The cutaneous vasculature is an accessible tissue that can be used to assess microvascular function in humans. Intradermal microdialysis is a minimally invasive technique used to investigate mechanisms of vascular smooth muscle and endothelial function in the cutaneous circulation. This technique allows for the pharmacological dissection of the pathophysiology of microvascular endothelial dysfunction as indexed by decreased nitric oxide-mediated vasodilation, an indicator of cardiovascular disease development risk. In this technique, a microdialysis probe is placed in the dermal layer of the skin, and a local heating unit with a laser Doppler flowmetry probe is placed over the probe to measure the red blood cell flux. The local skin temperature is clamped or stimulated with direct heat application, and pharmacological agents are perfused through the probe to stimulate or inhibit intracellular signaling pathways in order to induce vasodilation or vasoconstriction or to interrogate mechanisms of interest (co-factors, antioxidants, etc.). The cutaneous vascular conductance is quantified, and mechanisms of endothelial dysfunction in disease states can be delineated.
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Quantification and interpretation of nitric oxide-dependent cutaneous vasodilation during local heating.
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Department of Health and Human Physiology, The University of Iowa, Iowa City, Iowa, United States.
Human cutaneous microdialysis approaches for assessing nitric oxide (NO)-dependent blood flow include local heating (LH) of the skin until a plateau is reached, followed by infusion of a NO synthase inhibitor such as -nitro-l-arginine methyl ester (l-NAME); however, varied methods of quantifying and expressing NO-dependent vasodilation can obfuscate data interpretation and reproducibility. We retrospectively assessed NO-dependent vasodilation during LH to 39°C or 42°C, calculated as the ) absolute contribution of the NO-dependent component (along with baseline and the non-NO-dependent component) to the total cutaneous vascular conductance (CVC) response to LH, normalized to maximal CVC (%CVC); ) difference in %CVC (Δ%CVC) between the LH plateau and post-NO synthase inhibition (l-NAME plateau; Δ%CVC = LH plateau - l-NAME plateau); ) percentage of the LH plateau attributable to Δ%CVC (%plateau = Δ%CVC/LH plateau × 100); and ) %plateau when correcting for baseline. The LH plateaus during 39°C and 42°C were 48 ± 17%CVC (9 ± 5% baseline; 2 ± 4% non-NO dependent; 36 ± 15% NO dependent) and 88 ± 10%CVC (15 ± 8% baseline; 9 ± 10% non-NO dependent; 64 ± 13% NO dependent), respectively.
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December 2024
Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada.
We evaluated reactive oxygen species (ROS) modulation of cutaneous vasodilation during local and whole body passive heating in young and older adults. Cutaneous vascular conductance normalized to maximum vasodilation (%CVC) was assessed in young and older adults (10/group) using laser-Doppler flowmetry at four dorsal forearm sites treated with ) Ringer solution (control), ) 100 µM apocynin (NADPH oxidase inhibitor), ) 10 µM allopurinol (xanthine oxidase inhibitor), or ) 10 µM tempol (superoxide dismutase mimetic), via intradermal microdialysis during local () and whole body heating (). In , forearm skin sites were set at 33°C during baseline and then progressively increased to 39°C and 42°C (30 min each).
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Noll Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, United States.
The transcriptional regulator nuclear factor-κB (NF-κB) is a mediator of endothelial dysfunction. Inhibiting NF-κB with salsalate is used to investigate inflammatory mechanisms contributing to accelerated cardiovascular disease risk. However, in the absence of disease, inhibition of NF-κB can impact redox mechanisms, resulting in paradoxically decreased endothelial function.
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Institue of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8574, Japan.
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