orabase and Lung-Diseases

We aimed to examine effectiveness of sodium hyaluronate-carboxymethly cellulose (NaH/CMC) for sealing pulmonary air leaks during postoperative period.. The study was conducted in 16 male Sprague-Dawley rats. A linear insicion (length= 0.2 cm, depth= 0.1 cm) to the lung parenchyma on the inflated by a cutter was made. The animals were randomly divided; the control group (n= 8) and NaH/CMC-treated group (the study group, n= 8). Control group was left for physiologic healing while a NaH/CMC membrane was applied over the the incisional area in the study group. Then the pressure point where the air leakage observed was noted.. No polymorphonucleer leucocytes (PMNL) infiltration was detected in control group, whereas PMNL infiltration was 0.38 ± 0.5 cell per 100 high field in study group (p= 0.234). The degree of macrophage, lymphocyte infiltration and the mean fibroblast count were found to be higher in study group compared with control group (p= 0.007, p= 0.02, p= 0.05, respectively). The mean pressure value for air leak to occur in the control group was 43.50 ± 9.55 mmHg whereas it was 73.75 ± 16.68 mmHg in the study group (p< 0.001).. The data revealed that bioabsorbable NaH/CMC membrane accelerates healing with preserving the expansile character of lung parenchyma even in high ventilation pressures. However, further studies are required to assess the prevent impact of the pulmonary air-leak for NaH/CMC membrane.

Topics: Animals; Carboxymethylcellulose Sodium; Humans; Hyaluronic Acid; Lung; Lung Diseases; Male; Pneumothorax; Postoperative Period; Rats; Rats, Sprague-Dawley

The mechanism of bleomycin (Bleo)-induced pulmonary injury is not fully understood. Elevated levels of lung phospholipase A2 (PLA2) have been previously reported following intratracheal (IT) instillation of Bleo, but the role of this enzyme in the pathogenesis of lung injury is not clear. In this pilot study, we have evaluated the effect of a cell impermeable inhibitor of PLA2 (CME) on Bleo-induced pulmonary inflammation in hamsters. Pulmonary injury was induced by a single IT instillation of Bleo (1 unit/0.5 ml saline). Three groups of male Syrian hamsters were evaluated: 1) BLEO-CME animals received IT Bleo and daily intraperitoneal (IP) injections of CME (1 mumole/kg), starting 1 day before IT instillation; 2) BLEO-SAL animals--received IT Bleo and IP injections of saline and 3) SAL-SAL animals--treated with IT and IP administrations of saline. Animals were sacrificed 14 days after IT treatment and lung injury was evaluated histologically by a semiquantitative morphologic index and by a differential cell count of bronchoalveolar lavage fluid. CME treatment significantly ameliorated Bleo-induced lung injury compared to BLEO-SAL animals (P < 0.05). The percentage of neutrophiles in bronchoalveolar lavage fluid was reduced from 17.7 +/- 3.2% (mean +/- S.E.) in BLEO-SAL group to 7.3 +/- 1.7% in BLEO-CME group (P < 0.05), achieving levels comparable to SAL-SAL control animals. These results suggest that treatment with an extracellular PLA2 inhibitor-CME abates Bleo-induced pulmonary injury. This may indicate an active role of PLA2 in the pathogenesis of interstitial pulmonary fibrosis.

Topics: Animals; Bleomycin; Carboxymethylcellulose Sodium; Cricetinae; Enzyme Inhibitors; Injections, Intraperitoneal; Lung Diseases; Male; Mesocricetus; Phosphatidylethanolamines; Phospholipases A; Phospholipases A2; Pilot Projects; Pulmonary Alveoli; Pulmonary Fibrosis; Sodium Chloride

Recurrent respiratory papillomatosis is a disease caused by a virus in the Papovaviridae family. It tends to recur in the laryngotracheal tree, and treatment is surgical removal with a CO2 laser and suspension microlaryngoscopy. Some patients may require these procedures every few weeks, and a systemic agent to control disease would be ideal for them. Care must be taken in the selection of an agent, as these lesions, similar to other papova virus-induced lesions, are most susceptible to malignant degeneration in the presence of a carcinogen. Eight patients were given 10 courses of polyriboinosinic-polyribocytidylic acid [poly(I,C)-LC] in an attempt to control their disease. The three who were tested were able to produce good titers of interferon. The rate of disease progression was probably slowed in four patients, as reflected by a decrease in the requirement for surgery; however, the medication appeared to be relatively toxic in effective doses. Four of 10 courses were held for hepatotoxicity, and mild hepatotoxicity occurred in four more. One course was held for thrombocytopenia associated with bleeding at the tracheostomy site. We conclude that in its presently available form, poly(I,C)-LC is too toxic to be administered long term for control of this disease.

Topics: Adult; Carboxymethylcellulose Sodium; Child; Child, Preschool; Drug Evaluation; Female; Humans; Interferon Inducers; Kidney; Liver; Lung Diseases; Male; Methylcellulose; Middle Aged; Papillomaviridae; Poly I-C; Polylysine; Polyomaviridae; Recurrence; Respiratory Tract Infections

Topics: Bronchography; Carboxymethylcellulose Sodium; Contrast Media; Humans; Lung Diseases; Methylcellulose