Effects of Postprandial Lipemia Combined With Disturbed Blood Flow on the Flow-Mediated Dilation, Oxidative Stress, and Endothelial Microvesicles in Healthy Subjects.

Gustavo S M Araujo,Aline Lopes Dalmazo,Fernanda Marciano Consolim-Colombo,Allan R K Sales,Katia De Angelis,Grazia M Guerra,Amanda Araujo,Natalia G Rocha,Maria C C Irigoyen,Thiago O C Silva,Diego Faria,Helena M N Rocha,João E Izaias

doi:10.3389/fphys.2022.812942

Abstract

AimsBoth postprandial lipemia (PPL) and disturbed blood flow (DBF) induce endothelial dysfunction. However, the interactive effect of these stimuli on endothelial function is currently unknown. In the present study, we tested whether PPL plus DBF causes a greater reduction in flow-mediated dilation (FMD) than PPL and if this response is associated with elevations in oxidative stress and endothelial microvesicles (EMVs).MethodsEighteen individuals (aged 28 ± 1yrs, 3 females, and BMI 24.43 ± 0.8kg/m2) randomly underwent two experimental sessions: PPL and PPL plus DBF. FMD and venous blood samples were obtained at baseline and 30, 70, and 110 min after stimulation. PPL was induced by fat overload via mozzarella pizza ingestion and DBF by forearm cuff inflation to 75 mm Hg per 30 min. Lipidic profile, oxidative stress (thiobarbituric acid reactive substances, TBARS; ferric reducing/antioxidant power, FRAP; hydrogen peroxide, H2O2) and EMVs were measured in blood samples.ResultsHypertriglyceridemia was observed in both sessions. Retrograde shear rate and oscillatory index responses were significantly higher in the PPL plus DBF compared with PPL. PPL plus DBF evoked a greater reduction in FMD than did PPL and EMVs, NADPH oxidase, and H2O2 similarly increased in both sessions, but TBARS and FRAP did not change.ConclusionThese data indicate that the association of PPL plus DBF additively impairs endothelium-dependent function in 110 min after stimulus in healthy individuals, despite a similar increase in oxidative stress and EMVs. Further studies are needed to understand the mechanisms associated with the induced-endothelial dysfunction by association of PPL and DBF.

Highlights

Coronary arterial disease is the main cause of death and reduction in quality of life worldwide, leading to enormous economic consequences (Mathers and Loncar, 2006; Stone et al, 2012)
Postprandial lipidemia-induced vascular endothelial dysfunction is thought to be mediated by oxidative stress resulting from an increased lipid load within the cell, in turn leading to increased oxidative metabolism and excess production of reactive oxygen species (ROS) (Ramírez-Vélez, 2011; Zhao et al, 2021)
The metabolic responses to fat load in both postprandial lipidemia (PPL) and PPL plus DBF sessions are displayed in the Figures 2A–E

Summary

Introduction

Coronary arterial disease is the main cause of death and reduction in quality of life worldwide, leading to enormous economic consequences (Mathers and Loncar, 2006; Stone et al, 2012). It is well known that geometrically irregular arterial regions including bifurcations, branches, and curvatures, which are characterized by low time-average shear stress and high oscillatory blood flow profiles (i.e., disturbed blood flow, DBF), are markedly susceptible to the development of atherosclerosis (Chiu and Chien, 2011; Davies et al, 2013). These findings are supported by cell culture and isolated vessel studies that demonstrate that endothelial injury and pathologic vascular remodeling are induced by DBF. The interactive effect of blood flow disturbances and PPL on endothelial function is currently unknown

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