[The adventitia reduces left ventricular dynamic afterload via smooth muscle activation-dependent mechanisms]

Ventricular dynamic afterload depends on arterial viscoelastic and geometric properties. Vasoactive factors produced in the adventitia modulate arterial tone. However, it is still not known whether the adventitia is involved in determining the magnitude of the dynamic afterload. The aim of this study was to investigate the role played by the adventitia, via smooth muscle-dependent mechanisms, in determining dynamic afterload.

The diameter, pressure and flow in brachiocephalic trunks from sheep were measured before and after removal of the adventitia, both in vivo with muscular reactivity preserved (n=8) and in vitro with muscular reactivity abolished (n=8). All studies were performed under similar hemodynamic conditions. Dynamic afterload was determined from elastic and viscous arterial responses, elastic and viscous work, arterial characteristic impedance, and pulse wave velocity. Comparison of in vivo and in vitro findings enabled smooth muscle-dependent changes to be evaluated.

Only in vivo, did removal of the adventitia lead to a reduction in vessel diameter (17.32 [2.02] vs 15.46 [1.28] mm) and to increases in elastic (7.21 [1.39] vs 15.59 [3.00] x 10(6) dyn.cm(-2)) and viscous (5.16 [2.04] vs 9.87 [2.00] x 10(5) dyn.s.cm(-2)) arterial responses, elastic (6.15 [1.08] vs 9.20 [0.76] x 10(-2) J/m2) and viscous work (11.61 [2.25] vs 15.20 [2.37] x 10(-3) J/m2), impedance (223.97 [136.11] vs 396.33 [182.27] dyn x s x cm(-3)), and pulse wave velocity (397.70 [31.21] vs 598.78 [28.04] cm.s(-1)) (P<.05). The reduction in diameter and the increases in elastic and viscous responses are evidence of muscular activation.

The adventitia may contribute to the control of ventricular dynamic afterload by means of mechanisms dependent on muscular tone.