• Michael A Flierl, Daniel Rittirsch, Markus S Huber-Lang, J Vidya Sarma, and Peter A Ward.
• Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109-0602, United States of America.
• Mol. Med. 2008 May 1;14(5-6):327-36.

AbstractSeptic cardiomyopathy is a well-described complication of severe sepsis and septic shock. However, the interplay of its underlying mechanisms remains enigmatic. Consequently, we constantly add to our pathophysiological understanding of septic cardiomyopathy. Various cardiosuppressive mediators have been discovered, as have multiple molecular mechanisms (alterations of myocardial calcium homeostasis, mitochondrial dysfunction, and myocardial apoptosis) that may be involved in myocardial dysfunction during sepsis. Finally, the detrimental roles of nitric oxide and peroxynitrite have been unraveled. Here, we describe our present understanding of systemic, supracellular, and cellular molecular mechanisms involved in sepsis-induced myocardial suppression.

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