Key result
Mathematical models of nitric oxide diffusion and convection predict much lower NO values than in vivo experimental measurements in the microcirculation.
This review highlights the discrepancies between mathematical models and experimental measurements of nitric oxide in the microcirculation, emphasizing the need to better understand NO signaling and storage mechanisms.
Discrepancies between NO models and measurements caution against overreliance on current simulations in vascular research; leaves open NO storage and signaling mechanisms for further study.
Several apparent paradoxes are evident when one compares mathematical predictions from models of nitric oxide (NO) diffusion and convection in vasculature structures with experimental measurements of NO (or related metabolites) in animal and human studies. Values for NO predicted from mathematical models are generally much lower than in vivo NO values reported in the literature for experiments, specifically with NO microelectrodes positioned at perivascular locations next to different sizes of blood vessels in the microcirculation and NO electrodes inserted into a wide range of tissues supplied by the microcirculation of each specific organ system under investigation. There continues to be uncertainty about the roles of NO scavenging by hemoglobin versus a storage function that may conserve NO, and other signaling targets for NO need to be considered. This review describes model predictions and relevant experimental data with respect to several signaling pathways in the microcirculation that involve NO.
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Buerk et al. (2011) conducted a review in Nitric oxide signaling in the microcirculation. Nitric oxide was evaluated. Mathematical models of nitric oxide diffusion and convection predict much lower NO values than in vivo experimental measurements in the microcirculation.
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