Document Detail


Inhibition of 20-HETE attenuates diabetes-induced decreases in retinal hemodynamics.
MedLine Citation:
PMID:  21658386     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The mechanisms of early diabetes-induced decreases in retinal blood flow have yet to be fully determined. The aim of this study was to explore the hypothesis that 20-hydroxyeicosatetraenoic acid (20-HETE) plays a role in the early decrease of retinal hemodynamics in diabetic mice. 20-HETE has been implicated previously in the diabetes-enhanced vasoconstriction of mesenteric and renal vessels; however, its role in the diabetic retinal microcirculation has not been investigated. Diabetes was induced by multiple low-dose injections of streptozotocin (STZ; 50 mg/kg for 5 consecutive days), then ∼2 weeks later the mice were administered daily intraperitoneal injections with or without the 20-HETE inhibitor HET0016 (2.5 mg/kg/day) for the following 2 weeks. Non-diabetic age-matched mice were included as controls. Intravital microscopy was used to obtain measurements of retinal vascular diameters and red blood cell (RBC) velocities for the feed arterioles and draining venules extending out of and into the optic disk. From these values, wall shear rates and blood flow rates were calculated. Diabetes induced approximately 30-40% decreases in RBC velocity, wall shear rate, and blood flow rate. These decreases were attenuated to 5-10% in the mice given HET0016. In summary, the 20-HETE inhibitor HET0016 is able to attenuate the retinal hemodynamic changes induced by diabetes.
Authors:
Zhongli Wang; Amit Singh Yadav; Wendy Leskova; Norman R Harris
Related Documents :
17485096 - Atherogenic lipoprotein phenotype and ldl size and subclasses in patients with peripher...
8202496 - Insulin promotes the biosynthesis and secretion of apolipoprotein b-48 by altering apol...
8462776 - Metabolism by human endothelial cells of very low density lipoprotein subfractions isol...
3931466 - Effects of glyburide therapy on lipoproteins in non-insulin-dependent diabetes mellitus.
7600746 - Good blood glucose control characterizes patients without retinopathy after long diabet...
7601726 - Dietary protein and(or) energy restriction in mares: plasma glucose, insulin, nonesteri...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-05-30
Journal Detail:
Title:  Experimental eye research     Volume:  93     ISSN:  1096-0007     ISO Abbreviation:  Exp. Eye Res.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-07-18     Completed Date:  2011-09-09     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  0370707     Medline TA:  Exp Eye Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  108-13     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Molecular & Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Amidines / pharmacology*
Animals
Blood Flow Velocity / physiology
Diabetes Mellitus, Experimental / physiopathology,  prevention & control*
Diabetic Retinopathy / physiopathology,  prevention & control*
Erythrocytes / physiology
Hydroxyeicosatetraenoic Acids / antagonists & inhibitors*
Injections, Intraperitoneal
Male
Mice
Mice, Inbred C57BL
Regional Blood Flow / physiology
Retinal Vessels / drug effects*,  physiopathology
Grant Support
ID/Acronym/Agency:
EY017599/EY/NEI NIH HHS; R01 EY017599-04/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Amidines; 0/Hydroxyeicosatetraenoic Acids; 0/N-hydroxy-N'-(4-butyl-2-methylphenyl)formamidine; 79551-86-3/20-hydroxy-5,8,11,14-eicosatetraenoic acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Cyclohexanol analogues are positive modulators of GABA(A) receptor currents and act as general anaes...
Next Document:  LRRK2 directly phosphorylates Akt1 as a possible physiological substrate: Impairment of the kinase a...