PhD defence G.M. (Gianmarco) Balestra

Brief summary of the doctoral thesis:

In this thesis we further developed and characterized our phosphorimetric method for near-simultaneous measurements of microcirculatory and mitochondrial oxygenation in the heart in vivo. In two animal models, right ventricular pressure overload and endotoxemia, we addressed the oxygenation level in the microcirculation and mitochondria. In both diseases no myocardial oxygen shortage was found. Our results suggest reprogramming of mitochondrial metabolic pathways and mitochondrial dysfunction as mechanisms for organ dysfunction in right ventricular pressure overload and endotoxemia, respectively. Elevated troponin levels were measured in animals treated with norepinephrine. Usual drug regimen according to sepsis treatment guidelines might therefore be associated with myocardial damage. Finally, it could be hypothesized that the mitochondrial mechanisms with altered metabolism and function represent a generic defense mechanism to severe cellular challenges as they have been described in a large number of cardiac, pulmonary, hepatic, neurologic and psychiatric diseases.