Effects of sensory nerve blockade on cutaneous microvascular responses to ischemia-reperfusion injury.

Abstract

Examine the effects of sensory nerve blockade on cutaneous post-occlusive reactive hyperemia (PORH) and local thermal hyperemia (LTH) following prolonged upper limb ischemia. In nine males [28years (standard deviation:6)], volar forearm skin blood flux normalized to maximum vasodilation (%SkBFmax) was assessed at control (CTRL) and sensory nerve blockade (EMLA) treated sites during the PORH response following 20-min of complete arm ischemia and during rapid LTH (33-42°C, 1°C·20s-1, held for ~30-min+20-min at 44°C) before and after ischemia-reperfusion (IR) injury. EMLA increased mean [95% confidence-interval] PORH amplitude by 21%SkBFmax ([9,33]; p=0.003), delayed time to peak by 111s ([40,182]; p=0.007) and increased area under the curve by 19,462%SkBFmax·s ([11,346,27,579]; p<0.001) compared to CTRL. For LTH, EMLA delayed onset time by 76s ([46,106]; p<0.001) Pre-IR and by 46s ([27,65]; p<0.001) Post-IR compared to CTRL. Post-IR onset time was delayed for CTRL by 26s ([8,43]; p=0.007), but was not different for EMLA (p>0.050) compared to Pre-IR. EMLA delayed time to initial peak by 24s ([4,43]; p=0.022, Main time effect) and it attenuated the initial peak by 27%SkBFmax ([12,43]; p=0.002) Pre-IR and by 16%SkBFmax ([3,29]; p=0.020) post-IR compared to CTRL. Post-IR, the initial peak was not different for CTRL (p>0.050), but it was increased by 16%SkBFmax ([5,26]; p=0.005) for EMLA compared to Pre-IR. Neither EMLA nor IR altered the steady-state heating plateau (all p>0.050). For the current model of IR injury, sensory nerves appear to have a negligible influence on the LTH response in non-glabrous forearm skin once vasodilation has been initiated.