Key result
Patients with newly diagnosed, untreated primary hypertension exhibited significantly faster hypoxia-induced NADH accumulation in the skin during early transient ischemia compared to healthy individuals.
Why the study?
To compare dynamic changes in 460-nm forearm skin fluorescence reflecting cellular NADH content during transient ischaemia between healthy individuals and patients with newly diagnosed, untreated essential hypertension.
Do dynamic changes in skin NADH fluorescence during transient ischaemia differ between patients with newly diagnosed untreated essential hypertension and healthy individuals?
Cross-Sectional (n=81)
Do dynamic changes in skin NADH fluorescence during transient ischaemia differ between patients with newly diagnosed untreated essential hypertension and healthy individuals?
Patients with untreated essential hypertension exhibit quicker hypoxia-induced NADH accumulation during skin ischaemia, suggesting impaired protective mechanisms against early cellular hypoxia.
Answers are grounded in this paper and cite their sources.
May indicate early hypoxia vulnerability in untreated hypertension; hypothesis-generating for NADH fluorescence in risk assessment, should not yet change practice.
The reduced form of nicotinamide adenine dinucleotide (NADH) is crucial in cellular metabolism. During hypoxia, NADH accumulation results from anaerobic cytoplasmic glycolysis and impaired mitochondrial function. This study aimed to compare the dynamic changes in the 460-nm forearm skin fluorescence, which reflects cellular NADH content, during transient ischaemia between healthy individuals and patients with newly diagnosed, untreated essential hypertension (HA). Sixteen healthy volunteers and sixty-five patients with HA underwent non-invasive measurement of forearm skin NADH content using the Flow Mediated Skin Fluorescence (FMSF) method at rest and during a 100-s transient ischaemia induced by inflation of the brachial cuff. The fluorescent signal was sampled at 25 Hz. All samples were normalised to the end of the ischaemic phase, which is the most stable phase of the whole recording. Slope values of 1 s linear regressions were determined for every 25-sample neighbouring set. The 1-s slopes in the early phase of skin ischaemia, indicating quicker hypoxia-induced NADH accumulation in skin, were significantly higher in patients with HA than in healthy individuals. These findings suggest that some protecting mechanisms postponing the early consequences of early cellular hypoxia and premature NADH accumulation during skin ischaemia are impaired in patients with untreated HA. Further studies are needed to investigate this phenomenon.
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Pawlak-Chomicka et al. (2023) conducted a cross-sectional in Primary Hypertension (n=81). Primary hypertension vs. Healthy individuals was evaluated on 1-s slopes of 460-nm forearm skin fluorescence linear regression during the early phase of skin ischemia (p=<0.05). Patients with newly diagnosed, untreated primary hypertension exhibited significantly faster hypoxia-induced NADH accumulation in the skin during early transient ischemia compared to healthy individuals.
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