Effect of hypercholesterolemia on transendothelial EBD–albumin permeability and lipid accumulation in porcine iliac arteries

LaMack, Jeffrey A.; Himburg, Heather A.; Friedman, Morton H.

doi:10.1016/j.atherosclerosis.2005.04.020

Cited by 9 publications

(7 citation statements)

References 36 publications

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“…In agreement with our observation, LaMack et al . indicated that endothelial permeability to albumin in hypercholesterolemic pigs was higher than in those on a normal diet [18]. Our results indicate that acidosis increased aortic endothelial permeability in animals with a normal diet, but did not further increase endothelial permeability in the hypercholesterolemic group.…”

Section: Discussionmentioning

confidence: 47%

Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Khazaei¹,

Nematbakhsh²

2012

aoms

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IntroductionMetabolic acidosis is present in end stage renal disease. There is a link between enhanced endothelial permeability and accelerated atherosclerosis. In this study, we investigated the effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide (NO) concentration in normal and high-cholesterol fed rabbits.Material and methodsTwenty-four male rabbits were divided into four groups: normal, hypercholesterolemic, acidemic, and hypercholesterolemic plus acidemic. Acidosis and hypercholesterolemia were induced by drinking water containing ammonium chloride (NH4Cl), and cholesterol-rich animal chow (1%), respectively. After 6 weeks, blood samples were taken and endothelial permeability was measured using the Evans blue dye injection method.ResultsHypercholesterolemic animals had higher aortic endothelial permeability compared with normal groups (16.18 ±0.91 µg EB/g tissue vs. 12.89 ±0.66 µg EB/g tissue, p < 0.05). Acidosis significantly increased endothelial permeability in the normal group (17.10 ±0.56 µg/g tissue vs. 12.89 ± 0.66 µg/g tissue; p < 0.05) but did not further increase endothelial permeability in hypercholesterolemic animals (16.18 ±0.91 µg EB/g tissue vs. 17.29 ±0.46 µg EB/g tissue; p > 0.05). Serum total cholesterol, low density lipoprotein (LDL) and NO concentrations in hypercholesterolemic animals were significantly higher than the normal group and acidosis could not change them either in the normal or in the high-cholesterol diet group.ConclusionsAlterations of serum lipids and NO are not the main mechanism for accelerated atherosclerosis during metabolic acidosis. Acidosis increases aortic endothelial permeability at least in a normal diet which may be a possible mechanism for progression of atherosclerosis processes in end-stage renal disease.

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Section: Discussionmentioning

confidence: 47%

Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Khazaei¹,

Nematbakhsh²

2012

aoms

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“…Furthermore, experimental data support the relationship between LDL concentration and endothelial permeability (43), whereas a highfat diet in swine has been shown to increase the endothelial permeability compared with that in animals fed a normal diet (20). Conversely, small alterations of endothelial permeability have a great effect on LDL endothelial uptake (53,56).…”

Section: Discussionmentioning

confidence: 86%

Patient-specific computational modeling of subendothelial LDL accumulation in a stenosed right coronary artery: effect of hemodynamic and biological factors

Sakellarios

Papafaklis

Siogkas

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Atherosclerosis is a systemic disease with local manifestations. Low-density lipoprotein (LDL) accumulation in the subendothelial layer is one of the hallmarks of atherosclerosis onset and ignites plaque development and progression. Blood flow-induced endothelial shear stress (ESS) is causally related to the heterogenic distribution of atherosclerotic lesions and critically affects LDL deposition in the vessel wall. In this work we modeled blood flow and LDL transport in the coronary arterial wall and investigated the influence of several hemodynamic and biological factors that may regulate LDL accumulation. We used a three-dimensional model of a stenosed right coronary artery reconstructed from angiographic and intravascular ultrasound patient data. We also reconstructed a second model after restoring the patency of the stenosed lumen to its nondiseased state to assess the effect of the stenosis on LDL accumulation. Furthermore, we implemented a new model for LDL penetration across the endothelial membrane, assuming that endothelial permeability depends on the local lumen LDL concentration. The results showed that the presence of the stenosis had a dramatic effect on the local ESS distribution and LDL accumulation along the artery, and areas of increased LDL accumulation were observed in the downstream region where flow recirculation and low ESS were present. Of the studied factors influencing LDL accumulation, 1) hypertension, 2) increased endothelial permeability (a surrogate of endothelial dysfunction), and 3) increased serum LDL levels, especially when the new model of variable endothelial permeability was applied, had the largest effects, thereby supporting their role as major cardiovascular risk factors.

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“…After injection, practically all Evans blue binds to albumin and as a result only enters the vessel wall and perivascular area if there is a defect endothelial barrier [15-17]. In this study, the dye was used to ease the localization of the balloon-injured LAD segment and to macroscopically confirm that the balloon injury had caused increased vessel wall permeability.…”

Section: Methodsmentioning

confidence: 99%

CMR Assessment of endothelial damage and angiogenesis in porcine coronary arteries using gadofosveset

Pedersen

Thrysøe

Paaske

et al. 2011

Journal of Cardiovascular Magnetic Resonance

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BackgroundEndothelial damage and angiogenesis are essential for atherosclerotic plaque development and destabilization. We sought to examine whether contrast enhanced cardiovascular magnetic resonance (CMR) using gadofosveset could show endothelial damage and neovessel formation in balloon injured porcine coronary arteries.Methods and ResultsData were obtained from seven pigs that all underwent balloon injury of the left anterior descending coronary artery (LAD) to induce endothelial damage and angiogenesis. Between one - 12 days (average four) after balloon injury, in vivo and ex vivo T1-weighted coronary CMR was performed after intravenous injection of gadofosveset. Post contrast, CMR showed contrast enhancement of the coronary arteries with a selective and time-dependent average expansion of the injured LAD segment area of 45% (p = 0.04; CI95 = [15%-75%]), indicating local extravasation of gadofosveset. Vascular and perivascular extravasation of albumin (marker of endothelial leakiness) and gadofosveset was demonstrated with agreement between Evans blue staining and ex vivo CMR contrast enhancement (p = 0.026). Coronary MRI contrast enhancement and local microvessel density determined by microscopic examination correlated (ρ = 0.82, p < 0.001).ConclusionContrast enhanced coronary CMR with gadofosveset can detect experimentally induced endothelial damage and angiogenesis in the porcine coronary artery wall.

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Effect of hypercholesterolemia on transendothelial EBD–albumin permeability and lipid accumulation in porcine iliac arteries

Cited by 9 publications

References 36 publications

Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Experimental research Effect of experimentally induced metabolic acidosis on aortic endothelial permeability and serum nitric oxide concentration in normal and high-cholesterol fed rabbits

Patient-specific computational modeling of subendothelial LDL accumulation in a stenosed right coronary artery: effect of hemodynamic and biological factors

CMR Assessment of endothelial damage and angiogenesis in porcine coronary arteries using gadofosveset

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