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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Publikationen des W. G. Kerckhoff-Instituts     Display Documents



ID: 428408.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Publikationen des W. G. Kerckhoff-Instituts
Novel soluble guanylyl cyclase stimulator BAY 41-2272 attenuates ischemia/reperfusion induced lung injury
Authors:Egemnazarov, B.; Sydykov, A.; Schermuly, R. T.; Weissmann, N.; Stasch, J. P.; Sarybaev, A. S.; Seeger, W.; Grimminger, F.; Ghofrani, H. A.
Date of Publication (YYYY-MM-DD):2008
Title of Journal:Am J Physiol Lung Cell Mol Physiol
Audience:Not Specified
Abstract / Description:The protective effects of nitric oxide (NO), a physiological activator of soluble guanylyl cyclase (sGC), have been reported in ischemia/reperfusion (I/R) syndrome of the lung. Therefore, we studied the effects of BAY 41-2272, a novel sGC stimulator, on I/R injury of the lung in an isolated intact organ model. Lung injury was assessed by measuring weight gain and microvascular permeability (capillary filtration coefficient, Kfc). Release of reactive oxygen species (ROS) into the perfusate was measured during early reperfusion by ESR spectroscopy. Rabbit lungs were treated with BAY 41-2272, L-NMMA 400, or NO to evaluate the effects on I/R induced lung injury. In untreated lungs a dramatic rise in Kfc values and weight gain during reperfusion were observed, these results were associated with increased ROS production. Both, BAY 41-2272 and L-NMMA significantly attenuated vascular leakage and suppressed ROS release. Additional experiments showed that BAY 41-2272 diminished phorbol-12-myristrate-13-acetate induced ROS production by NADPH-oxidase. A pharmacological inhibition of the enzyme with consequent reduction in ROS levels decreased I/R injury. Nitric oxide had only marginal effect on I/R injury. Thus, BAY 41-2272 protects against I/R induced lung injury by interfering with the activation of NADPH-oxidases. Key words: acute lung injury, nitric oxide, oxidative stress, ROS.
External Publication Status:published
Document Type:Article
Communicated by:N. N.
Affiliations:MPI für physiologische und klinische Forschung
Identifiers:URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=...
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