Smart smooth muscle spring-dampers

Abstract

Pulsatile pressure in arteries produces mechanical oscillations. Highfrequency vibrations tend to produce mechanical structure injures. Vascular smooth muscle (VSM) could react modulating viscoelasticity to protect the arterial wall, filtering the highest harmonics component present in the large and rapid slope of blood pressure. The aim of this study was to evaluate the filtering performance exerted by VSM in the human common carotid artery (CCA) in normotensive (NT, smart springdampers turned on), hypertensive (HT, smart spring-dampers in action) and angiotensin converting enzyme (ACE) inhibitors-treated hypertensive patients (HT-treated, smart spring-dampers tuned), and in harvested human CCA segments (smart spring-dampers turned off). Human carotid arteries in vitro experiments (n = 14) and in vivo studies (n = 24) were performed, using adaptive modeling techniques to calculate mechanical impedance and creep (τC) and stress relaxation (τSR) time constants. This adaptive procedure was tested in vitro in harvested CCA mounted in a circulation mock. A confirmatory measure of damping was achieved by using the half-power bandwidth method ( fC) derived from the pressure-diameter frequency dependence using Bode diagrams, i.e., a compliance transfer function (diameter/pressure). Energy dissipation was calculated from the imaginary part of this function. Low-pass frequency responses were verified with a flat plateau up to a relatively stable frequency corner fC in the Bode diagram of the complete third-order model. Simplified first-order model cutoff frequencies were 2.7, 2.8, and 3.0 Hz for NT, HT, and HT-treated, respectively, showing an interesting constancy between groups. Smooth muscle tonus proved to preserve fC as well as τC. Energy dissipation in hypertensive patients (n = 12) three-folded NT values and tended to be restored in HT-treated by means of a decrease in τSR. VSM acts as smart spring-dampers, dissipating high-frequency components that might have damaging effects. VSM alterations found in HT patients could have a mandatory directive of preserving dynamic range near NT values, suggesting that VSM modulates its degree of activation and/or the vessel wall remodeling in order to ensure a suitable protection role.