Contribution of sympathetic nervous system activation to endothelial ischemia reperfusion injury in healthy adults.

Ischemia-reperfusion injury (IRI) describes the phenomenon through which the restoration of blood flow following prolonged ischemia exacerbates tissue damage during reperfusion. IRI can be modeled by inducing 20-min arm ischemia followed by reperfusion. This model causes transient impairments in brachial artery flow mediated dilation (FMD); however, the contribution of the sympathetic nervous system to these reductions remains unknown. We hypothesized that muscle sympathetic nerve activity (MSNA) would increase during IRI and that these increases in MSNA would be associated with decreases in FMD. Twenty healthy adults (11 M/9F) completed a single visit in which brachial artery FMD was measured at rest and following arm IRI. MSNA was measured at rest and during arm ischemia. Changes in brachial artery FMD and MSNA were compared via paired t-tests, and the association between increases in MSNA during ischemia and decreases in FMD following IRI was assessed via Pearson's correlation coefficient analysis. FMD was reduced following IRI (Pre = 7.1 ± 3.2%, Post = 4.6 ± 3.2% p = 0.0001) while MSNA increased slightly (Pre = 15.7 ± 6.3 bursts/min, Post = 19.0 ± 7.4 bursts/min, p = 0.002); however, there was no relationship between increases in MSNA and decreases in FMD (p ≥ 0.21). These findings suggest that while arm IRI increases MSNA in healthy adults, the vascular and sympathetic responses to IRI are not correlated.