion of mucin due to goblet cell hyperplasia is frequently encountered in many chronic airway diseases, such as chronic bronchitis, bronchiectasis, bronchial asthma and cystic fibrosis. Even in normal individuals, viral infection or bacterial pneumonia frequently provoke huge amounts of bronchial secretions which may cause airway obstruction. The production of mucin was regulated by epidermal growth factor (EGF) in vitro. To know whether this EGF system regulates mucin secretion in vivo and Pseudomonas also stimulates the mucin secretion by the same pathway, we studied these relationships in the cultured rat tracheal epithelial cells. METHODS: Rat tracheal epithelial cells were obtained by pronase dissociation from the male Fisher 344 rats. When cells became confluent, they were divided into 6 groups and stimulated with either EGF for 24 hours or Pseudomonas extracts for 12 hours with or without selective EGF-R tyrosine kinase inhibitor tyrphostin AG1478. RESULTS: We found that both EGF and Pseudomonas extracts phosphorylated the tyrosine residue in the EGF receptor from the rat tracheal epithelial cells and this tyrosine phosphorylation was nearly completely blocked by selective EGF-R tyrosine kinase inhibitor tyrphostin AG1478. The mucin secretion was also stimulated by either EGF or Pseudomonas extracts but more strong secretion of mucin and MUC5AC gene expression in the rat tracheal epithelial cell was done by Pseudomonas extracts. CONCLUSION: These data suggest that Pseudomonas secretes the mucin by way of the EGF receptor and MUC5AC gene expression and the inhibitors of EGF receptor tyrosine phosphorylation would be useful to prevent the huge production of mucin due to Pseudomonas aeruginosa lung infection.
Animal ; Blotting, Western ; Cells, Cultured ; Comparative Study ; Epidermal Growth Factor/*metabolism/pharmacology ; Epithelial Cells/drug effects/*secretion ; Gene Expression ; Male ; Models, Animal ; Mucins/drug effects/*genetics/*secretion ; *Pseudomonas aeruginosa ; RNA, Messenger/analysis ; Rats ; Rats, Inbred F344 ; Reverse Transcriptase Polymerase Chain Reaction ; Sensitivity and Specificity ; Trachea/cytology/drug effects/*microbiology/*secretion

Aim of the present study is to investigate activation effect of nobiletin on cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel activity. CFTR-mediated iodide influx assay and patch-clamp tests were done on FRT cells stably co-transfected with human CFTR and EYFP/H148Q. Nobiletin potently activated CFTR chloride channel activity in a dose- and time-dependent manner. The CFTR blocker CFTR(inh)-172 could completely reverse the effect. Preliminary mechanism study indicated that nobiletin activated CFTR chloride channel through a direct binding way. In addition, ex vivo tests done on mice trachea showed that nobiletin time-dependently stimulated submucosal gland fluid secretion. Nobiletin may be a therapeutic lead compound in treating CFTR-related diseases including disseminated bronchiectasis.
Animals ; Benzoates ; pharmacology ; Cystic Fibrosis Transmembrane Conductance Regulator ; antagonists & inhibitors ; drug effects ; metabolism ; Dose-Response Relationship, Drug ; Epithelial Cells ; metabolism ; Exocrine Glands ; secretion ; Flavones ; administration & dosage ; pharmacology ; Humans ; Mice ; Patch-Clamp Techniques ; Rats ; Rats, Inbred F344 ; Thiazolidines ; pharmacology ; Thyroid Gland ; cytology ; Time Factors ; Trachea ; secretion