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Journal of Aerosol Medicine and Pulmonary Drug Delivery 2015-Aug

Joint Intratracheal Surfactant-Antibacterial Therapy in Experimental Pseudomonas-Induced Pneumonia.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
הקישור נשמר בלוח
Alexei A Birkun
Anatoly V Kubyshkin
Nikolai Y Novikov
Yuri L Krivorutchenko
Michael I Fedosov
Olga N Postnikova
Anatoly A Snitser

מילות מפתח

תַקצִיר

BACKGROUND

The application of an exogenous pulmonary surfactant as a carrier for intratracheally administered antimicrobials represents a promising therapeutic modality that is still on its way to clinical practice. Owing to its ability to decrease surface tension, exogenous surfactant may enhance delivery of antibiotics into foci of pulmonary infection, thus increasing efficiency and safety of topical antimicrobial therapy in bacterial lung diseases.

OBJECTIVE

To assess potential interactions between exogenous surfactant and amikacin in vitro, and to study the effects of their joint intratracheal instillation in rats with acute pneumonia caused by Pseudomonas aeruginosa.

METHODS

The antibacterial and surface-active properties of amikacin (Amicil, Kievmedpreparat, Ukraine), porcine pulmonary surfactant (Suzacrin, Docpharm, Ukraine), and their combination were studied in vitro using standard microbiologic procedures and modified Pattle method (estimation of bubble diameter). Similar methods were utilized to study bacterial contamination of lungs and blood, and to assess the surface activity of bronchoalveolar wash (BAW) in 119 Wistar rats, including infected (intratracheal introduction of P. aeruginosa ATCC 27853) and noninfected animals. Histopathologic findings, differential leukocyte counts, and oxygenation parameters were recorded.

RESULTS

Antibacterial and surface-active properties of the surfactant and amikacin remained unimpaired in vitro. In rats anti-pseudomonal and anti-inflammatory effects of the surfactant-amikacin mixture were more pronounced (p<0.05) than effects of pure amikacin as evidenced by recorded rates of bacterial growth and granulocytic response. The combined therapy considerably restricted tissue damage and mitigated reduction of BAW surface activity.

CONCLUSIONS

The advantages of the joint surfactant-amikacin therapy of Pseudomonas-induced pneumonia may suggest further clinical trials.

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