Figure 2.

From Ferguson et al[37], with adaptation from Gutterman et al[62]. In a healthy heart, arteriolar endothelium produces NO, prostacyclin (PGI2, and EETs) as well as low levels of hydrogen peroxide, which support a quiescent non proliferative state. With the onset of disease (A), flow through the microvasculature releases hydrogen peroxide, creating a proinflammatory environment throughout the organ, potentially leading to hypertrophy, fibrosis, and atherosclerosis. In B, with bypass grafting of ischemic myocardium, the microvascular health of the myocardium is “normalized”. NO: Nitric oxide; PGI2: Prostacyclin; EET: Epoxyeicosatrienoic acids.