Coupling arterial windkessel with peripheral vasomotion: modeling the effects on low-frequency oscillations.
Arterial pressure (AP) and heart rate (HR) waves have long been recognized as an important sign of cardiovascular regulation, however, the underlying interactions involving vasomotion, arterial mechanisms and neural regulation have not been clarified. With the aid of simple dynamical models consisting of active peripheral vascular districts (PVDs) fed by a compliant/resistant arterial tree, the relationship between local AP and flow and systemic AP waves were analyzed. A PVD was described as a nonlinear flow regulation loop. Various feedback dynamics were experimented and general properties were focused. The PVDs displayed a region of active flow compensation against pressure changes, in which self-sustained low-frequency (LF, 0.1 Hz) appeared. Oscillations critically depended on parameter, Teq, analogous to a windkessel time constant, proportional to arterial compliances: a value of about 2 s (consistent with a normal pulse pressure) performed a buffering effect essential for LF oscillations in peripheral flow; conversely, stiffer arteries damped LF vasomotion. Two PVDs fed by a common compliance oscillated in phase opposition; the consequent negative interference cancelled systemic AP waves, even in presence of large peripheral oscillations. The partial disruption of phase opposition by a common neural drive oscillating at a LF proximal to that of the PVDs unveiled LF waves in AP. Also, several PVDs with randomly different natural frequencies displayed a tendency to reciprocal cancellation, while a limited neurally induced phase alignment unmasked LF oscillations at systemic level. It is concluded that vasomotion, arterial compliances and, neural drives are all elements which may cooperate in forming AP waves.