Indexes from a parametric model of the interactions between heart period and arterial pressure variabilities

A linear model for the evaluation of causal interactions between heart period (HP) and systolic arterial pressure (SAP) variabilities was applied to experimental data from conscious dogs and clinical data from mild hypertensive subjects. The structure of the model is designed in order to identify the source of low frequency (LF) spontaneous oscillations and the pathways conveying respiratory effects on the variabilities at high frequency (HF); in the meanwhile mechanical as well as baroreceptive mechanisms are evaluated. Different mechanisms coexist in the generation of both rhythms. LF is enhanced by arterial pressure (AP) regulation, but different sources affect the sinus node during coronary artery occlusion (CAO). A respiration to HP pathway is prevalent in dogs, while a respiration to SAP pathway is important in humans and is enhanced in dogs during sympathetic stimuli.