IN-VIVO IN-VITRO COMPARISON OF RAT ABDOMINAL-AORTA WALL VISCOSITY - INFLUENCE OF ENDOTHELIAL FUNCTION

Arterial wall viscosity (AWV) is a potential source of energy dissipat ion in circulation. That arteries, which are known to be markedly visc ous in vitro, have lower viscosity in vivo has been suggested but not demonstrated under similar pressure conditions. Endothelium, which may modulate AWV through smooth muscle tone, could contribute to the low level of viscosity in vivo. Our objectives were first to compare AWV o f the rat abdominal aorta, in vivo and In vitro, with similar pulse-pr essure waves, and second, to determine whether endothelial function in fluences AWV in vivo and in vitro. The diameter of the abdominal aorta and distending pressure were measured in vivo and in vitro with a hig h-resolution echotracking system and a micromanometer, respectively. A WV was calculated as the area of the pressure-volume curve hysteresis. After in vivo examination, the arterial segments were isolated in vit ro and submitted to resynthesized pressure waves identical to those re corded in vivo. Deendothelialization was performed in vivo by balloon rubbing; then arteries were examined either in vivo or in vitro. AWV w as markedly lower in vivo than in vitro (6.6 +/- 0.7 versus 22.7 +/- 3 .7 J . m(-1) . 10(-5), respectively; P<.001). After deendothelializati on, a sustained 40% increased AMV was observed during a 15-minute foll ow-up (P<.01). In vitro, deendothelialized arteries have a 64% higher AWV than segments with endothelium (P<.01). Our results indicate that the physiological effective viscosity, measured in vivo in intact anim als, is threefold lower than the intrinsic viscosity of the arterial w all, measured in vitro. Endothelium removal determines a sustained inc rease in AWV, either in vivo or in vitro. These results suggest that a ctive mechanisms compensate for intrinsic viscosity under physiologica l conditions. One of these energy-saving mechanisms might be dependent on normal endothelial function.