Objective: Ischemia-reperfusion (IR) injury causes tissue injury and endothelial dysfunction. There is evidence that oxidative stress plays an important role.
Methods: We tested if IR-induced endothelial dysfunction could be prevented by administration of the antioxidant vitamin C. Twenty-six healthy male subjects and eight male patients with peripheral arterial disease (PAD) were enrolled in this randomised placebo-controlled study. Forearm blood flow (FBF) measurements in response to the vasodilators acetylcholine (ACh; endothelium-dependent agonist) or nitroglycerin (NTG; endothelium-independent) were performed before and after forearm ischemia for 20 min. FBF responses were reassessed during reperfusion with intra-arterial co-administration of 24 mg/min vitamin C or placebo. In six volunteers responses to the NO-synthase inhibitor N-monomethyl-L-arginine (L-NMMA) were also assessed before and after ischemia with and without vitamin C.
Results: ACh-induced vasodilation was blunted in subjects receiving placebo after reperfusion (p<0.05 versus baseline). Administration of vitamin C completely prevented impaired responsiveness. NTG-induced vasodilation was not affected by reperfusion or vitamin C. This finding was consistent in patients with PAD and impaired endothelial function, where local vitamin C infusion restored FBF reactivity to ACh before and after IR injury (p<0.05 versus baseline). Again, NTG-induced vasodilation was not affected. Blunted L-NMMA responses seen during reperfusion could be completely reversed by vitamin C.
Conclusions: Our data indicate that IR-induced vascular injury can be prevented by administration of antioxidants.
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http://dx.doi.org/10.1016/j.atherosclerosis.2007.06.011 | DOI Listing |
Curr Cardiol Rep
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Pediatric Advanced Heart Failure and Heart Transplant Program, University of Mississippi Medical Center, 2500 N State Street, Jackson, MS, USA.
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Department of Thoracic Surgery, The 1st Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, Jiangxi, PR China; Jiangxi Hospital of China-Japan Friendship Hospital, National Regional Center for Respiratory Medicine, Nanchang 330000, Jiangxi, PR China; Jiangxi Institute of Respiratory Disease, The 1st Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330000, Jiangxi, PR China. Electronic address:
Hyperhomocysteinemia (HHcy) is associated with the development and progression of chronic cardiovascular diseases through the deleterious effects of high levels of homocysteine (Hcy) on the cardiovascular system. However, the exact mechanism of action of Hcy on the acute injury of the cardiovascular system following ischemia/reperfusion (I/R) remains unclear. The present study demonstrated that copper mobilization occurs during cardiac I/R, and the interactive toxic effect of Hcy and mobile Cu during cardiac I/R induces necroptosis of cardiac microvascular endothelial cells (CMECs) and thus enhances cardiac dysfunction.
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School of Medicine, Vita-Salute San Raffaele University, Milan, Italy; Division of head and neck, Ophthalmology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy. Electronic address:
Focal capillary ectasia in the macular region can manifest in distinct clinical scenarios, which can be categorized into two main entities: perifoveal vascular anomalous complex (PVAC) and telangiectatic capillaries (TelCaps). PVAC represents a primary, idiopathic condition, whereas TelCaps occur secondary to underlying vascular disorders, including diabetic macular edema and retinal vein occlusion. We provide a comprehensive analysis of these two entities, encompassing their clinical presentations, multimodal imaging findings, histological evidence, and differential diagnosis from other retinal microvascular abnormalities, such as Type 1 macular telangiectasia, adult-onset Coats disease, Type 3 macular neovascularization in age-related macular degeneration, and retinal arterial macroaneurysms.
View Article and Find Full Text PDFStem Cells Transl Med
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Developmental and Stem Cell Biology Program, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4.
Disruption of developmental processes affecting the fetal lung leads to pulmonary hypoplasia. Pulmonary hypoplasia results from several conditions including congenital diaphragmatic hernia (CDH) and oligohydramnios. Both entities have high morbidity and mortality, and no effective therapy that fully restores normal lung development.
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Pulmonary endothelial cell (EC) activation is a key factor in acute respiratory distress syndrome (ARDS). In sepsis, increased glycolysis leads to lactate buildup, which induces lysine lactylation (Kla) on histones and other proteins. However, the role of protein lactylation in EC dysfunction during sepsis-induced ARDS remains unclear.
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