Ocular perfusion abnormalities in diabetes

被引:114
作者
Ciulla, TA
Harris, A
Latkany, P
Piper, HC
Arend, O
Garzozi, H
Martin, B
机构
[1] Indiana Univ, Sch Med, Dept Ophthalmol, Indianapolis, IN 46260 USA
[2] Midwest Eye Inst, Indianapolis, IN USA
[3] Manhattan Eye Ear & Throat Hosp, New York, NY 10021 USA
[4] Eye Care Ctr, Fishers, NY USA
[5] Rhein Westfal TH Aachen, Sch Med, Dept Ophthalmol, Aachen, Germany
[6] Haemek Med Ctr, Dept Ophthalmol, Afula, Israel
[7] Indiana Univ, Med Sci Program, Bloomington, IN USA
来源
ACTA OPHTHALMOLOGICA SCANDINAVICA | 2002年 / 80卷 / 05期
关键词
diabetes; diabetic retinopathy; ocular perfusion; blood flow; choroid; choriocapillaris; retinal circulation; pericyte; endothelial cel;
D O I
10.1034/j.1600-0420.2002.800503.x
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose: To review the role of ocular perfusion in the pathophysiology of diabetic retinopathy, one of the leading causes of irreversible blindness in the industrialized world. Methods: We carried out a Medline search of the literature published in English or with English abstracts from 1966 to 2000 using various combinations of relevant key words. Results: Hyperglycaemia leads to a wide variety of vascular abnormalities at the microvascular and macrovascular levels, including abnormal autoregulation. Conclusion: Three major aspects of ocular perfusion in diabetic retinopathy require additional investigation. Firstly, the precise mechanisms that link elevated glucose to dysfunction of retinal vascular cells need to be identified. Secondly, those factors that lead to both capillary dropout and to angiogenesis, twin processes that are linked to tissue hypoxia and lead to excess perfusion, increased risk of extravascular leakage and frank haemorrhage, must be carefully delineated. Finally, once specific knowledge of disease fundamentals has been amassed, tests of therapies to reverse or prevent these pathological processes can move forward.
引用
收藏
页码:468 / 477
页数:10
相关论文
共 139 条
[1]   Vascular endothelial growth factor-induced retinal permeability is mediated by protein kinase C in vivo and suppressed by an orally effective beta-isoform-selective inhibitor [J].
Aiello, LP ;
Bursell, SE ;
Clermont, A ;
Duh, E ;
Ishii, H ;
Takagi, C ;
Mori, F ;
Ciulla, TA ;
Ways, K ;
Jirousek, M ;
Smith, LEH ;
King, GL .
DIABETES, 1997, 46 (09) :1473-1480
[2]  
Alder VA, 1998, AUST NZ J OPHTHALMOL, V26, P267
[3]   Overview of studies on metabolic and vascular regulatory changes in early diabetic retinopathy [J].
Alder, VA ;
Su, EN ;
Yu, DY ;
Cringle, S ;
Yu, P .
AUSTRALIAN AND NEW ZEALAND JOURNAL OF OPHTHALMOLOGY, 1998, 26 (02) :141-148
[4]  
Ansari NH, 1998, J TOXICOL ENV HEAL A, V54, P467
[5]   INFLUENCE OF PERICYTES ON CAPILLARY ENDOTHELIAL-CELL GROWTH [J].
ANTONELLIORLIDGE, A ;
SMITH, SR ;
DAMORE, PA .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 140 (04) :1129-1131
[6]  
Applegate RA, 1997, INVEST OPHTH VIS SCI, V38, P783
[7]   PERIFOVEAL MICROCIRCULATION WITH NON-INSULIN-DEPENDENT DIABETES-MELLITUS [J].
AREND, O ;
WOLF, S ;
REMKY, A ;
SPONSEL, WE ;
HARRIS, A ;
BERTRAM, B ;
REIM, M .
GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY, 1994, 232 (04) :225-231
[8]   MACULAR MICROCIRCULATION IN CYSTOID MACULOPATHY OF DIABETIC-PATIENTS [J].
AREND, O ;
REMKY, A ;
HARRIS, A ;
BERTRAM, B ;
REIM, M ;
WOLF, S .
BRITISH JOURNAL OF OPHTHALMOLOGY, 1995, 79 (07) :628-632
[9]   THE RELATIONSHIP OF MACULAR MICROCIRCULATION TO VISUAL-ACUITY IN DIABETIC-PATIENTS [J].
AREND, O ;
WOLF, S ;
HARRIS, A ;
REIM, M .
ARCHIVES OF OPHTHALMOLOGY, 1995, 113 (05) :610-614
[10]  
Arend O, 1997, INVEST OPHTH VIS SCI, V38, P1819