Comparison of laser-Doppler flowmetry with biochemical indicators of endothelial dysfunction related to early microangiopathy in Type 1 diabetic patients

Biomarkers of oxidative stress and endothelial dysfunction in glucose intolerance and diabetes mellitus

“…In the present study, NAGase activity was significantly higher in GI and DM2 groups in comparison with the controls. Accordingly, previous reports have shown that NAGase activity is increased in DM2 individuals when compared to healthy subjects [45][46][47]. NAGase is a lysosomic glycoproteic enzyme synthesized by various cells, including endothelial cells and smooth muscle cells of blood vessels [17].…”

“…Oxidative stress may damage the endothelial cells from vessels leading to the release of this lysosomic enzyme into the extracellular fluids. Skrha et al [46] showed a high correlation between NAGase activity and either blood flow or brachial artery diameter measurements through doppler ultrasonagraphy, routinely used to evaluate endothelial function. Moreover, it has been demonstrated a positive correlation between NAGase activity, protein glycation and arterial blood pressure in individuals with type 1 DM [48].…”

Risk of Macrovascular Complications in Type 2 Diabetes Mellitus: Endothelial Microparticle Profiles

“…Microalbuminuria and retinal vascular abnormalities are associated with an increased risk of macrovascular events [9,10,11]. Endothelial dysfunction may be estimated clinically by changes in circulation examined by venous plethysmography or laser-Doppler flowmetry, or by determining the levels of biochemical markers and endothelial progenitor cells [12,13,14]. A broader appreciation of endothelial dysfunction can be obtained by study of the levels of direct products of endothelial cells that change when they become activated or apoptotic.…”

Effects of local cooling on sacral skin perfusion response to pressure: Implications for pressure ulcer prevention

“…Increased perfusion after a period of tissue ischemia is a normal physiological response referred to as reactive hyperemia [24]. The response has been used in previous studies to investigate vascular diseases, endothelial dysfunction [25,26], and microvascular function following pharmacological intervention [27]. Several mechanisms are involved in the response, including accumulation of metabolic vasodilators, vascular smooth muscle relaxation [28,29], and response from sensory nerves [27].…”

“…Since little evidence exists to support the use of one time series parameter over another relative to pressure-induced stress or damage [27], we analyzed multiple parameters used in previous studies to characterize this response, including baseline skin blood flow, peak SBF [23,26,29,32], normalized peak SBF [17,31,33], time to peak [17,23,25,26,31,32], and perfusion area [26,29,34].…”