A validated reduced-order dynamic model of nitric oxide regulation in coronary arteries.

Nitric Oxide (NO) provides myocardial oxygen demands of the heart during exercise and cardiac pacing and also prevents cardiovascular diseases such as atherosclerosis and platelet adhesion and aggregation. However, the direct in vivo measurement of NO in coronary arteries is still challenging. To address this matter, a mathematical model of dynamic changes of calcium and NO concentration in the coronary artery was developed for the first time. The model is able to simulate the effect of NO release in coronary arteries and its impact on the hemodynamics of the coronary arterial tree and also to investigate the vasodilation effects of arteries during cardiac pacing. For these purposes, flow rate, time-averaged wall shear stress, dilation percent, NO concentration, and Calcium (Ca2+) concentration within coronary arteries were obtained. In addition, the impact of hematocrit on the flow rate of the coronary artery was studied. It was seen that the behavior of flow rate, wall shear stress, and Ca2+ is biphasic, but the behavior of NO concentration and the dilation percent is triphasic. Also, by increasing the Hematocrit, the blood flow reduces slightly. The results were compared with several experimental measurements to validate the model qualitatively and quantitatively. It was observed that the presented model is well capable of predicting the behavior of arteries after releasing NO during cardiac pacing. Such a study would be a valuable tool to understand the mechanisms underlying vessel damage, and thereby to offer insights for the prevention or treatment of cardiovascular diseases.