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Einfluss von (-)-Epigallocatechin-3-gallat auf den Lungenschaden im Rahmen des kardiopulmonalen Bypasses mittels Herz-Lungen-Maschine in einem Schweinemodell

Background: Lung dysfunction constitutes a severe complication after major cardiac surgery with cardiopulmonary bypass (CPB), substantially contributing to postoperative morbidity and mortality. The current possibilities of preventive and therapeutic interventions, however, remain insufficient. We, therefore, investigated the effects of intraoperative application of the antioxidant and anti-inflammatory green tea polyphenol epigallocatechin-3-gallate (EGCG) on CPB-associated lung injury.
Materials and methods: Thirty piglets (8 - 15 kg) were divided into four groups: sham-operated and saline-treated control group (n = 7); sham-operated and EGCG-treated control group (EGCG-control group; n = 7); CPB group (n = 10); and CPB + EGCG group (n = 6). The CPB groups underwent 120 min of CPB followed by 90 min of recovery time. In the CPB + EGCG group, EGCG (10 mg/kg body weight) was administered intravenously before and after CPB. Hemodynamic monitoring, blood gas analysis, hematoxylin-eosin staining, and immunohistochemistry of lung tissue were performed.
Results: Histologic examination revealed thickening of the alveolar wall and enhanced alveolar neutrophil infiltration in the CPB group (P < 0.05) compared with those in the control group, which was prevented by EGCG (P < 0.05). In the CPB group, higher formation of poly(ADP-ribose) and nuclear translocation of apoptosis-inducing factor were detected in comparison with those in the control group (P < 0.001), which were both reduced in the CPB + EGCG group (P < 0.001). Compared with the control group, the EGCG-control group
showed thickening of the alveolar wall and increased neutrophil infiltration (P < 0.05).
Conclusions: CPB leads to lung edema, pulmonary neutrophil infiltration, and presumably initiation of poly(ADP-ribose) polymerase-dependent cell death signaling in the lung. EGCG appears to attenuate CPB-associated lung injury, suggesting that this may provide a novel pharmacologic approach.

Identiferoai:union.ndltd.org:DRESDEN/oai:qucosa.de:bsz:15-qucosa-213299
Date17 November 2016
CreatorsKasper, Bernhard
ContributorsUniversität Leipzig, Medizinische Fakultät, Prof. Dr. med. Stefan Dhein, Prof. Dr. med Dietrich Pfeiffer, Prof. Dr. med. Farhad Bakhtiary
PublisherUniversitätsbibliothek Leipzig
Source SetsHochschulschriftenserver (HSSS) der SLUB Dresden
Languagedeu
Detected LanguageEnglish
Typedoc-type:doctoralThesis
Formatapplication/pdf

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