Abatay H.Payne S.J.STEPHEN JOHN PAYNE2022-05-242022-05-242010https://www.scopus.com/inward/record.uri?eid=2-s2.0-77958011877&doi=10.1007%2f978-3-642-14515-5_220&partnerID=40&md5=04226d4b696e5988ba27d92e4444c503https://scholars.lib.ntu.edu.tw/handle/123456789/611827Vasomotion (rhythmic oscillations in vascular tone) has been suggested to act as a protective mechanism under conditions of low perfusion, acting to increase oxygen delivery to tissue when blood pressure is reduced, although this is not proven. It is thought that vasomotion may occur due to instabilities in the myogenic response (changes in blood vessel diameter in response to transmural pressure changes) and it has been hypothesized that the vasomotion observed on Nitric Oxide (NO) blockade is caused by the fact that the myogenic system is stabilized by the NO behavior. We investigated this behavior through a coupled mathematical model of NO transport and the myogenic response. The coupled model is then simulated at baseline, elevated and decreased values of blood pressure for the two cases: with and without NO dynamics (the latter to mimic the case with NO blockade). The results show that as the NO flow dependent system is coupled with the myogenic system, the vessel diameter becomes stable (i.e. oscillations are abolished) for baseline and high pressure values (but not at low pressure), but that it exhibits oscillations at all values of blood pressure without the NO coupling. ? 2010 International Federation for Medical and Biological Engineering.Autoregulationsmyogenic responseNO flow dependent systemPhysiological modelingVasomotionBiomechanicsBiomedical engineeringBiophysicsBloodBlood pressureBlood vesselsComputer simulationMathematical modelsNitric oxideOxygenPhysiologyTechnical presentationsPhysiological modelsAnalysis of the effects of nitric oxide on vasomotionconference paper10.1007/978-3-642-14515-5_2202-s2.0-77958011877