Integrated model of endothelial NO regulation and systemic circulation for the comparison between pulsatile and continuous perfusion.

Many experimental studies concerning nitric oxide (NO) release from endothelium and its vasodilative action are available in the literature, but no analytical description or modeling of these phenomena can be found. On the contrary, a large modeling literature is available concerning the other cardiovascular control mechanisms, such as the myogenic and metabolic control. In order to analytically describe these phenomena, a model of the endothelial control (defined in the Laplace domain and based on experimental data) was implemented and integrated with a lumped-parameter model of the systemic circulation, consisting of large artery segments and peripheral networks. The endothelial regulation model was based on the hypothesis proposed by Kuchan and Frangos, considering that NO release from the endothelium is generated by two parallel paths. The whole model was then applied to study the different vascular constriction or dilation under continuous or pulsatile perfusion, in order to better understand the clinical evidences of a poor organ perfusion in the presence of continuous with respect to pulsatile cardiopulmonary bypass. According to the experimental evidences, the main results obtained from the model revealed a widespread vascular constriction under continuous perfusion with respect to pulsatile. This result remains constant in the presence of different conditions of blood parameters and flow waveform.