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Vascular Perfusion (vascular + perfusion)
Selected AbstractsCirculation in normal and inflamed dental pulpENDODONTIC TOPICS, Issue 1 2007ELLEN BERGGREEN In the pulp, arteries branch into a capillary network before they leave the pulp as venules through the apical foramina. The tissue has low compliance, as it is enclosed in dentin, and has a relatively high blood flow and blood volume. The interstitial fluid pressure (IFP) and colloid osmotic pressure are relatively high whereas the net driving blood pressure is low. The high pulsatile IFP is probably the major force for propelling lymph in the dental pulp. Vasodilation in neighboring tissue as well as arteriovenous (AV) shunts in the pulp itself can contribute to a fall in total and coronal pulpal blood flow, respectively. The pulp blood flow is under nervous, humoral, and local control. Inflammatory vascular responses, vasodilation, and increased vessel permeability induce an increase in IFP that can be followed by a temporarily impaired blood flow response. Lipopolysaccharides (LPS) from bacteria may cause endothelial activation in the pulp, leading to vasoconstriction and reduced vascular perfusion. Lymphatic vessels are identified with specific lymphatic markers in the pulp but so far, little is known about their function. Because of the special circulatory conditions in the pulp, there are several clinical implications that need to be considered in dental treatment. Received 13 February 2009; accepted 28 August 2009. [source] Hip ulcer secondary to foreign body reaction and vacuum-assisted closure therapy: report of a caseINTERNATIONAL WOUND JOURNAL, Issue 1 2005Gabriela Moreno-Coutiño MD Abstract Patients who have a foreign body reaction are at risk of developing chronic ulcers secondary to necrosis, due to the inflammation present in the affected tissues or trauma, worsened by alterations in the vascular perfusion. These ulcers represent a therapeutic challenge for both physicians and patients. [source] Characterization of human liver dendritic cells in liver grafts and perfusatesLIVER TRANSPLANTATION, Issue 3 2006Brenda M. Bosma It is generally accepted that donor myeloid dendritic cells (MDC) are the main instigators of acute rejection after organ transplantation. The aim of the present study was to characterize MDC in human donor livers using liver grafts and perfusates as a source. Perfusates were collected during ex vivo vascular perfusion of liver grafts pretransplantation. MDC, visualized in wedge biopsies by immunohistochemistry with anti-BDCA-1 monoclonal antibody (mAb), were predominantly observed in the portal fields. Liver MDC, isolated from liver wedge biopsies, had an immature phenotype with a low expression of CD80 and CD83. Perfusates were collected from 20 grafts; perfusate mononuclear cells (MNC) contained 1.5% (range, 0.3-6.6%) MDC with a viability of 97 ± 2%. Perfusates were a rich source of hepatic MDC since 0.9 × 106 (range, 0.11-4.5 × 106) MDC detached from donor livers during vascular perfusion pretransplantation. Perfusate MDC were used to further characterize hepatic MDC. Perfusate MDC expressed less DC-LAMP (P = 0.000), CD80 (P = 0.000), CD86 (P = 0.003), and CCR7 (P = 0.014) than mature hepatic lymph node (LN) MDC, and similar CD86 (P = 0.140) and CCR7 (P = 0.262) as and more DC-LAMP (P = 0.007) and CD80 (P = 0.002) than immature blood MDC. Perfusate MDC differed from blood MDC in producing significantly higher amounts of interleukin (IL)-10 in response to lipopolysaccharide (LPS), and in being able to stimulate allogeneic T-cell proliferation. In conclusion, human donor livers contain exclusively immature MDC that detach in high numbers from the liver graft during pretransplantation perfusion. These viable MDC have the capacity to stimulate allogeneic T-cells, and thus may represent a major player in the induction of acute rejection. Liver Transpl 12: 384,393, 2006. © 2006 AASLD. [source] Abdominal compartment syndrome after liver transplantationLIVER TRANSPLANTATION, Issue 1 2005Alexander E. Handschin The abdominal compartment syndrome is a well-known complication after abdominal trauma and is increasingly recognized as a potential risk factor for renal failure and mortality after adult orthotopic liver transplantation (OLT). We present a case report of a young patient who presented with acute liver failure complicated by an acute pancreatitis. The patient developed an acute abdominal compartment syndrome after OLT. Transurethral measurement of intraabdominal pressure indicated an abdominal compartment syndrome associated with impaired abdominal vascular perfusion, including liver perfusion. Renal insufficiency was immediately reversed after decompressive bedside laparotomy. The abdominal compartment syndrome is a potential source of posttransplant renal insufficiency and liver necrosis in OLT. It remains, however, a rarely described complication after liver transplantation, despite the presence of significant factors that contribute to elevated intraabdominal pressure. (Liver Transpl 2005;11:98,100.) [source] Antivascular Tumor Eradication by Hypericin-mediated Photodynamic Therapy,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 5 2002Bin Chen ABSTRACT Photodynamic therapy (PDT) with hypericin has been shown to inhibit tumor growth in different tumor models, and tumor vascular damage was suggested to be mainly responsible for the antitumoral effect. Here, we demonstrate tumor vascular damage and its consequence on local tumor control after hypericin-mediated PDT by using both short and long drug,light intervals. Radiation-induced fibrosarcoma-1 tumors were exposed to laser light at either 0.5 or 6 h after a 5 mg/kg dose of hypericin. Tumor perfusion was monitored by fluorescein dye,exclusion assay and by Hoechst 33342 staining of functional blood vessels. Significant reduction in tumor perfusion was found immediately after both PDT treatments. A complete arrest of vascular perfusion was detected by 15 h after the 0.5 h-interval PDT, whereas well-perfused areas could still be found at this time in tumors after the 6 h-interval PDT. A histological study confirmed that primary vascular damage was involved in both PDT treatments. Tumor cells appeared intact shortly after light treatment, degenerated at later hours and became extensively pycnotic at 24 h after the 0.5 h-interval PDT. PDT under this condition led to complete tumor cure. In contrast, significant numbers of viable tumor cells, especially at the tumor periphery, were found histologically at 24 h after the 6 h-interval PDT. No tumor cure was obtained when PDT was performed at this time. Our results strongly suggest that targeting the tumor vasculature by applying short drug,light interval PDT with hypericin might be a promising way to eradicate solid tumors. [source] Morphological changes induced in the pig kidney by extracorporeal shock wave lithotripsy: Nephron injuryTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2003Youzhi Shao Abstract While shock wave lithotripsy (SWL) is known to cause significant damage to the kidney, little is known about the initial injury to cells along the nephron. In this study, one kidney in each of six juvenile pigs (6,7 weeks old) was treated with 1,000 shock waves (at 24 kV) directed at a lower pole calyx with an unmodified HM-3 lithotripter. Three pigs were utilized as sham-controls. Kidneys were fixed by vascular perfusion immediately after SWL or sham-SWL. Three of the treated kidneys were used to quantitate lesion size. Cortical and medullary samples for light (LM) and transmission electron microscopy (TEM) were taken from the focal zone for the shock waves (F2), the contralateral kidney, and the kidneys of sham-SWL pigs. Because preservation of the tissue occurred within minutes of SWL, the initial injury caused by the shock waves could be separated from secondary changes. No tissue damage was observed in contralateral sham-SWL kidneys, but treated kidneys showed signs of injury, with a lesion of 0.2% ± 0.1% of renal volume. Intraparenchymal hemorrhage and injury to tubules was found at F2 in both the cortex and medulla of SWL-treated kidneys. Tubular injury was always associated with intraparenchymal bleeding, and the range of tissue injury included total destruction of tubules, focal cellular fragmentation, necrosis, cell vacuolization, and membrane blebbing. The initial injury caused by SWL was cellular fragmentation and necrosis. Cellular vacuolization, membrane blebbing, and disorganization of apical brush borders appear to be secondary changes related to hypoxia. Anat Rec Part A 275A:979,989, 2003. © 2003 Wiley-Liss, Inc. [source] Tumour growth following portal branch ligation in an experimental model of liver metastases,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2010O. Kollmar Background: Portal branch ligation (PBL) is being used increasingly before hepatectomy for colorectal metastases. This study evaluated the effect of PBL on angiogenesis, growth factor expression and tumour growth in a mouse model of hepatic colorectal metastases. Methods: CT26.WT cells were implanted into the left liver lobe of BALB/c mice. Animals underwent PBL of the left liver lobe or sham treatment. Angiogenesis, microcirculation, growth factor expression, cell proliferation and tumour growth were studied over 14 and 21 days by intravital multifluorescence microscopy, laser Doppler flowmetry, immunohistochemistry and western blotting. Results: Left hilar blood flow and tumour microcirculation were significantly diminished during the first 7 days after PBL. This resulted in tumour volume being 20 per cent less than in sham controls by day 14. Subsequently, PBL-treated animals demonstrated recovery of left hilar blood flow and increased expression of hepatocyte growth factor and transforming growth factor ,, associated with increased cell proliferation and acceleration of growth by day 21. Conclusion: PBL initially reduced vascular perfusion and tumour growth, but this was followed by increased growth factor expression and cell proliferation. This resulted in delayed acceleration of tumour growth, which might explain the stimulated tumour growth observed occasionally after PBL. Copyright © 2010 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Long-term study of vascular perfusion effects following arteriovenous sheathotomy for branch retinal vein occlusionACTA OPHTHALMOLOGICA, Issue 3 2010Mahiul M. K. Muqit Abstract. Purpose:, To evaluate the perfusion effects and long-term visual outcome of pars plana vitrectomy (PPV) combined with arteriovenous sheathotomy (AVS) with or without triamcinolone for nonischaemic branch retinal vein occlusion (NI-BRVO). Methods:, Prospective, interventional case series of eight patients with NI-BRVO and haemorrhagic macular oedema. Patients underwent PPV and AVS (n = 5), or PPV, AVS and intravitreal triamcinolone (IVT, n = 3). A masked grading technique assessed fundus photographs and fluorescein angiography (FFA) following surgery. Scanning laser ophthalmoscopy/optical coherence tomography (SLO/OCT) evaluated macular oedema and outer retinal architecture. Main outcomes examined included visual acuity (VA), retinal reperfusion, collateral vessel regression, vascular dilatation, cystoid macular oedema (CMO), and ocular neovascularization. Results:, Seven of eight patients underwent uncomplicated surgery, with increased intraretinal perfusion and reduced engorgement of distal retinal veins. The mean pre-logMAR VA was 0.8 (SD 0.17) and did not improve significantly after surgery (post-logMAR 0.6, SD 0.38; p = 0.11, paired t -test). SLO/OCT showed persistent CMO in four patients, and subfoveal thinning of the photoreceptor layer. Collateral vessels disappeared at the blockage site post-AVS in 7/8 eyes, and this was associated with improved retinal perfusion. Six of eight patients developed epiretinal membrane. No patients developed ocular neovascularization. The average follow-up was 34.5 months. Conclusions:, PPV with AVS is a safe procedure, and adjunctive IVT had no additional effects on vascular perfusion. Successful decompressive surgery was followed by disappearance of collateral vessels at the BRVO blockage site and was a clinical marker for intravascular reperfusion. Long-term epiretinal gliosis and subfoveal photoreceptor atrophy limited functional and visual recovery. [source] | |||||||||||||