Delayed window of improvements in skin microvascular function following a single bout of remote ischaemic preconditioning.

NEW FINDINGS What is the central question of this study? Animal infarct studies indicate a delayed window of cardiac protection following remote ischaemic preconditioning (RIPC); however, the presence and duration of this delayed effect have not been examined in the in vivo human microvasculature. What is the main finding and its importance? Local heating- and Ach-induced cutaneous vasodilation was significantly increased 24 and 48 hrs after a single bout of RIPC, respectively. Neither response persisted beyond ∼48 hrs. SNP-induced cutaneous vasodilation was not altered. These findings reveal a delayed increase in microvascular endothelial function following a single bout of RIPC. ABSTRACT Remote ischaemic preconditioning (RIPC) induces protective effects from ischemia-reperfusion (IR) injury. In the myocardium and conduit vasculature, a single bout of RIPC confers delayed protection that begins 24 hours afterward and lasts 2-3 days. However, the extent and the timeline in which a single bout of RIPC affects the human microvasculature is unclear. We hypothesized that a single bout of RIPC results in a delayed increase in skin microvascular function. Sixteen healthy participants (age = 23 ± 4 years, 7 males, 9 females; MAP = 82 ± 7 mmHg) were recruited to measure cutaneous microvascular function immediately prior to a single bout of RIPC and then 24hr, 48hr, 72hr, and a week after the bout. RIPC consisted of 4 repetitions of 5 minutes of arm blood flow occlusion interspersed by 5 minutes reperfusion. Skin blood flow responses to local heating (Tloc = 42°C), acetylcholine (Ach), and sodium nitroprusside (SNP) were measured by laser speckle contrast imaging and expressed as cutaneous vascular conductance (CVC = PU∙mmHg-1 ). Local heating vasodilatation was increased 24 and 48 hours after RIPC (1.05±0.07 vs. 1.18±0.07, 1.24±0.08 PU∙mmHg-1 ; ΔCVC, pre- vs 24, 48 hrs post-RIPC, P<0.05). Ach-induced cutaneous vasodilatation increased significantly 48 hours after RIPC (0.71±0.07 vs. 0.93±0.12 PU∙mmHg-1 ; ΔCVC, pre- vs 48 hrs post-RIPC, P<0.05) and returned to baseline thereafter. SNP-mediated vasodilatation did not change. Thus, a single bout of RIPC elicits a delayed response in the microvasculature, resulting in an improved endothelial-dependent cutaneous vasodilatation response that peaked ∼48 hrs post-RIPC. This article is protected by copyright. All rights reserved.