Apoptosis contributes to septic cardiomyopathy and is improved by simvastatin therapy

• Published in: Shock (Augusta, Ga.) Vol. 29; no. 4; p. 497
• Main Authors: Buerke, Ute, Carter, Justin M, Schlitt, Axel, Russ, Martin, Schmidt, Hendrik, Sibelius, Ulf, Grandel, Ulrich, Grimminger, Friedrich, Seeger, Werner, Mueller-Werdan, Ursula, Werdan, Karl, Buerke, Michael
• Format: Journal Article
• Language: English
• Published: United States 01.04.2008
• Subjects: Animals; Apoptosis - drug effects; Cardiomyopathies - drug therapy; Cardiomyopathies - etiology; Cardiomyopathies - physiopathology; Exotoxins - toxicity; Heart - drug effects; Heart - physiopathology; Hemodynamics - drug effects; In Situ Nick-End Labeling; In Vitro Techniques; Myocardium - metabolism; Myocardium - pathology; Necrosis; Rats; Sepsis - chemically induced; Sepsis - complications; Sepsis - drug therapy; Simvastatin - therapeutic use; Tumor Necrosis Factor-alpha - metabolism; Tumor Suppressor Protein p53 - metabolism

Bacterial toxins cause cardiac dysfunction and death through an inflammatory process, but the mechanism remains unclear. Simvastatin is recognized as having anti-inflammatory properties beyond its lipid-lowering effects. We examined Staphylococcus aureus alpha-toxin in isolated heart and in vivo mod...