Lumped Parameter Outflow Models for 1-D Blood Flow Simulations:Effect on Pulse Waves and Parameter Estimation

Several lumped parameter,or zero-dimensional(0-D),models of the microcirculation are coupled in the time domain to the nonlinear,one-dimensional(1-D)equations of blood flow in large arteries.A linear analysis of the coupled system,together with in vivo observations,shows that:(i)an inflow resistance that matches the characteristic impedance of the terminal arteries is required to avoid non-physiological wave reflections;(ii)periodic mean pressures and flow distributions in large arteries depend on arterial and peripheral resistances,but not on the compliances and inertias of the system,which only affect instantaneous pressure and flow waveforms;(iii)peripheral inertias have a minor effect on pulse waveforms under normal conditions;and(iv)the time constant of the diastolic pressure decay is the same in any 1-D model artery,if viscous dissipation can be neglected in these arteries,and it depends on all the peripheral compliances and resistances of the system.Following this analysis,we propose an algorithm to accurately estimate peripheral resistances and compliances from in vivo data.This algorithm is verified against numerical data simulated using a 1-D model network of the 55 largest human arteries,in which the parameters of the peripheral windkessel outflow models are known a priori.Pressure and flow waveforms in the aorta and the first generation of bifurcations are reproduced with relative root-mean-square errors smaller than 3%.

Plasma Neuropeptide Y Levels in Vasovagal Syncope in Children

Background： Vasovagal syncope （VVS） is the most common cause of syncope in children. Neuropeptide Y （NPY） plays an important role in the regulation of blood pressure （BP）, as well as myocardial contractility. This study aimed to explore the role of plasma NPY in VVS in children. Methods： Fifty-six children who were diagnosed with VVS （VVS group） using head-up tilt test （HUT） and 31 healthy children who were selected as controls （control group） were enrolled. Plasma NPY concentrations were detected. The independent t-test was used to compare the data of the VVS group with those of the control group. The changes in plasma NPY levels in the VVS group during the HUT, as well as hemodynamic parameters, such as heart rate （HR）, BP, total peripheral vascular resistance （TPVR）, and cardiac output （CO）, were evaluated using the paired t-test. Furthermore, the correlations between plasma NPY levels and hemodynamic parameters were analyzed using bivariate correlation analysis. Results： The BP, HR, and plasma NPY （0.34 ± 0.12 pg/ml vs. 0.46 ± 0.13 pg/ml） levels in the supine position were statistically low in the VVS group compared to levels in the control group （all P 〈 0.05）. Plasma NPY levels were positively correlated with the HR （Pearson, R = 0.395, P 〈 0.001） and diastolic BP （Pearson, R = 0.311, P = 0.003） when patients were in the supine position. When patients in the VVS group were in the supine position, elevated TPVR （4.6 ± 3.7 mmHg·min-1·L-1 vs. 2.5 ± 1.0 mmHg·min-1·L-1, respectively, P 〈 0.001;1 mmHg = 0.133 kPa） and reduced CO （1.0 ± 0.7 L/min vs. 2.4 ± 1.3 L/min, respectively, P 〈 0.001） were observed in the positive-response period compared with baseline values. The plasma NPY levels were positively correlated with TPVR （Spearman, R = 0.294, P = 0.028） but negatively correlated with CO in the positive-response period during HUT （Spearman, R = -0.318, P = 0.017）. Conclusions： Plasma NPY may contribute to the pathogenesis of VVS by increasing the TPVR and decreasing the CO during orthostatic regulation.