Isolated rat mesenteric resistance arteries were mounted in an arteriograph and subjected to pulsatility or not in?vitro. Arteries were perfused with a physiologic salt solution without circulating cells.
After 180 minutes, flow-mediated dilation was higher and pressure-induced myogenic tone lower in arteries subjected to pulsatility. Without pulsatility, reactive oxygen species and markers of inflammation (monocyte chemotactic protein 1 and tumor necrosis factor ¦Á) were higher than baseline. In perfused mesenteric beds under similar conditions, tumor necrosis factor ¦Á was higher in perfusate after 180 minutes of nonpulsatility (5.7 ¡À 1.6 pg/mL vs 1.1 ¡À 0.4 pg/mL; P?<?.01). In arteries treated with the antioxidant 4-hydroxy-2,2,6,6-tetramethylpiperidin-1-oxyl (tempol), flow-mediated dilation and myogenic tone were similar in nonpulsatile and pulsatile arteries; monocyte chemotactic protein 1 and nuclear factor ¦ÊB expression levels were not increased in tempol-treated nonpulsatile arteries.
Absence of pulsatility in resistance arteries increased oxidative stress, which in turn induced inflammation and preferentially altered pressure and flow-dependent tone, which play a key role in control of local blood flow.