Immunohistochemical evaluation of three nitric oxide synthase isoforms in human saphenous vein exposed to different degrees of distension pressures

Viaro, Fernanda; Capellini, Verena Kise; Celotto, Andréa Carla; Carlotti, Carlos Gilberto; Rodrigues, Alfredo José; Reis, Graziela Saraiva; Augusto, Viviane dos Santos; Évora, Paulo Roberto Barbosa

doi:10.1016/j.carpath.2009.11.002

Cited by 14 publications

(16 citation statements)

References 35 publications

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“…11,17,18 The immunohistochemical data With respect to the immunohistochemical expression of NOS isoforms, positive staining associated with eNOS, iNOS and nNOS was observed in all vein layers and in all groups, confirming the findings of previous studies. 7,13,18,19 In the present study, expression of eNOS in the endothelium was not decreased, confirming the findings of Dalio et al 11 Shear stress in the presence of flow is a stimulus for eNOS endothelial expression, resulting in consequential synthesis and release of NO in the remaining endothelium. 14,15 In addition, expression of eNOS was not reduced in the venous walls of HSVs from non-diabetic patients.…”

Section: The Experimental Modelsupporting

confidence: 91%

Effects of elevated perfusion pressure and pulsatile flow on human saphenous veins isolated from diabetic and non-diabetic patients

Rosique

Tirapelli

et al. 2012

Diabetes and Vascular Disease Research

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Objective: This study was carried out to determine high pressure and pulsatile flow perfusion effects on human saphenous vein (HSV) segments obtained from diabetic and non-diabetic patients. Methods: The veins were perfused with oxygenated Krebs solution for 3 h, with a pulsatile flow rate of 100 mL/ min and pressures of 250 × 200 or 300 × 250 mmHg. After perfusion, veins were studied by light microscopy; nitric oxide synthase (NOS) isoforms, CD34 and nitrotyrosine immunohistochemistry and tissue nitrite/nitrate (NO x ) and malondialdehyde (MDA) quantification. Results: Light microscopy revealed endothelial denuding areas in all HSV segments subjected to 300 × 250 mmHg perfusion pressure, but the luminal area was similar. The percentage of luminal perimeter covered by endothelium decreased as perfusion pressures increased, and significant differences were observed between groups. The endothelial nitric oxide synthase (eNOS) isoform immunostaining decreased significantly in diabetic patients' veins independent of the perfusion pressure levels. The inducible NOS (iNOS), neuronal NOS (nNOS) and nitrotyrosine immunostaining were similar. Significant CD34 differences were observed between the diabetic 300 × 250 mmHg perfusion pressure group and the non-diabetic control group. Tissue nitrite/nitrate and MDA were not different among groups. Conclusions: Pulsatile flow and elevated pressures for 3 h caused morphological changes and decreased the eNOS expression in the diabetic patients' veins.

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Section: The Experimental Modelsupporting

confidence: 91%

Effects of elevated perfusion pressure and pulsatile flow on human saphenous veins isolated from diabetic and non-diabetic patients

Rosique

Tirapelli

et al. 2012

Diabetes and Vascular Disease Research

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“…A study by Viaro et al illustrates that even briefly distending vessels ex vivo with relatively modest pressures can impact the endothelium. Pressurizing human SV at 300 mmHg for as short as 15 s resulted in nearly complete denudation of the endothelium as detected by immunostaining for eNOS [85]. Exposure to 200 mmHg for 15 s decreased endothelial coverage to approximately half of that in unpressurized controls, though these differences did not reach statistical significance [85].…”

Section: Endotheliummentioning

confidence: 98%

“…A number of studies show that pressurization of human SV can denude the endothelium [84][85][86][87][88]. A study by Viaro et al illustrates that even briefly distending vessels ex vivo with relatively modest pressures can impact the endothelium.…”

Section: Endotheliummentioning

confidence: 99%

Biomechanics and Mechanobiology of Saphenous Vein Grafts

Gooch

Firstenberg

Shrefler

et al. 2018

Journal of Biomechanical Engineering

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Within several weeks of use as coronary artery bypass grafts (CABG), saphenous veins (SV) exhibit significant intimal hyperplasia (IH). IH predisposes vessels to thrombosis and atherosclerosis, the two major modes of vein graft failure. The fact that SV do not develop significant IH in their native venous environment coupled with the rapidity with which they develop IH following grafting into the arterial circulation suggests that factors associated with the isolation and preparation of SV and/or differences between the venous and arterial environments contribute to disease progression. There is strong evidence suggesting that mechanical trauma associated with traditional techniques of SV preparation can significantly damage the vessel and might potentially reduce graft patency though modern surgical techniques reduces these injuries. In contrast, it seems possible that modern surgical technique, specifically endoscopic vein harvest, might introduce other mechanical trauma that could subtly injure the vein and perhaps contribute to the reduced patency observed in veins harvested using endoscopic techniques. Aspects of the arterial mechanical environment influence remodeling of SV grafted into the arterial circulation. Increased pressure likely leads to thickening of the medial wall but its role in IH is less clear. Changes in fluid flow, including increased average wall shear stress, may reduce IH while disturbed flow likely increase IH. Nonmechanical stimuli, such as exposure to arterial levels of oxygen, may also have a significant but not widely recognized role in IH. Several potentially promising approaches to alter the mechanical environment to improve graft patency are including extravascular supports or altered graft geometries are covered.

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“…The term endothelial dysfunction has now become synonymous with reduced nitric oxide production [11, 12]. Loss of endothelial nitric oxide production by denudation predisposes to vasospasm, vascular smooth muscle cell proliferation, platelet aggregation, leukocyte migration, and adhesion [13, 14].…”

Section: Introductionmentioning

confidence: 99%

Intimal thickness associated with endothelial dysfunction in human vein grafts

Sexton

Hocking

et al. 2013

Journal of Surgical Research

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Objectives Intimal hyperplasia is a complex process thought to be initiated by injury and is the leading cause of vein graft failure. In this investigation we hypothesized that basal intimal thickness in human saphenous vein is a predictor of endothelial dysfunction and potentially intimal hyperplasia. Methods Human saphenous veins were obtained during coronary artery bypass surgery. The segments were contracted with phenylephrine, and relaxed with carbachol to determine endothelial-dependent relaxation. Vein segments were fixed in 10% buffered formalin, and cultured for 14 days in high serum and then fixed in formalin. The fixed tissues were stained with Verhoeff-Van Gieson and average intimal and medial thicknesses were calculated using light microscopy and a computerized image analysis system. Results Human saphenous veins displayed variable amounts of basal intimal thickness ranging from 18.80 to 241.3 µm. Endothelial-dependent relaxation of the veins was highly variable with values ranging from 0 to 27.59%. Human saphenous vein with basal intimal thickness greater than 120mm had significantly less endothelial-dependent relaxation (8.90±6.32%) than those with basal intimal thickness less than 120mm (21.97±10.64%). Endothelial dysfunction correlated with basal intimal thickness > 120µm (P = 0.02). Basal intimal thickness also correlated with increased intimal thickness after 14 days in organ culture (P=0.0001). Conclusions Basal intimal thickness greater than 120 µm is a predictor of endothelial dysfunction, and since greater basal intimal thickness also correlated with increased intimal thickness after organ culture, basal intimal thickness may predict vein graft failure due to intimal hyperplasia.

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Immunohistochemical evaluation of three nitric oxide synthase isoforms in human saphenous vein exposed to different degrees of distension pressures

Cited by 14 publications

References 35 publications

Effects of elevated perfusion pressure and pulsatile flow on human saphenous veins isolated from diabetic and non-diabetic patients

Effects of elevated perfusion pressure and pulsatile flow on human saphenous veins isolated from diabetic and non-diabetic patients

Biomechanics and Mechanobiology of Saphenous Vein Grafts

Intimal thickness associated with endothelial dysfunction in human vein grafts

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