期刊
EXPERIMENTAL PHYSIOLOGY
卷 106, 期 6, 页码 1380-1388出版社
WILEY
DOI: 10.1113/EP089438
关键词
endothelial function; iontophoresis; laser speckle contrast; local heating; skin blood flow; vascular adaptation
类别
资金
- Iowa State University
Remote ischaemic preconditioning (RIPC) induces delayed enhancement in endothelium-dependent cutaneous vasodilatory response, as shown by increased skin microvascular responses to local heating and ACh 24 and 48 hours post-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 degrees 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 (Delta CVC, 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 (Delta CVC, 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 similar to 48 h post-RIPC.
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