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Influence of Ischaemia‐Reperfusion Injury on Sensory Nerve Control of Vasodilation During a Subsequent Bout of Local Skin Heating in the Forearm

Cutaneous sensory nerves play a vital role in moderating microcirculatory blood flow by releasing vasodilatory neuropeptides in response to various stimuli including local heating. Ischaemia‐reperfusion (I‐R) injury is associated with altered sensory nerve conduction and depletion of sensory neuropeptide stores, which may contribute to an impaired vasodilatory response to local skin heating following the initial ischemic insult. In ten participants we evaluated the contribution of sensory nerves in driving the vasodilatory response to local heating in forearm skin before and after 20 minutes of ischaemia induced by inflating (220 mmHg) a standard blood pressure cuff around the arm. Red blood cell flux, an index of skin blood flow, was examined using laser‐Doppler probes with integrated local heating units. Flux values were then divided by mean arterial pressure and reported as cutaneous vascular conductance (CVC). Local heating was initiated prior to ischaemia and 20 minutes after the release of cuff occlusion at separate skin sites. At each site local temperature was controlled at 33°C and then increased (3°C min−1) to 42°C and held for ~30 min. Following this, local temperature was increased to 44°C for 20 min. Responses were compared between sites with sensory nerves blocked via local anaesthetic (EMLA) cream and untreated (UNTR) sites before and after I‐R. At UNTR sites, I‐R itself had no effect on CVC during the initial vasodilation (5%; P>0.05). However, relative to the UNTR site before I‐R, EMLA reduced CVC during the initial vasodilation by 45% before ischaemia and 20% after I‐R (both P<0.05). Neither I‐R nor EMLA treatment altered CVC during the secondary plateau at 42°C or at maximum heating to 44°C (all P>0.05). I‐R injury caused a significant delay in vasodilatory onset of 36% (P<0.05) at the UNTR site compared to delays of ~76% at EMLA sites before and after I‐R (both P<0.05). The time to initial vasodilatory peak between UNTR sites was unchanged by I‐R (2%; P>0.05). Conversely, it was significantly delayed by 24% (P<0.05) with EMLA application before I‐R, but not after (17%; P>0.05). We conclude that cutaneous sensory nerve impairment caused by 20 minutes of forearm I‐R injury significantly impairs the kinetics of the response to a rapid, non‐painful local heating stimulus, which may be associated with a higher temperature threshold for initiating vasodilation post‐ischaemia. This alteration of sensory nerve function may contribute to persistent tissue hypoxia and impaired thermoregulatory responses to local skin or whole body heating following an initial ischemic insult if temperature is not adequately controlled.