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

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 [28 years (standard deviation:6)], volar forearm skin blood flux normalized to maximum vasodilation (%SkBF_max) 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·20 s^-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%SkBF_max ([9,33]; p = 0.003), delayed time to peak by 111 s ([40,182]; p = 0.007) and increased area under the curve by 19,462%SkBF_max·s ([11,346,27,579]; p < 0.001) compared to CTRL. For LTH, EMLA delayed onset time by 76 s ([46,106]; p < 0.001) Pre-IR and by 46 s ([27,65]; p < 0.001) Post-IR compared to CTRL. Post-IR onset time was delayed for CTRL by 26 s ([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 24 s ([4,43]; p = 0.022, Main time effect) and it attenuated the initial peak by 27%SkBF_max ([12,43]; p = 0.002) Pre-IR and by 16%SkBF_max ([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%SkBF_max ([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.