Mechanical ventilation during experimental sepsis increases deposition of advanced glycation end products and myocardial inflammation

摘要

IntroductionIncreasing evidence links advanced glycation end products (AGE) including N^ε-(carboxymethyl)lysine (CML) to the development of heart failure. Accumulation of AGE leads to myocardial inflammation, which is considered as one of the possible mechanisms underlying sepsis-induced cardiac dysfunction. We hypothesized that mechanical ventilation (MV) augmented sepsis-induced myocardial CML deposition and inflammation.