Differential effects of wave reflections and peripheral resistance on aortic blood pressure: a model-based study.
It has been generally accepted that arterial system wave reflections act to increase aortic blood pressure and the load placed on the left ventricle. Using a mathematical model of the coupled left ventricle-arterial system, we predict that this is not the case. With the model, two aspects of wave reflection, the global reflection coefficient [TG(omega)] and the pulse wave velocity (cph), were adjusted independently. In addition, TG(omega) and cph could be altered independently of the direct-current properties of the arterial system model. Reduction of TG(omega) yielded increases in stroke volume (SV) as well as in peak systolic (Ps), diastolic (Pd), and mean aortic (Pao) pressures and, hence, increased the load on the left ventricle. SV and Pao increased only in the range where strong reflection occurs. Reduced cph also yielded higher pressures, whereas increased cph resulted in reduced Pao and Pd but increased Ps. The changes in pressures and SV in response to altered TG(omega) and cph were relatively small compared with absolute levels. Simulated vasoconstriction and vasodilation further demonstrated the much greater importance of peripheral resistance on pressure and SV levels and lead to the prediction that pressure reduction in vasodilation occurs not because of, but in spite of, reduced wave reflections. We conclude that these results have not yet been observed experimentally, because reflection cannot yet be separated from the direct-current properties of the arterial system; therefore wave reflections themselves have not yet been adequately studied in the intact animal.
Berger
D S
DS
Department of Biomedical Engineering, Rutgers University, Piscataway, New Jersey 08855.
Li
J K
JK
Noordergraaf
A
A
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology*; D001783:Blood Flow Velocity; D001794:Blood Pressure; D006801:Humans; D008729:Methoxamine / Q000494:pharmacology; D008955:Models, Cardiovascular; D009599:Nitroprusside / Q000494:pharmacology; D011673:Pulsatile Flow; D013318:Stroke Volume; D014655:Vascular Resistance; D014661:Vasoconstriction; D014664:Vasodilation
D009599:Nitroprusside; D008729:Methoxamine