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

What is the central question of this study? Animal infarct studies indicate a delayed window of cardiac protection after remote ischaemic preconditioning (RIPC); however, the presence and duration of this delayed effect have not been examined in human microvasculature in vivo. What is the main finding and its importance? Cutaneous vasodilatation induced by local heating or ACh was increased significantly 24 and 48 h after a single bout of RIPC, respectively. Neither response persisted beyond ∼48 h. Sodium nitroprusside-induced cutaneous vasodilatation was not altered. These findings reveal a delayed increase in microvascular endothelial function after a single bout of RIPC.

Remote ischaemic preconditioning (RIPC) induces protective effects from ischaemia-reperfusion injury. In the myocardium and conduit vasculature, a single bout of RIPC confers delayed protection that begins 24 h afterwards and lasts for 2-3 days. However, the extent and the time line in which a single bout of RIPC affects the human microvasculature are 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; seven males, nine females; MAP, 82 ± 7 mmHg) were recruited to measure cutaneous microvascular function immediately before a single bout of RIPC and 24, 48 and 72 h and 1 week after the bout. The RIPC consisted of four repetitions of 5 min of arm blood flow occlusion interspersed by 5 min reperfusion. Skin blood flow responses to local heating (local temperature of 42°C), ACh and sodium nitroprusside were measured by laser speckle contrast imaging and expressed as the cutaneous vascular conductance (CVC; in perfusion units per millimetre of mercury). Vasodilatation in response to local heating was increased 24 and 48 h after RIPC (ΔCVC, 1.05 ± 0.07 vs. 1.18 ± 0.07 and 1.24 ± 0.08 PU mmHg^-1 , pre- vs. 24 and 48 h post-RIPC; P < 0.05). Acetylcholine-induced cutaneous vasodilatation increased significantly 48 h after RIPC (ΔCVC, 0.71 ± 0.07 vs. 0.93 ± 0.12 PU mmHg^-1 , pre- vs. 48 h post-RIPC; P < 0.05) and returned to baseline thereafter. Sodium nitroprusside-mediated vasodilatation did not change. Thus, a single bout of RIPC elicited a delayed response in the microvasculature, resulting in an improvement in the endothelium-dependent cutaneous vasodilatory response that peaked ∼48 h post-RIPC.