Suppression of Intimal Hyperplasia in a Rabbit Model of Arterial Balloon Injury by Enalaprilat But Not Dimethyl Sulfoxide

1994 ◽  
Vol 8 (2) ◽  
pp. 158-165 ◽  
Author(s):  
Michael M. Law ◽  
Michael D. Colburn ◽  
George E. Hajjar ◽  
Hugh A. Gelabert ◽  
William J. Quiñones-Baldrich ◽  
...  
Keyword(s):  
Dimethyl Sulfoxide ◽  
Intimal Hyperplasia ◽  
Rabbit Model ◽  
Balloon Injury

NO synthesis is involved in structural and functional effects of ACE inhibitors in injured arteries

1996 ◽  
Vol 270 (1) ◽  
pp. H298-H305 ◽  
Author(s):  
E. Van Belle ◽  
B. Vallet ◽  
J. L. Auffray ◽  
C. Bauters ◽  
M. Hamon ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ace Inhibitors ◽  
Intimal Hyperplasia ◽  
Vascular Function ◽  
Ace Inhibitor ◽  
White Male ◽  
Rabbit Model ◽  
Balloon Injury

Angiotensin-converting enzyme (ACE) inhibitors reduce intimal hyperplasia after balloon injury. A role for nitric oxide (NO) has been suggested in this effect. Because recent data suggest that NO may modulate some features of endothelial cells and because endothelial cells are involved in the control of intimal hyperplasia, we investigated the role of NO synthesis in the effect of an ACE inhibitor, perindopril, on neoendothelial dysfunction and intimal hyperplasia in a rabbit model of unilateral iliac balloon injury. New Zealand White male rabbits received placebo, perindopril, or cotreatment with perindopril and NG-nitro-L-arginine methyl ester (L-NAME) and were evaluated 4 wk after the injury. Fifteen rabbits (5 in each group) were used to assess in vitro vasoreactivity and twenty-four (8 in each group) for morphometric analysis. In injured vessels, neoendothelium-dependent relaxation in ACE inhibitor-treated animals was improved compared with placebo (P < 0.05) and restored to the level of noninjured vessels (NS). The improvement observed with ACE inhibitor was abolished by cotreatment with L-NAME (P < 0.05). In the same vessels, no effect was observed on neoendothelium-independent vasoreactivity. The improved neoendothelial dysfunction with ACE inhibitor was associated with a 66% reduction in intimal thickening (P < 0.01). The effect was also reversed by cotreatment with L-NAME (P < 0.01). In noninjured vessels, treatment did not alter vasoreactivity or morphology of the vessel wall. These results suggest that NO synthesis may play a key role in the improvement of vascular function seen with ACE inhibitor in balloon-injured vessels.

scholarly journals Effect of gene delivery of NOS isoforms on intimal hyperplasia and endothelial regeneration after balloon injury

Gene Therapy ◽  
2006 ◽  
Vol 14 (5) ◽  
pp. 396-404 ◽  
Author(s):  
R Cooney ◽  
S O Hynes ◽  
F Sharif ◽  
L Howard ◽  
T O'Brien
Keyword(s):  
Gene Delivery ◽  
Intimal Hyperplasia ◽  
Balloon Injury ◽  
Endothelial Regeneration ◽  
Nos Isoforms

Abstract 117: Heparin Derived Oligosaccharide Inhibits Vascular Intimal Hyperplasia in Balloon Injured Carotid Artery and the Mechanism Involved

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
He Shuying ◽  
Wu Jie
Keyword(s):  
Growth Factor ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Intimal Hyperplasia ◽  
Serum Lipids ◽  
Rabbit Model ◽  
High Cholesterol Diet ◽  
Type I ◽  
Monocyte Chemoattractant Protein 1 ◽  
Expression Levels

To determine the effects of heparin-derived oligosaccharides (HDOs) on vascular intimal hyperplasia (IH) in balloon-injured carotid artery and the mechanism involved. The animal model was established by rubbing the endothelia within the common carotid artery (CCA) of male rabbits along with a high-cholesterol diet. The arterial IH was testified by histopathological changes of the CCA. Serum lipids were detected using automated biochemical analysis; Expression of mRNAs corresponding to vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), vascular cell adhesion molecule-1 (VCAM-1), monocyte chemoattractant protein-1 (MCP-1), scavenger receptor class B type I (SR-BI) and ATP-binding cassette transporter A1 (ABCA-1) were analyzed using reverse transcription polymerase chain reaction assays. Expressions of VEGF, VCAM-1, MCP-1, SR-BI and ABCA-1 proteins were detected by western blotting. Enzyme-linked immunosorbent assays were used to quantify expression levels of VEGF and bFGF. The results implied that administration of HDO significantly inhibited common carotid artery histopathology and restenosis that was induced by balloon injury. Treatment with HDO also significantly decreased mRNA and protein expression levels of VEGF, bFGF, VCAM-1, MCP-1, and SR-BI in the arterial wall, however ABCA-1 expression levels were elevated. HDO treatment led to a reduction in various serum lipids (total cholesterol, triglycerides, high-density and low-density lipoproteins). We concluded that, in a rabbit model, HDO can ameliorate IH and the mechanisms might involved VEGF, bFGF, VCAM-1, MCP-1, SR-BI and ABCA-1.

scholarly journals Ovariectomy and augmentation of intimal hyperplasia after balloon injury of the rat carotid artery

2000 ◽  
Vol 82 ◽  
pp. 191
Author(s):  
Tomoko Ishibashi ◽  
Satoshi Obayashi ◽  
Takeshi Aso ◽  
Hiroshi Azuma
Keyword(s):  
Carotid Artery ◽  
Intimal Hyperplasia ◽  
Balloon Injury

Function and role of voltage-gated sodium channel NaV1.7 expressed in aortic smooth muscle cells

2009 ◽  
Vol 296 (1) ◽  
pp. H211-H219 ◽  
Author(s):  
Kentaro Meguro ◽  
Haruko Iida ◽  
Haruhito Takano ◽  
Toshihiro Morita ◽  
Masataka Sata ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Cells ◽  
Intimal Hyperplasia ◽  
Muscle Cells ◽  
Rt Pcr ◽  
Balloon Injury ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Voltage Gated

Voltage-gated Na+ channel currents ( INa) are expressed in several types of smooth muscle cells. The purpose of this study was to evaluate the expression of INa, its functional role, pathophysiology in cultured human (hASMCs) and rabbit aortic smooth muscle cells (rASMCs), and its association with vascular intimal hyperplasia. In whole cell voltage clamp, INa was observed at potential positive to −40 mV, was blocked by tetrodotoxin (TTX), and replacing extracellular Na+ with N-methyl-d-glucamine in cultured hASMCs. In contrast to native aorta, cultured hASMCs strongly expressed SCN9A encoding NaV1.7, as determined by quantitative RT-PCR. INa was abolished by the treatment with SCN9A small-interfering (si)RNA ( P < 0.01). TTX and SCN9A siRNA significantly inhibited cell migration ( P < 0.01, respectively) and horseradish peroxidase uptake ( P < 0.01, respectively). TTX also significantly reduced the secretion of matrix metalloproteinase-2 6 and 12 h after the treatment ( P < 0.01 and P < 0.05, respectively). However, neither TTX nor siRNA had any effect on cell proliferation. L-type Ca2+ channel current was recorded, and INa was not observed in freshly isolated rASMCs, whereas TTX-sensitive INa was recorded in cultured rASMCs. Quantitative RT-PCR and immunostaining for NaV1.7 revealed the prominent expression of SCN9A in cultured rASMCs and aorta 48 h after balloon injury but not in native aorta. In conclusion, these studies show that INa is expressed in cultured and diseased conditions but not in normal aorta. The NaV1.7 plays an important role in cell migration, endocytosis, and secretion. NaV1.7 is also expressed in aorta after balloon injury, suggesting a potential role for NaV1.7 in the progression of intimal hyperplasia.

scholarly journals 870. NOS Isoforms, Intimal Hyperplasia and Endothelial Regeneration after Balloon Injury

2006 ◽  
Vol 13 ◽  
pp. S335
Author(s):  
Ronan Cooney ◽  
Sean O. Hynes ◽  
Sharif Faisal ◽  
Timothy O'Brien
Keyword(s):  
Intimal Hyperplasia ◽  
Balloon Injury ◽  
Endothelial Regeneration ◽  
Nos Isoforms

Topical application of β-radiation to reduce intimal hyperplasia after carotid artery balloon injury in rabbit

2002 ◽  
Vol 3 (1) ◽  
pp. 16-19 ◽  
Author(s):  
David Rosenthal ◽  
Scott L Stevens ◽  
C.S Skillern ◽  
Eric D Wellons ◽  
Keith Robinson ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Topical Application ◽  
Intimal Hyperplasia ◽  
Balloon Injury

scholarly journals Cilostazol as a noninferiority pharmacologic option to paclitaxel in early intimal hyperplasia inhibition after venous balloon angioplasty in a rabbit model: a preliminary study

2020 ◽  
Vol 1 ◽  
pp. 200-206
Author(s):  
Rodrigo Lozano-Corona ◽  
Hugo Laparra-Escareno ◽  
Javier E. Anaya-Ayala ◽  
Alejandro Zentella-Dehesa ◽  
Jesus J. Baquera-Heredia ◽  
...  
Keyword(s):  
Balloon Angioplasty ◽  
Intimal Hyperplasia ◽  
Rabbit Model ◽  
Preliminary Study
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