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Sökning: WFRF:(Mellander Stefan 1960)

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1.
  • Fogelstrand, Per, 1971, et al. (författare)
  • Increased Vascular Injury Reduces the Degree of Intimal Hyperplasia following Angioplasty in Rabbits.
  • 2011
  • Ingår i: Journal of vascular research. - : S. Karger AG. - 1423-0135 .- 1018-1172. ; 48:4, s. 307-15
  • Tidskriftsartikel (refereegranskat)abstract
    • Background/Aims: Formation of intimal hyperplasia following angioplastic procedures can lead to complications, including restenosis and accelerated atherosclerosis. The vessel wall media is a main source of neointimal cells. However, evidence suggests that there are additional cell sources, such as the adventitia. Here we investigate whether an extensive loss of vascular smooth muscle cells (VSMCs) in the media results in less intimal hyperplasia or if there is compensatory cell recruitment from the adventitia. Methods:A balloon catheter was pulled through the rabbit carotid artery 4 times (major injury) or 2 times (minor injury). Adventitial cells were labeled with 5-bromo-2-deoxyuridine or PKH26. Results:The major injury, but not the minor injury, resulted in a complete loss of VSMCs in large parts of the media and significant leukocyte infiltration. The major injury resulted in less neointima compared with the minor injury. The thinnest neointima was seen at the most injured parts of the media in the major injury group. Cell-tracking experiments showed that the media, but not the adventitia, served as a source of neointimal cells. Conclusion: An augmented angioplastic injury with extensive VSMC loss in rabbits reduced the degree of intimal hyperplasia. No compensatory recruitment of neointimal cells from the adventitia occurred.
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2.
  • Heckenkamp, J, et al. (författare)
  • Photodynamic therapy reduces intimal hyperplasia in prosthetic vascular bypass grafts in a pig model.
  • 2007
  • Ingår i: European journal of vascular and endovascular surgery. - : Elsevier BV. - 1078-5884. ; 34:3, s. 333-9
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Bypass surgery has a failing frequency of 30% during the first year, mainly due to intimal hyperplasia (IH). This negative effect is most pronounced in artificial grafts. Photodynamic therapy (PDT) is a technique in which light activates photosensitizer dyes to produce free-radicals resulting in an eradication of cells in the vascular wall. The aim of this study was to determine the effectiveness of PDT to reduce IH in a preclinical porcine PTFE bypass model. MATERIAL AND METHODS: Ten pigs were used. After a pilot PDT dosimetry study (n=3) PTFE grafts were bilaterally placed into the circulation as bypasses from the common to the external iliac arteries (n=7). The right sides served as controls (C). Before implantation of the left grafts, the arterial connecting sites of the left distal anastomoses were PDT-treated. The arteries were pressurized at 180 mmHg for 5 minutes with the photosensitizer Methylene Blue (330 microg/ml), and thereafter endoluminally irradiated with laser light (lambda = 660 nm, 100 mW/cm(2), 150 J/cm(2)). After 4 weeks the specimens were retrieved and formalin fixed. Cross sections through the midportions of the distal anastomoses and the grafts were used for histology, immunohistochemistry to identify inflammatory cells and morphometric evaluation (n=7). RESULTS: No systemic side effects and no graft occlusions were noted. PDT-treated anastomoses showed reduced IH in the mid-portions of the anastomoses (Area of IH: microm(2)/microm graft: C: 6970+/-1536, PDT: 2734+/-2560; P<0.005) as well as in the grafts (C: 5391+/-4031, PDT: 777+/-1331; P<0.02). The number of inflammatory cells per microscopic field was increased after PDT (C: 24+/-16, PDT: 37+/-15; P<0.009). CONCLUSIONS: Adjuvant PDT, performed in an endovascular fashion, was a safe method to reduce prosthetic graftstenosis in a preclinical setting. This study underscores the clinical potential of PDT to inhibit the development of clinical bypass graftstenosis.
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3.
  • Leonhardt, Henrik, 1963, et al. (författare)
  • Endovascular management of acute bleeding arterioenteric fistulas.
  • 2008
  • Ingår i: Cardiovascular and interventional radiology. - : Springer Science and Business Media LLC. - 1432-086X .- 0174-1551. ; 31:3, s. 542-9
  • Tidskriftsartikel (refereegranskat)abstract
    • The objective of this study was to review the outcome of endovascular transcatheter repair of emergent arterioenteric fistulas. Cases of abdominal arterioenteric fistulas (defined as a fistula between a major artery and the small intestine or colon, thus not the esophagus or stomach), diagnosed over the 3-year period between December 2002 and December 2005 at our institution, were retrospectively reviewed. Five patients with severe enteric bleeding underwent angiography and endovascular repair. Four presented primary arterioenteric fistulas, and one presented a secondary aortoenteric fistula. All had massive persistent bleeding with hypotension despite volume substitution and transfusion by the time of endovascular management. Outcome after treatment of these patients was investigated for major procedure-related complications, recurrence, reintervention, morbidity, and mortality. Mean follow-up time was 3 months (range, 1-6 months). All massive bleeding was controlled by occlusive balloon catheters. Four fistulas were successfully sealed with stent-grafts, resulting in a technical success rate of 80%. One patient was circulatory stabilized by endovascular management but needed immediate further open surgery. There were no procedure-related major complications. Mean hospital stay after the initial endovascular intervention was 19 days. Rebleeding occurred in four patients (80%) after a free interval of 2 weeks or longer. During the follow-up period three patients needed reintervention. The in-hospital mortality was 20% and the 30-day mortality was 40%. The midterm outcome was poor, due to comorbidities or rebleeding, with a mortality of 80% within 6 months. In conclusion, endovascular repair is an efficient and safe method to stabilize patients with life-threatening bleeding arterioenteric fistulas in the emergent episode. However, in this group of patients with severe comorbidities, the risk of rebleeding is high and further intervention must be considered. Patients with cancer may only need treatment for the acute bleeding episode, and an endovascular approach has the advantage of low morbidity.
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4.
  • Mellander, Stefan, 1960, et al. (författare)
  • Healing of PTFE grafts in a pig model recruit neointimal cells from different sources and do not endothelialize.
  • 2005
  • Ingår i: European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery. - : Elsevier BV. - 1078-5884. ; 30:1, s. 63-70
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: The aim of this study was to analyze the cellular sources for the neointima and the cell type that is lining the lumen in artificial grafts implanted in pigs. MATERIALS AND METHODS: We used polytetrafluoroethylene grafts as bypasses from the common to the external iliac arteries. The animals were sacrificed after 1, 4, 7, 14, 21, 30, 60 and 90 days. Morphological, immunohistochemical and electron microscope assessments were made. RESULTS: After 7 days a circumferential neoadventitia was formed. At day 14 isolated cellular islets of proliferating cells were observed on the luminal side of the graft without connection to the neoadventitia or the adjacent arteries. In the anastomotic regions at day 14 we observed an isolated neointima in contact with the adjacent artery. The cells lining the lumen had characteristics of both smooth muscle cells and endothelial cells. CONCLUSIONS: Our study suggests that in artificial porcine grafts, the perivascular tissue, the blood and the adjacent artery contribute to the formation of the neointima. The luminal surface is covered by a hybrid cell with both smooth muscle cell and endothelial cell properties.
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5.
  • Mellander, Stefan, 1960 (författare)
  • On cellular sources for intimal hyperplasia after vascular interventions
  • 2007
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Vascular interventions for the treatment of symptomatic atherosclerosis fail in up to 40 % of the cases during the first year. One important reason is the development of a narrowing process known as intimal hyperplasia (IH). The cells forming IH resemble smooth muscle cells (SMCs) from the media of the arterial wall. Therefore the media has generally been regarded as the cellular origin for IH. However, there are reports indicating that other cellular sources might be involved. The aim of this thesis was to investigate which cellular sources participate in the development of intimal hyperplasia after bypass surgery and balloon injury. Furthermore, we wanted to investigate, if the inhibition of one cellular source could reduce initimal hyperplasia. Studies were made in pig and rabbit. Specific aims were: 1/ To evaluate the blood, the adjacent artery, the media, the adventitia, and the surrounding tissue as cellular sources to intimal hyperplasia 2/ To evaluate the contribution of blood-borne mononuclear cells to IH 3/ To evaluate, if depletion of the cells in the media reduces intimal hyperplasia after vascular interventions. We found that the adjacent artery at the anastomoses and the surrounding tissue contributed cells in a bypass model in pig. Blood-borne mononuclear cells were labeled ex vivo and retransfused after bypass implantation and balloon injury in pig. These cells were later found in the IH. Some of these cells co-expressed markers for smooth muscle cells suggesting a trandifferation from a blood-borne mononuclear to a tissue forming cell. In a ballon injury model in rabbit we found that the media with its SMCs was the main cellular source and that adventitial cells did not contribute to the IH. After depletion of the medial SMCs by a more severe balloon trauma in rabbit and by photodynamic therapy in the bypass model in pig we found less IH compared with controls, suggesting the media and its cells to be an important source after both interventions. In conclusion, the results presented in this thesis show that cells from the media, the surrounding tissue, the adjacent artery, and blood-borne mononuclear cells can contribute to IH. By depletion of the cells in the media, intimal hyperplasia following both bypass surgery and balloon injury is reduced.
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