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局部压力引起的脉络膜血流改变。

Alteration in choroidal blood flow produced by local pressure.

作者信息

Ivert Lena, Kong Jian, Gouras Peter

机构信息

Department of Ophthalmology, St. Erik's Eye Hospital, Karolinska Institute, Polhemsgatan 50, 112 82, Stockholm, Sweden.

出版信息

Graefes Arch Clin Exp Ophthalmol. 2006 Oct;244(10):1339-44. doi: 10.1007/s00417-006-0292-8. Epub 2006 Mar 17.

Abstract

BACKGROUND

To investigate how transient pressure applied to the retinal pigment epithelium (RPE) layer and choroid affects choroidal blood flow in rabbits.

METHODS

Twelve rabbits underwent vitrectomy and local retinectomy. In nine of the rabbits a glass rod was used to exert brief pressure on the RPE layer and choroid. Three of the rabbits had no pressure indentation and were considered to be controls. The choroidal circulation was studied by indocyanine green (ICG) angiography. The retina and choroid were studied by postmortem histology.

RESULTS

Pressure on the RPE layer and choroid caused nonfluorescence in segments of retinal arteries and veins and reduced fluorescence in adjacent choroidal capillaries, producing a black region at the pressure site in the angiograms. The size of this region decreased during the angiogram, often accompanied by the appearance of fine channels considered to be flow through the partially blocked vessels; the obstructed ends of the vessels became increasingly hyperfluorescent. These changes lasted for about 24 h before the choroidal circulation recovered. Histology showed evidence of thrombotic-like material in choroidal arteries and veins at the areas of absent perfusion. After local retinectomies, there was no evidence of thrombosis in control eyes where no pressure had been applied.

CONCLUSION

Brief pressure on the RPE and choroid causes immediate reduction in flow through choroidal vessels, which appears to be due to local thrombosis in small segments of these vessels that resolves slowly. This may reflect a tendency for thrombi to form rapidly in choroidal vessels; it may also depend on neural reflexes causing vasoconstriction. The long time course of recovery could result in retinal ischemia and may underlie the pathophysiology of other pressure insults to the choroid.

摘要

背景

研究短暂施加于视网膜色素上皮(RPE)层和脉络膜的压力如何影响兔脉络膜血流。

方法

12只兔接受玻璃体切除术和局部视网膜切除术。其中9只兔用玻璃棒对RPE层和脉络膜施加短暂压力。3只兔未施加压力凹陷,作为对照。通过吲哚菁绿(ICG)血管造影研究脉络膜循环。通过死后组织学研究视网膜和脉络膜。

结果

对RPE层和脉络膜施加压力导致视网膜动脉和静脉节段无荧光,相邻脉络膜毛细血管荧光减弱,在血管造影片的压力部位产生黑色区域。该区域大小在血管造影过程中减小,常伴有被认为是通过部分阻塞血管的血流的细小通道出现;血管阻塞端荧光逐渐增强。这些变化持续约24小时,之后脉络膜循环恢复。组织学显示灌注缺失区域的脉络膜动脉和静脉中有类似血栓的物质。局部视网膜切除术后,未施加压力的对照眼中无血栓形成证据。

结论

对RPE和脉络膜的短暂压力导致脉络膜血管血流立即减少,这似乎是由于这些血管小节段局部血栓形成且消退缓慢所致。这可能反映了脉络膜血管中血栓快速形成的倾向;也可能取决于引起血管收缩的神经反射。恢复时间长可能导致视网膜缺血,可能是脉络膜其他压力损伤病理生理学的基础。

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