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Tissue Hypoxia (tissue + hypoxia)
Selected AbstractsTISSUE HYPOXIA AS A THERAPEUTIC TARGET IN ACUTE KIDNEY INJURYCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2009Roger G Evans No abstract is available for this article. [source] Theoretical Simulation of Oxygen Transport to Brain by Networks of Microvessels: Effects of Oxygen Supply and Demand on Tissue HypoxiaMICROCIRCULATION, Issue 4 2000T.W. SECOMB ABSTRACT Objective: Simulations of oxygen delivery by a three-dimensional network of microvessels in rat cerebral cortex were used to examine how the distribution of partial pressure of oxygen (PO2) in tissue depends on blood flow and oxygen consumption rates. Methods: Network geometry was deduced from previously published scanning electron micrographs of corrosion casts. A nonlinear least-squares method, using images obtained at three different angles, was used to estimate vessel locations. The network consisted of 50 segments in a region 140 µm × 150 µm × 160 µm. A Green's function method was used to predict the PO2 distribution. Effects of varying perfusion and consumption were examined, relative to a control state with consumption 10 cm3O2/100 g per min and perfusion 160 cm3/100 g per min. Results: In the control state, minimum tissue PO2 was 7 mm Hg. A Krogh-type model with the same density of vessels, but with uniform spacing, predicted a minimum tissue PO2 of 23 mm Hg. For perfusion below 60% of control, tissue hypoxia (PO2 <1 mm Hg) was predicted. When perfusion was reduced by 75%, the resulting hypoxia could be eliminated by a 31% reduction in oxygen consumption rate. Conclusions: The simulations suggest that tissue hypoxia resulting from a severe decrease in brain perfusion, as can occur in stroke, may be avoided by a moderate decrease in oxygen consumption rate. [source] Differential levels of tissue hypoxia in the developing chicken heartDEVELOPMENTAL DYNAMICS, Issue 1 2006Jamie Wikenheiser Abstract Tissue hypoxia plays a critical role in normal development, including cardiogenesis. Previously, we showed that oxygen concentration, as assessed by the hypoxia indicator EF5, is lowest in the outflow tract (OFT) myocardium of the developing chicken heart and may be regulating events in OFT morphogenesis. In this study, we identified additional areas of the embryonic chicken heart that were intensely positive for EF5 within the myocardium in discrete regions of the atrial wall and the interventricular septum (IVS). The region of the IVS that is EF5-positive includes a portion of the developing central conduction system identified by HNK-1 co-immunostaining. The EF5 positive tissues were also specifically positive for nuclear-localized hypoxia inducible factor 1, (HIF-1,), the oxygen-sensitive component of the hypoxia inducible factor 1 (HIF-1) heterodimer. The pattern of the most intensely EF5-stained myocardial regions of the atria and IVS resemble the pattern of the major coronary vessels that form in later stages within or immediately adjacent to these particular regions. These vessels include the sinoatrial nodal artery that is a branch of the right coronary artery within the atrial wall and the anterior/posterior interventricular vessels of the IVS. These findings indicate that a portion of the developing central conduction system and the patterning of coronary vessels may be subject to a level of regulation that is dependent on differential oxygen concentration within cardiac tissues and subsequent HIF-1 regulation of gene expression. Developmental Dynamics 235:115,123, 2006. © 2005 Wiley-Liss, Inc. [source] Drug-induced methaemoglobinaemia presenting with angina following the use of dapsoneINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 5 2003A. Salamat Summary Anaemia may result in tissue hypoxia which may induce or exacerbate symptoms of ischaemia. Tissue hypoxia may however also result from the presence of haemoglobin with altered oxygen-binding characteristics. Drug-induced methaemoglobinaemia in which oxygen is irreversibly bound to haemoglobin may complicate the use of some common drugs. This condition may result in severe tissue hypoxia, which is rapidly and cheaply reversed by methylene blue. [source] Lactate: physiology and clinical utilityJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2008Sarah E. Allen DVM Abstract Objective: To review the physiology of lactate production and metabolism, the causes of lactic acidosis, and the current applications of lactate monitoring in humans and animals. Data sources: Human and veterinary studies. Summary: Lactate production is the result of anaerobic metabolism. Tissue hypoxia due to hypoperfusion is the most common cause of lactic acidosis. Studies in critically ill humans have shown that serial lactate monitoring can be used to assess the severity of illness and response to therapy. Several veterinary studies have also shown lactate as a useful tool to assess severity of illness. Conclusions: Lactate measurement in critically ill veterinary patients is practical and can provide information to assess severity of illness. Further veterinary studies are needed to establish the value of serial lactate measurements for prognostic and therapeutic purposes. Information regarding lactate measurement in cats is limited, and further studies are warranted. [source] Role of VEGF and tissue hypoxia in patterning of neural and vascular cells recruited to the embryonic heartDEVELOPMENTAL DYNAMICS, Issue 11 2009Hongbin Liu Abstract We hypothesized that oxygen gradients and hypoxia-responsive signaling may play a role in the patterning of neural or vascular cells recruited to the developing heart. Endothelial progenitor and neural cells are recruited to and form branched structures adjacent to the relatively hypoxic outflow tract (OFT) myocardium from stages 27,32 (ED6.5,7.5) of chick development. As determined by whole mount confocal microscopy, the neural and vascular structures were not anatomically associated. Adenoviral delivery of a VEGF trap dramatically affected the remodeling of the vascular plexus into a coronary tree while neuronal branching was normal. Both neuronal and vascular branching was diminished in the hearts of embryos incubated under hyperoxic conditions. Quantitative analysis of the vascular defects using our recently developed VESGEN program demonstrated reduced small vessel branching and increased vessel diameters. We propose that vascular and neural patterning in the developing heart share dependence on tissue oxygen gradients but are not interdependent. Developmental Dynamics 238:2760,2769, 2009. © 2009 Wiley-Liss, Inc. [source] Differential levels of tissue hypoxia in the developing chicken heartDEVELOPMENTAL DYNAMICS, Issue 1 2006Jamie Wikenheiser Abstract Tissue hypoxia plays a critical role in normal development, including cardiogenesis. Previously, we showed that oxygen concentration, as assessed by the hypoxia indicator EF5, is lowest in the outflow tract (OFT) myocardium of the developing chicken heart and may be regulating events in OFT morphogenesis. In this study, we identified additional areas of the embryonic chicken heart that were intensely positive for EF5 within the myocardium in discrete regions of the atrial wall and the interventricular septum (IVS). The region of the IVS that is EF5-positive includes a portion of the developing central conduction system identified by HNK-1 co-immunostaining. The EF5 positive tissues were also specifically positive for nuclear-localized hypoxia inducible factor 1, (HIF-1,), the oxygen-sensitive component of the hypoxia inducible factor 1 (HIF-1) heterodimer. The pattern of the most intensely EF5-stained myocardial regions of the atria and IVS resemble the pattern of the major coronary vessels that form in later stages within or immediately adjacent to these particular regions. These vessels include the sinoatrial nodal artery that is a branch of the right coronary artery within the atrial wall and the anterior/posterior interventricular vessels of the IVS. These findings indicate that a portion of the developing central conduction system and the patterning of coronary vessels may be subject to a level of regulation that is dependent on differential oxygen concentration within cardiac tissues and subsequent HIF-1 regulation of gene expression. Developmental Dynamics 235:115,123, 2006. © 2005 Wiley-Liss, Inc. [source] Effect of transition metal ions (cobalt and nickel chlorides) on intestinal iron absorptionEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2004G. O. Latunde-Dada Abstract Background, Haem biosynthesis may regulate intestinal iron absorption through changes in cellular levels of ,-aminolaevulinic acid (ALA), haem and perhaps other intermediates. CoCl2 and NiCl2 are activators of haem oxygenase, the rate-limiting enzyme in haem catabolism. Co2+ and Ni2+ may also regulate and increase iron absorption through a mechanism that simulates hypoxic conditions in the tissues. Design, We assayed intestinal iron absorption in mice dosed with CoCl2 or NiCl2. The effects of these metal ions on splenic and hepatic levels of ALA synthase and dehydratase as well as urinary levels of ALA and phosphobilinogen were also assayed. Results, While Co2+ enhanced iron absorption when administered to mice at doses of 65, 125 and 250 µmoles kg,1 body weight, Ni2+ was effective only at the highest dose. Ni2+ but not Co2+ at the highest dose reduced urinary ALA in the treated mice. Both metals ions increased splenic expression of haem oxygenase 1 and iron regulated protein 1, proteins involved, respectively, in haem degradation and iron efflux. Co2+ induced erythropoietin expression. Conclusions, The data suggest that while the effect of Ni2+ on iron absorption could be explained by effects on ALA, the effect of Co2+ may not be explained simply by changes in haem metabolism; therefore, effects mediated by alterations of specific haemoproteins by mechanisms that simulate tissue hypoxia could be important. [source] Immunodetection of GLUT1, p63 and phospho-histone H1 in invasive head and neck squamous carcinoma: correlation of immunohistochemical staining patterns with keratinizationHISTOPATHOLOGY, Issue 6 2006D E Burstein Aims :,To examine invasive head and neck squamous carcinomas for expression of GLUT1, a glucose transporter and marker of increased glucose uptake, glycolytic metabolism and response to tissue hypoxia; p63, a p53 homologue that is a marker of the undifferentiated proliferative basaloid phenotype; and phospho-histone H1, a marker of activation of the cell cycle-promoting cyclin-dependent kinases 1 and 2. Methods :,Routinely processed slides from 34 invasive squamous carcinomas, including 25 with intraepithelial components, were immunostained with anti-GLUT1 (Chemicon), anti-p63 (4A4, Santa Cruz), and antiphospho-histone H1 (monoclonal 12D11). Results :,In keratinizing carcinomas, all three markers were most commonly immunodetected peripherally, with loss of expression in central keratinized zones. In contrast, in non-keratinizing carcinomas, p63 and phospho-histone H1 expression was most commonly observed throughout tumour nests and anti-GLUT1 stained in a pattern suggestive of hypoxia-induced expression (,antistromal' staining), in which cells at the tumour,stromal interface were GLUT1, and cells in central, perinecrotic zones showed progressive induction of GLUT1. Intraepithelial components also displayed basal and ,antibasal' GLUT1 staining patterns, homologous to the pro- and antistromal patterns in invasive carcinoma; basal patterns in intraepithelial lesions appeared to be more predictive of keratinizing invasive carcinoma and antibasal intraepithelial staining more predictive of non-keratinizing poorly differentiated carcinomas. Conclusions :,Keratinizing and non-keratinizing squamous carcinomas differ in expression patterns of GLUT1, p63 and phospho-histone H1. In the former, all three markers were typically suppressed in conjunction with keratinization; in the latter, GLUT1 expression was more likely to occur in a hypoxia-inducible pattern and expression of p63 and phospho-histone H1 was unsuppressed. GLUT1 expression patterns in intraepithelial lesions may be predictive of the differentiation status of the associated invasive carcinoma. [source] Drug-induced methaemoglobinaemia presenting with angina following the use of dapsoneINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 5 2003A. Salamat Summary Anaemia may result in tissue hypoxia which may induce or exacerbate symptoms of ischaemia. Tissue hypoxia may however also result from the presence of haemoglobin with altered oxygen-binding characteristics. Drug-induced methaemoglobinaemia in which oxygen is irreversibly bound to haemoglobin may complicate the use of some common drugs. This condition may result in severe tissue hypoxia, which is rapidly and cheaply reversed by methylene blue. [source] Selective induction of mucin-3 by hypoxia in intestinal epitheliaJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2006Nancy A. Louis Abstract Epithelial cells line mucosal surfaces (e.g., lung, intestine) and critically function as a semipermeable barrier to the outside world. Mucosal organs are highly vascular with extensive metabolic demands, and for this reason, are particularly susceptible to diminished blood flow and resultant tissue hypoxia. Here, we pursue the hypothesis that intestinal barrier function is regulated in a protective manner by hypoxia responsive genes. We demonstrate by PCR confirmation of microarray data and by avidin blotting of immunoprecipitated human Mucin 3 (MUC3), that surface MUC3 expression is induced in T84 intestinal epithelial cells following exposure to hypoxia. MUC3 RNA is minimally detectable while surface protein expression is absent under baseline normoxic conditions. There is a robust induction in both the mRNA (first evident by 8 h) and protein expression, first observed and maximally expressed following 24 h hypoxia. This is followed by a subsequent decline in protein expression, which remains well above baseline at 48 h of hypoxia. Further, we demonstrate that this induction of MUC3 protein is associated with a transient increase in the barrier restorative peptide, intestinal trefoil factor (ITF). ITF not only colocalizes with MUC3, by confocal microscopy, to the apical surface of T84 cells following exposure to hypoxia, but is also found, by co-immunoprecipitation, to be physically associated with MUC3, following 24 h of hypoxia. In exploration of the mechanism of hypoxic regulation of mucin 3 expression, we demonstrated by luciferase assay that the full-length promoter for mouse Mucin 3 (Muc3) is hypoxia-responsive with a 5.08,±,1.76-fold induction following 24 h of hypoxia. Furthermore, analysis of both the human (MUC3A) and mouse (Muc3) promoters revealed potential HIF-1 binding sites which were shown by chromatin immunoprecipitation to bind the pivotal hypoxia-regulating transcription factor HIF-1,. Taken together, these studies implicate the HIF-1, mediated hypoxic induced expression of mucin 3 and associated ITF in the maintenance of intestinal barrier function under hypoxic conditions. J. Cell. Biochem. 99: 1616,1627, 2006. © 2006 Wiley-Liss, Inc. [source] Membrane-bound, ATP-dependent energy systems and tissue hypoxia in human gastric mucosaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2 2000Gyula Mózsik First page of article [source] A multilocus candidate approach identifies ACE and HIF1A as susceptibility genes for celluliteJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 8 2010E Emanuele Abstract Background, Cellulite is a common complex cosmetic problem for many post-adolescent women characterised by relief alterations of the skin surface, which give the skin an orange-peel appearance. Although genetic factors have been suggested to play a role in the development of cellulite, the genetic background of this condition remains unclear. We therefore conducted a multi-locus genetic study examining the potential associations of candidate gene variants in oestrogen receptors, endothelial function/adipose tissue hypoxia, lipid metabolism, extracellular matrix homeostasis, inflammation and adipose tissue biology, with the risk of cellulite. Methods, Using a case,control study of 200 lean women with cellulite and 200 age- and BMI-matched controls (grade 0 according to Nurnberger,Muller scale), we examined the association of cellulite with 25 polymorphisms in 15 candidate genes. Results, Two of the 25 polymorphisms were significantly associated with cellulite at the P < 0.01 level. After allowance for age, body mass index, the prevalence of contraceptive use and smoking in logistic regression analysis, the multivariable-adjusted odds ratios for cellulite were 1.19 (95% CI: 1.10,1.51; P < 0.01) for ACE rs1799752 and 0.61 (95% CI: 0.45,0.88, P < 0.01) for HIF1A rs11549465. Conclusions, This study, which demonstrates an independent role of ACE and HIF1A in predisposing to cellulite, may provide novel information on the pathophysiology of this common cosmetic problem, and offer a topic for research for novel beautification interventions. [source] Critical role of the vascular endothelial cell in health and disease: a review articleJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 2 2004Todd C. Duffy DVM Abstract Objective: To review the human and veterinary literature on the role of the vascular endothelial cell in health, as well as during hypoxic and inflammatory disease states. Data sources: Data from human and veterinary literature were reviewed through a Pubmed search and a manual search of the references listed in articles covering some aspect of vascular endothelial cell function. Human data synthesis: The development of techniques that allow the maintenance and growth of endothelial cells in culture has produced an explosion of new research in the area of endothelial cell physiology. This plethora of data has revealed the critical role that vascular endothelial cells play in both health and disease states. Interspecies variations can occur with respect to the vascular endothelial cell physiology and its response to pathologic conditions. Veterinary data synthesis: There is a paucity of information regarding the role of the vascular endothelial cell in health or disease of small animals. Many human studies use species cared for by veterinarians, providing information that may be applied to small animals and that may be used to construct future studies. Conclusion: An organ system itself, the vascular endothelium is an essential component of all organs in the body. The endothelial cell lining functions to maintain selective permeability between the blood and the tissue it supplies, regulate vascular tone, sustain blood fluidity through regulation of coagulation, and modulate interaction of leukocytes with the interstitium and inflammatory reactions. During disease states, the endothelial cell functions locally to limit the boundaries of the disease process. If these functions are not controlled, they can become a part of the pathogenic process, contributing to blood stasis and thrombosis, potentiation of local inflammation and interstitial edema formation, subsequent tissue hypoxia, and multiple organ dysfunction. Pharmacological investigations targeting the modulation of endothelial function during disease states have not yet advanced treatment protocols. Since all critically ill animals are at risk for some degree of endothelial cell dysfunction, treatment regimens should focus on promoting capillary blood flow and tissue oxygen delivery. [source] Theoretical Simulation of Oxygen Transport to Brain by Networks of Microvessels: Effects of Oxygen Supply and Demand on Tissue HypoxiaMICROCIRCULATION, Issue 4 2000T.W. SECOMB ABSTRACT Objective: Simulations of oxygen delivery by a three-dimensional network of microvessels in rat cerebral cortex were used to examine how the distribution of partial pressure of oxygen (PO2) in tissue depends on blood flow and oxygen consumption rates. Methods: Network geometry was deduced from previously published scanning electron micrographs of corrosion casts. A nonlinear least-squares method, using images obtained at three different angles, was used to estimate vessel locations. The network consisted of 50 segments in a region 140 µm × 150 µm × 160 µm. A Green's function method was used to predict the PO2 distribution. Effects of varying perfusion and consumption were examined, relative to a control state with consumption 10 cm3O2/100 g per min and perfusion 160 cm3/100 g per min. Results: In the control state, minimum tissue PO2 was 7 mm Hg. A Krogh-type model with the same density of vessels, but with uniform spacing, predicted a minimum tissue PO2 of 23 mm Hg. For perfusion below 60% of control, tissue hypoxia (PO2 <1 mm Hg) was predicted. When perfusion was reduced by 75%, the resulting hypoxia could be eliminated by a 31% reduction in oxygen consumption rate. Conclusions: The simulations suggest that tissue hypoxia resulting from a severe decrease in brain perfusion, as can occur in stroke, may be avoided by a moderate decrease in oxygen consumption rate. [source] Childhood cirrhosis, hepatopulmonary syndrome and liver transplantationPEDIATRIC TRANSPLANTATION, Issue 3 2008Gokhan Tumgor Abstract:, Objectives:, The hepatopulmonary syndrome (HPS) is characterized as a triad: liver disease, intrapulmonary vascular dilatatiton, and arterial hypoxemia. The aim of this study is to analyze outcome of children with HPS in liver transplant era. Methods:, Between September 1996 and November 2006, 172 cirrhotic patients (median age 5 years; range 0.2,22 years, M/F; 97/75) were followed at Ege University Pediatric Gastroenterology, Hepatology and Nutrition Unit. All patients were evaluated by chest radiography, arterial blood gas analysis, and alveolar-arterial oxygen tension difference, contrast echocardiography (CEE) after and before the liver transplantation. Results:, HPS was diagnosed in 33 patients (19%) by CEE. None of them had pulmonary hypertension. HPS was not found related to etiology of the liver disease. Portal hypertension was found related to the development of HPS (75.7% in patients with HPS and 54.6% in others, p = 0.02). 17 of 33 patients with HPS underwent liver transplantation. Preoperative and postoperative period of these patients was uneventful. Patients were extubated in the operating room except for two. Median follow up of transplanted children was 1.9 year (range; 0.75,10 years). Arterial blood gas analysis and CEE positivity regressed in all of them by postoperative 6th month. Conclusions:, HPS is a serious and important complication of cirrhotic children that leads to tissue hypoxia and central cyanosis. HPS seems reversible after liver transplantation in all patients. [source] Impairment of endothelial cell differentiation from bone marrow,derived mesenchymal stem cells: New insight into the pathogenesis of systemic sclerosisARTHRITIS & RHEUMATISM, Issue 6 2007P. Cipriani Objective Systemic sclerosis (SSc) is a disorder characterized by vascular damage and fibrosis of the skin and internal organs. Despite marked tissue hypoxia, there is no evidence of compensatory angiogenesis. The ability of mesenchymal stem cells (MSCs) to differentiate into endothelial cells was recently demonstrated. The aim of this study was to determine whether impaired differentiation of MSCs into endothelial cells in SSc might contribute to disease pathogenesis by decreasing endothelial repair. Methods MSCs obtained from 7 SSc patients and 15 healthy controls were characterized. The number of colony-forming unit,fibroblastoid colonies was determined. After culture in endothelial-specific medium, the endothelial-like MSC (EL-MSC) phenotype was assessed according to the surface expression of vascular endothelial growth factor receptors (VEGFRs). Senescence, chemoinvasion, and capillary morphogenesis studies were also performed. Results MSCs from SSc patients displayed the same phenotype and clonogenic activity as those from controls. In SSc MSCs, a decreased percentage of VEGFR-2+, CXCR4+, VEGFR-2+/CXCR4+ cells and early senescence was detected. After culturing, SSc EL-MSCs showed increased expression of VEGFR-1, VEGFR-2, and CXCR4, did not express CD31 or annexin V, and showed significantly decreased migration after specific stimuli. Moreover, the addition of VEGF and stromal cell,derived factor 1 to cultured SSc EL-MSCs increased their angiogenic potential less than that in controls. Conclusion Our data strongly suggest that endothelial repair may be affected in SSc. The possibility that endothelial progenitor cells could be used to increase vessel growth in chronic ischemic tissues may open up new avenues in the treatment of vascular damage caused by SSc. [source] Eight Hours of Hypotensive versus Normotensive Resuscitation in a Porcine Model of Controlled Hemorrhagic ShockACADEMIC EMERGENCY MEDICINE, Issue 9 2008David E. Skarda MD Abstract Objectives:, The aim of this study was to compare hypotensive and normotensive resuscitation in a porcine model of hemorrhagic shock. Methods:, This was a prospective, comparative, randomized survival study of controlled hemorrhagic shock using 28 male Yorkshire-Landrace pigs (15 to 25 kg). In 24 splenectomized pigs, the authors induced hemorrhagic shock to a systolic blood pressure (sBP) of 48 to 58 mm Hg (,35% bleed). Pigs were randomized to undergo normotensive resuscitation (sBP of 90 mm Hg, n = 7), mild hypotensive resuscitation (sBP of 80 mm Hg, n = 7), severe hypotensive resuscitation (sBP of 65 mm Hg, n = 6), or no resuscitation (n = 4). The authors also included a sham group of animals that were instrumented and splenectomized, but that did not undergo hemorrhagic shock (n = 4). After the initial 8 hours of randomized pressure-targeted resuscitation, all animals were resuscitated to a sBP of 90 mm Hg for 16 hours. Results:, Animals that underwent severe hypotensive resuscitation were less likely to survive, compared with animals that underwent normotensive resuscitation. Mean arterial pressure (MAP) decreased with hemorrhage and increased appropriately with pressure-targeted resuscitation. Base excess (BE) and tissue oxygen saturation (StO2) decreased in all animals that underwent hemorrhagic shock. This decrease persisted only in animals that were pressure target resuscitated to a sBP of 65 mm Hg. Conclusions:, In this model of controlled hemorrhagic shock, initial severe hypotensive pressure-targeted resuscitation for 8 hours was associated with an increased mortality rate and led to a persistent base deficit (BD) and to decreased StO2, suggesting persistent metabolic stress and tissue hypoxia. However, mild hypotensive resuscitation did not lead to a persistent BD or to decreased StO2, suggesting less metabolic stress and less tissue hypoxia. [source] Retinal oxygenation in diabetic retinopathyACTA OPHTHALMOLOGICA, Issue 2009SH HARDARSON Purpose Diabetic retinopathy (DR) is believed to cause retinal tissue hypoxia by damaging retinal capillaries. The purpose of this study was to examine the effect of diabetic retinopathy on oxygen saturation in retinal arterioles and venules. Methods The retinal oximeter (Oxymap ehf., Reykjavik, Iceland) is composed of a fundus camera, beam splitter and light filters. Specialized software calculates relative oxygen saturation from light absorption at two wavelengths of light (605nm and 586nm). One first or second degree temporal arteriole and venule were measured in one eye of 31 healthy individual and 28 patients with diabetic retinopathy. The diabetic patients had background DR (n=6), macular oedema (n=7), untreated preproliferative or proliferative DR (n=7) or stable proliferative DR after treatment (n=8). Statistical analyses were performed with an unpaired t-test, one-way ANOVA and Dunnett's post test. Results Retinal arteriolar saturation was 93±4% (n=31, mean±SD) in healthy subjects and 101±6% (n=28) in patients with DR (p<0.0001). Retinal venular saturation was 58±6% in healthy subjects and 67±8% in diabetic patients (p<0.0001). Arteriolar and venular saturation was higher in all subgroups of diabetic patients (see methods) than in healthy subjects. Conclusion Increased oxygen saturation in retinal vessels in diabetic retinopathy, also found by other researchers, is consistent with poor distribution of blood and oxygen to the retinal tissue rather than decreased total retinal blood flow. Poor distribution of oxygen may be caused by capillary dropouts and shunts as well as thickening of the capillary walls. Commercial interest [source] Pseudoexfoliatio capsulae and endothelin-1 plasma levelsACTA OPHTHALMOLOGICA, Issue S232 2000G. L. Possati M. Cellini Summary The authors found an increase of endothelin-1 (ET-1) plasma levels in patients with pseudoexfoliatio syndrome (PXS): 2.730±0.224 pg/ml vs 1.420±0.30S pg/ml. With Color Doppler Imaging (CDI) they found in PXS patients a decrease of peak systolic velocity values in the posterior ciliary arteries that were 12.725 ± 2.536 cm/sec vs 15.450 ± 3.173 cm/sec (p<0.049) while the resistance values were increased 0.640 ± 0.051 vs 0.548 ± 0.058 (p<0.001). The increase of ET-1 plasma levels may assess the vasospasm and uveal tissue hypoxia. [source] | |||||||||||||