Inadequate Myocardial Oxygen Supply/Demand in Experimental Pulmonary Hypertension
نویسندگان
چکیده
The increased workload of the right heart due to pulmonary hypertension increases oxygen consumption of right ventricular cardiomyocytes because the mitochondria have to operate at a higher rate. Hypertrophy can normalize right ventricular wall stress, thereby also normalizing the rate of oxygen consumption by mitochondria. However, hypertrophy may cause hypoxia in cardiomyocytes because intracellular diffusion distances for oxygen increase and capillary density decreases when the myocytes enlarge. Increased diffusion distances imply that the interstitial oxygen tension preventing core hypoxia in cardiomyocytes (PO2crit) increases, whereas reduced capillary density likely reduces interstitial PO2. In addition to the increased power output of the right ventricular myocytes, the rate of oxygen consumption of the cells also increases because their mechanical efficiency decreases (Wong et al., 2010). These changes can lead to oxidative stress (Redout et al., 2007) and may lead to apoptosis of RV cardiomyocytes (Ecarnot-Laubriet et al., 2002).
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