Non‐invasive in vivo human model of post‐ischaemic skin preconditioning by measurement of flow‐mediated 460‐nm autofluorescence

Abstract

Transient ischaemia and reperfusion (TIAR) induce early ischaemic preconditioning (IPC) in different tissues and organs, including the skin. IPC protects tissues by modifying the mitochondrial function and decreasing the amount of the reduced form of nicotinamide adenine dinucleotide (NADH). Skin 460-nm autofluorescence is proportional to the NADH content and can be non-invasively measured during TIAR. We propose a non-invasive in vivo human model of skin IPC for studying the effects of repeated TIARs on the NADH content.Methods: Fifty-one apparently healthy volunteers (36 women) underwent three 100-second forearm ischaemia episodes induced by inflation of brachial pressure cuff to the pressure of 60 mmHg above systolic blood pressure, followed by 500-second long reperfusion episodes. Changes in skin NADH content were measured using 460-nm fluorescence before and during each of the three TIARs. Results:The first two TIARs caused a significant reduction in the skin NADH content before (P = .0065) and during the third ischaemia (P = .0011) and reperfusion (P = .0003) up to 3.0%. During the third TIAR, the increase in skin NADH was 20% lower than during the first ischaemia (P = .0474). Conclusions: The measurement of the 460-nm fluorescence during repeated TIARs allows for a non-invasive in vivo investigation of human skin IPC. Although IPC reduces the overall NADH skin content, the most noticeable NADH reduction appears during ischaemia after earlier TIARs. Studying the skin model of IPC may provide new avenues for in vivo physiological, clinical and pharmacological research on mitochondrial metabolism.

Investigating the Ischaemic Phase of Skin NADH Fluorescence Dynamics in Recently Diagnosed Primary Hypertension: A Time Series Analysis

“…Transient and controlled ischaemia forces cells to shift into anaerobic metabolism with an increase in lactate and H+ [ 17 , 33 ]. Excessive H+ binds to NAD+ and causes NADH accumulation in mitochondria.…”

“…In brief, FMSF continuously and non-invasively measures the 460-nm fluorescent light emitted by the skin in response to earlier excitation by the 340-nm ultraviolet light. The ultraviolet light does not reach deeper than 0.5 mm from the skin surface, so the FMSF method provides information from the most superficial skin cells [ 12 , 17 , 18 ].…”

The Effect of Antihypertensive Drugs on NADH in Newly Diagnosed Primary Hypertension

“…The method involves a measurement of the intensity of the light emitted by NADH (in the 420–480 nm range) created by initial excitation of particles with an absorption wave (320–380 nm), reaching about 0.3–0.5 mm deep into the skin [ 5 , 16 ]. The measurement is taken on the skin of the forearm at rest, then during short-term controlled ischemia due to complete closure of the brachial artery by the blood pressure cuff and during reperfusion.…”