Early inhibition of myointimal proliferation by angiopeptin after balloon catheter injury in the rabbit

Foegh, Marie L.; Asotra, Satish; Conte, John V.; Howell, Marcus H.; Kagan, Elliott; Verma, Kiran; Ramwell, Peter W.

doi:10.1016/s0741-5214(94)70221-7

Cited by 37 publications

(20 citation statements)

References 34 publications

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“…Delaying treatment for as little as 8 h after injury abrogates the inhibitory effects of octreotide. This stresses the importance of early events immediately after vascular tissue injury, suggesting that octreotide inhibits the expression of early genes causally related to the response to vascular injury and thereby triggering vascular cell proliferation [11].…”

Section: Discussionmentioning

confidence: 89%

“…Subsequently, it has also been demonstrated that analogues of octreotide inhibit myointimal proliferation after air drying injury in the rat and balloon injury in the rabbit. Octreotide analogues have also been shown to inhibit chronic coronary vascular disease in rabbit and rat cardiac transplant models [7,11,12].…”

Section: Discussionmentioning

confidence: 99%

“…Vascular smooth muscle cell replication in allograft arteriosclerosis is accompanied by the synthesis of several peptide growth factors in the vascular wall. Octreotide analogues selectively reduce growth factor synthesis in the vascular wall and concomitantly block vascular smooth muscle cell replication [7,11,12].…”

Section: Discussionmentioning

confidence: 99%

“…Foegh et al [11] concluded that administration of an angiopeptin analogue of octreotide (2-200 Ìg/kg/day) significantly reduced intimal hyperplasia by approximately 50% in a balloon injury model in the rabbit when evaluated 3 weeks after injury. This inhibitory effect was unrelated to treatment duration and dose.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of Myointimal Proliferation by Octreotide in Canine Vein Interposition Grafts

Işcan

Saritaş

et al. 1998

Eur Surg Res

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Purpose: The aim of this study was to evaluate the efficacy of octreotide in modulating the progression of intimal hyperplasia in autogenous vein bypass grafts in a canine model. The effect of the drug on the progression of intimal hyperplasia was measured with the Gilman parameter, a measure used extensively as a wound-healing descriptor. Methods: 12 mongrel dogs were randomly and equally divided into two groups. The first group (octreotide group) was administered octreotide 20 µg/kg/day. The control group (group II) received saline solution by subcutaneous injection. Each dog had 8- to 10-cm segments of autogenous jugular vein bypassed to the femoral arteries. Quantitative data on luminel narrowing over time from intimal hyperplasia were compared from calculated Gilman parameters after image analysis of retrieved, histologically processed graft sections. Each vein graft was analyzed by computerized morphometric analysis. Results: The mean Gilman parameter for distal graft segments was 0.47 ± 0.17 mm in the control group and 0.25 ± 0.07 mm in the octreotide group 6 weeks after operation (p < 0.05). Distal graft segments between the control and octreotide groups were statistically significant. In proximal, medial and distal graft segments, the mean Gilman parameters were 0.51 ± 0.16 mm in the control group and 0.37 ± 0.18 mm in the octreotide group, the difference being statistically significant (p < 0.01). Conclusion: Octreotide significantly inhibits myointimal thickening, and these data support the efficacy of octreotide in reducing intimal hyperplasia in arterialized vein grafts during the short postoperative period. Further investigations are required to as certain whether this beneficial effect of octretide persists in the long term.

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibition of Myointimal Proliferation by Octreotide in Canine Vein Interposition Grafts

Işcan

Saritaş

et al. 1998

Eur Surg Res

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“…Angiopeptin is a synthetic somatostatin analogue with antiproliferative effects on vascular smooth muscle cells, although its exact mechanism of action is unclear. 73,74 De Scheerder et al 75 studied the effects of angiopeptin loaded onto stents coated with polyorganophosphazene, a polymer known to induce an exaggerated inflammatory and proliferative response. At 6 weeks, a significant difference in the minimum luminal diameter and neointimal area between angiopeptin-treated arteries and untreated controls was noted in this model of accelerated restenosis in porcine coronary arteries.…”

Section: Stents Coated With Corticosteroids and Antimitotic Agentsmentioning

confidence: 99%

Coated Stents for the Prevention of Restenosis: Part I

2002

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O ver the past decade, the use of endoluminal metallic stents has become common practice during percutaneous coronary intervention (PCI), especially after clinical trials showed evidence of decreased restenosis rates when compared with balloon angioplasty alone. [1][2][3] Although stents significantly reduce restenosis when compared with balloon angioplasty, restenosis rates in patients who receive stents are still 20% to 40% at 6 months. [1][2][3][4][5][6] Recently, the concept of using stents coated with agents that could potentially inhibit neointimal hyperplasia has emerged. These agents include biocompatible materials, anticoagulants, corticosteroids, and antimitotic agents. This 2-part article reviews animal studies, human observational studies, and results from randomized clinical trials investigating coated stents. Part I discusses the pathophysiology of in-stent restenosis, as well as animal studies investigating coated stents. Part II discusses human studies investigating coated stents. Pathophysiology of In-Stent RestenosisIn-stent restenosis is primarily due to neointimal hyperplasia. [7][8][9][10][11][12][13] Vessel injury by an angioplasty balloon or stent struts leads to the activation of platelets and mural thrombus formation. [13][14][15][16] The presence of vascular injury, mural thrombus, and a metallic foreign body activates circulating neutrophils and tissue macrophages. 12,13,17,18 These cellular elements release cytokines and growth factors that activate smooth muscle cells. 19 -23 Upregulation and expression of genes such as c-myc that regulate cell division ensues, leading to cell proliferation. 24,25 Production of matrix metalloproteinases is also upregulated, leading to remodeling of the extracellular matrix, and initiating smooth muscle cell migration. 26 -28 The end result of this cascade of events is the uncontrolled proliferation of smooth muscle cells around the vessel intima and the deposition of extracellular matrix material, which often lead to significant luminal narrowing 3 to 6 months after PCI (Figure 1). Coated StentsThe systemic administration of a variety of agents has not had a significant impact on post-PCI restenosis rates. 29 -34 Although there is some evidence that controlling mural thrombus formation may decrease neointimal hyperplasia, [35][36][37] antiplatelet agents have not reliably resulted in reductions in restenosis rates in clinical trials. 29,30 Similarly, the systemic administration of corticosteroids aimed at controlling the inflammatory process has not shown decreased restenosis rates. 31 The lack of effect of systemically administered agents may be due to inadequate drug concentrations at the site of stent insertion. The limited success of these agents in decreasing rates of in-stent restenosis, coupled with side effects, prompted the development of coated stents.Stent coatings can be divided into 2 categories, biocompatible materials and drug-eluting coatings (Table 1). Biocompatible materials currently under investigation are thought to be less th...

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Data Analysis, Report Writing, and Regulatory Documentation

Wells¹

2011

Pharmaceutical Toxicology in Practice

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Early inhibition of myointimal proliferation by angiopeptin after balloon catheter injury in the rabbit

Cited by 37 publications

References 34 publications

Inhibition of Myointimal Proliferation by Octreotide in Canine Vein Interposition Grafts

Inhibition of Myointimal Proliferation by Octreotide in Canine Vein Interposition Grafts

Coated Stents for the Prevention of Restenosis: Part I

Data Analysis, Report Writing, and Regulatory Documentation

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