Changes in the plasma concentration of soluble thrombomodulin in patients with severe carotid artery stenosis after eversion endarterectomy

Dósa, Edit; Szabó, Attila; Prohászka, Zoltán; Karádi, István; Rugonfalvi-Kiss, Szabolcs; Apor, Astrid; Járányi, Zsuzsanna; Hüttl, Kálmán; Selmeci, L.; Acsády, György; Füst, George; Entz, László

doi:10.1007/s00011-005-1354-9

Inflamm. res.

2005

DOI: 10.1007/s00011-005-1354-9

|View full text |Cite

Changes in the plasma concentration of soluble thrombomodulin in patients with severe carotid artery stenosis after eversion endarterectomy

Edit Dósa

Attila Szabó

Zoltán Prohászka

et al.

Abstract: Our present findings indicate that sTM may be adsorbed to the atherosclerotic plaques or inflamed endothelium in carotid arteries. The pathological significance of this adsorption remains to be determined.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2009

Publication Types

Select...

Article3

Relationship

Self Cite0

Independent3

Authors

Journals

Cited by 3 publications

(2 citation statements)

References 31 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Risk factors for early restenosis include alterations in the complement system, 2 increased serum growth factor levels, 3 or changes in the hemostatic factors. 4 Ischemia-reperfusion injury and endothelial damage promote neointima formation. In contrast with early restenosis, late restenosis is due to the progression of primary atherosclerosis.…”

mentioning

confidence: 99%

Selective phosphodiesterase-5 inhibition reduces neointimal hyperplasia in rat carotid arteries after surgical endarterectomy

Hirschberg¹,

Radovits²,

Loganathan³

et al. 2009

Thorac cardiovasc Surg

View full text Add to dashboard Cite

Objective: Long-term results of surgical vessel reconstruction are compromised by restenosis caused by neointimal hyperplasia. Recent studies suggest that reduced cyclic guanosine monophosphate signaling is associated with neointima formation. In a rat model of endarterectomy, we investigated the effect of pharmacologic inhibition of cyclic guanosine monophosphate degradation on neointima formation by using the selective phosphodiesterase-5 inhibitor vardenafil.Methods: Carotid endarterectomy was performed in male Sprague-Dawley rats by means of incision of the right common carotid artery with removal of intima. Four groups were studied: unoperated control rats (n ¼ 4), shamoperated rats (n ¼ 9), control rats with endarterectomy (n ¼ 9), or endarterectomized rats treated with vardenafil (10 mg/kg/day) postoperatively (n ¼ 9). After 3 weeks, vessel compartment areas were measured by means of conventional microscopy with hematoxylin and eosin staining. Immunohistochemical analysis was performed to confirm neointima formation and the local cyclic guanosine monophosphate content. Plasma levels of cyclic guanosine monophosphate were determined by means of enzyme immunoassay. Student's t test was used for statistical evaluation.Results: Immunohistochemical analysis demonstrated intensive staining for transforming growth factor b1 and a-smooth muscle actin in the control neointima. Vardenafil significantly reduced the stenosis grade (24.64% AE 7.46% vs 54.12% AE 10.30% in the control group, P<.05) and expression of transforming growth factor b1, as well as a-smooth muscle actin, in the neointima. The immunohistochemical score for cyclic guanosine monophosphate was higher in the treated neointima (4.80 AE 0.76 vs 2.84 AE 0.40 in the control group, P < .05), and increased plasma cyclic guanosine monophosphate levels were found by means of enzyme immunoassay as well (84.65 AE 12.77 pmol/mL vs 43.50 AE 3.30 pmol/mL in the control group, P < .05).Conclusions: Treatment with vardenafil can be considered a new possibility to prevent neointimal hyperplasia after endarterectomy.Carotid endarterectomy is the standard treatment of severe carotid stenosis.1 Operative repair is not without potential complications, one of which is postoperative restenosis. Despite technical problems, the main cause of early restenosis after surgical vessel reconstruction is neointimal hyperplasia. Risk factors for early restenosis include alterations in the complement system, 2 increased serum growth factor levels, 3 or changes in the hemostatic factors. Ischemia-reperfusion injury and endothelial damage promote neointima formation. In contrast with early restenosis, late restenosis is due to the progression of primary atherosclerosis. 5 Pathologically, the following processes contribute to early restenosis: the migration of smooth muscle cells (SMCs) from the medial to the intimal layer, the proliferation of SMCs, the deposition of extracellular matrix material, and alterations in apoptosis of neointimal cells. 6Our previous studies showed that nit...

show abstract

mentioning

confidence: 99%

Selective phosphodiesterase-5 inhibition reduces neointimal hyperplasia in rat carotid arteries after surgical endarterectomy

Hirschberg¹,

Radovits²,

Loganathan³

et al. 2009

Thorac cardiovasc Surg

View full text Add to dashboard Cite

show abstract

mentioning

confidence: 99%

Selective phosphodiesterase-5 inhibition reduces neointimal hyperplasia in rat carotid arteries after surgical endarterectomy

Hirschberg

Radovits

Loganathan

et al. 2009

The Journal of Thoracic and Cardiovascular Surgery

View full text Add to dashboard Cite

Objective: Long-term results of surgical vessel reconstruction are compromised by restenosis caused by neoin-timal hyperplasia. Recent studies suggest that reduced cyclic guanosine monophosphate signaling is associated with neointima formation. In a rat model of endarterectomy, we investigated the effect of pharmacologic inhibition of cyclic guanosine monophosphate degradation on neointima formation by using the selective phosphodi-esterase-5 inhibitor vardenafil. Methods: Carotid endarterectomy was performed in male Sprague-Dawley rats by means of incision of the right common carotid artery with removal of intima. Four groups were studied: unoperated control rats (n ¼ 4), sham-operated rats (n ¼ 9), control rats with endarterectomy (n ¼ 9), or endarterectomized rats treated with vardenafil (10 mg/kg/day) postoperatively (n ¼ 9). After 3 weeks, vessel compartment areas were measured by means of conventional microscopy with hematoxylin and eosin staining. Immunohistochemical analysis was performed to confirm neointima formation and the local cyclic guanosine monophosphate content. Plasma levels of cyclic guanosine monophosphate were determined by means of enzyme immunoassay. Student's t test was used for statistical evaluation. Results: Immunohistochemical analysis demonstrated intensive staining for transforming growth factor b1 and a-smooth muscle actin in the control neointima. Vardenafil significantly reduced the stenosis grade (24.64% AE 7.46% vs 54.12% AE 10.30% in the control group, P<.05) and expression of transforming growth factor b1, as well as a-smooth muscle actin, in the neointima. The immunohistochemical score for cyclic guanosine mono-phosphate was higher in the treated neointima (4.80 AE 0.76 vs 2.84 AE 0.40 in the control group, P < .05), and increased plasma cyclic guanosine monophosphate levels were found by means of enzyme immunoassay as well (84.65 AE 12.77 pmol/mL vs 43.50 AE 3.30 pmol/mL in the control group, P < .05). Conclusions: Treatment with vardenafil can be considered a new possibility to prevent neointimal hyperplasia after endarterectomy. Carotid endarterectomy is the standard treatment of severe carotid stenosis. 1 Operative repair is not without potential complications, one of which is postoperative restenosis. Despite technical problems, the main cause of early reste-nosis after surgical vessel reconstruction is neointimal hyperplasia. Risk factors for early restenosis include alterations in the complement system, 2 increased serum growth factor levels, 3 or changes in the hemostatic factors. 4 Ischemia-reperfusion injury and endothelial damage promote neointima formation. In contrast with early resteno-sis, late restenosis is due to the progression of primary atherosclerosis. 5 Pathologically, the following processes contribute to early restenosis: the migration of smooth muscle cells (SMCs) from the medial to the intimal layer, the proliferation of SMCs, the deposition of extracellular matrix material, and alterations in apoptosis of neointimal cells. 6 Our previous studies s...

show abstract

Association between estrogen receptor α gene polymorphisms and early restenosis after eversion carotid endarterectomy and carotid stenting

et al. 2009

View full text Add to dashboard Cite

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

hi@scite.ai

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Changes in the plasma concentration of soluble thrombomodulin in patients with severe carotid artery stenosis after eversion endarterectomy

Abstract: Our present findings indicate that sTM may be adsorbed to the atherosclerotic plaques or inflamed endothelium in carotid arteries. The pathological significance of this adsorption remains to be determined.

Cited by 3 publications

References 31 publications

Selective phosphodiesterase-5 inhibition reduces neointimal hyperplasia in rat carotid arteries after surgical endarterectomy

Selective phosphodiesterase-5 inhibition reduces neointimal hyperplasia in rat carotid arteries after surgical endarterectomy

Selective phosphodiesterase-5 inhibition reduces neointimal hyperplasia in rat carotid arteries after surgical endarterectomy

Association between estrogen receptor α gene polymorphisms and early restenosis after eversion carotid endarterectomy and carotid stenting

Contact Info

Product

Resources

About