Exogenous surfactant attenuation of ischemia–reperfusion injury in the lung through alteration of inflammatory and apoptotic factors
| Autor: | Jozef Kesecioglu, Cobi Jacoba Johanna Heijnen, Annemieke Kavelaars, Niels P. van der Kaaij, Burkhard Lachmann, Bart P. van Putte, Pieter M. Cobelens |
|---|---|
| Přispěvatelé: | University of Groningen |
| Rok vydání: | 2009 |
| Předmět: |
Lung Diseases
Male Pulmonary and Respiratory Medicine medicine.medical_specialty Administration Topical Ischemia Apoptosis Nitric Oxide Surfactant therapy Nitric oxide Rats Sprague-Dawley chemistry.chemical_compound Pulmonary surfactant Internal medicine Edema RAT MODEL medicine Animals Lung NITRIC-OXIDE Caspase 3 Interleukin-6 business.industry TRANSPLANTATION Pulmonary Surfactants respiratory system medicine.disease INTERLEUKIN-10 Rats Transplantation Disease Models Animal MICE Endocrinology medicine.anatomical_structure chemistry Reperfusion Injury Immunology Surgery medicine.symptom business Cardiology and Cardiovascular Medicine Reperfusion injury |
| Zdroj: | JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 137(4), 824-828. MOSBY-ELSEVIER |
| ISSN: | 0022-5223 |
| DOI: | 10.1016/j.jtcvs.2008.08.046 |
| Popis: | Objective: Lung ischemia-reperfusion injury is associated with impaired gas exchange from increased edema formation and surfactant inactivation. Surfactant replacement therapy is believed to improve gas exchange and lung function, but its effect on inflammation is less well understood. We therefore examined the effects of exogenous surfactant on inflammatory and apoptotic factors in the lung in a rat model of lung ischemia-reperfusion injury. Methods: The left lung in rats was subjected to ischemia for 120 minutes and reperfusion for as long as 240 minutes. Sham-treated animals underwent sham surgery and mechanical ventilation for equivalent times. Rats received porcine surfactant or saline solution intratracheally either before or just after ischemia. Lungs were analyzed histopathologically and for expressions of inducible nitric oxide, cytokines, and caspase-3. Results: Lung ischemia-reperfusion injury resulted in worse lung histopathologic characteristics than in sham-operation animals. At 2 hours of reperfusion, lung ischemia-reperfusion injury animals showed increased pulmonary caspase-3 expression. Moreover, lung ischemia-reperfusion injury resulted in inducible nitric oxide expression at all time points. Exogenous surfactant resulted in less inflammatory cell infiltration and edema in the lungs relative to saline-treated animals. Surfactant decreased activated caspase-3 expression and increased inducible nitric oxide expression relative to saline-treated animals. At 4 hours of reperfusion, surfactant increased interleukin 6 and 10 expressions in the lung. Conclusion: This study showed a significant improvement in lung histologic characteristics after surfactant therapy, accompanied by reduced apoptosis and increased anti-inflammatory cytokine levels. Interestingly, surfactant therapy also increased pulmonary inducible nitric oxide expression. |
| Databáze: | OpenAIRE |
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