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视网膜小动脉和大脑中动脉对高碳酸/高氧联合刺激的反应。

Retinal arteriolar and middle cerebral artery responses to combined hypercarbic/hyperoxic stimuli.

作者信息

Kisilevsky Mila, Mardimae Alexandra, Slessarev Marat, Han Jay, Fisher Joseph, Hudson Chris

机构信息

Department of Ophthalmology and Vision Science, University of Toronto, Toronto, Ontario, Canada.

出版信息

Invest Ophthalmol Vis Sci. 2008 Dec;49(12):5503-9. doi: 10.1167/iovs.08-1854. Epub 2008 May 23.

DOI:10.1167/iovs.08-1854
PMID:18502990
Abstract

PURPOSE

The relative effect of simultaneously administered oxygen and carbon dioxide on the retinal and cerebral vessels is still controversial. The purpose of this study was to quantify and compare the superior-temporal retinal arteriole (RA) and middle cerebral artery (MCA) responses to hypercarbic and combined hypercarbic/hyperoxic stimuli.

METHODS

Twelve young, healthy volunteers participated in the study. End-tidal pressure of carbon dioxide was raised and maintained at 22% from baseline (hypercarbia), while end-tidal pressures of oxygen (P(ET)O(2)) of 100 (normoxia), 500, and 300 mm Hg (hyperoxia) were instituted. RA diameter and blood velocity were measured with laser Doppler velocimetry and simultaneous vessel densitometry; MCA blood velocity was measured with transcranial Doppler ultrasound.

RESULTS

Normoxic hypercarbia increased RA blood velocity by +17% and calculated flow by +21%. Hypercarbia/hyperoxia-500 mm Hg decreased RA diameter by -8%, velocity by -16% and calculated flow by -29%. MCA blood velocity increased by +45% in response to normoxic hypercarbia, significantly greater than RA blood velocity (P < 0.001). Increase in P(ET)O(2) did not affect the hypercarbia-induced increase in MCA blood velocity.

CONCLUSIONS

Hyperoxia reversed hypercarbia-induced vasodilation in RA in a concentration-dependent manner. Hypercarbia induced greater vasodilation in the MCA than in the RA but MCA blood velocity was unaffected by increases in P(ET)O(2).

摘要

目的

同时给予氧气和二氧化碳对视网膜血管和脑血管的相对影响仍存在争议。本研究的目的是量化并比较颞上视网膜小动脉(RA)和大脑中动脉(MCA)对高碳酸血症以及联合高碳酸血症/高氧刺激的反应。

方法

12名年轻健康志愿者参与了本研究。将呼气末二氧化碳分压从基线水平升高并维持在22%(高碳酸血症),同时设定呼气末氧分压(P(ET)O(2))为100(常氧)、500和300 mmHg(高氧)。使用激光多普勒测速仪和同步血管密度测定法测量RA直径和血流速度;使用经颅多普勒超声测量MCA血流速度。

结果

常氧高碳酸血症使RA血流速度增加了17%,计算得出的血流量增加了21%。高碳酸血症/高氧-500 mmHg使RA直径减少了8%,血流速度减少了16%,计算得出的血流量减少了29%。MCA血流速度在常氧高碳酸血症时增加了45%,显著高于RA血流速度(P < 0.001)。P(ET)O(2)的增加并未影响高碳酸血症诱导的MCA血流速度增加。

结论

高氧以浓度依赖的方式逆转了高碳酸血症诱导的RA血管舒张。高碳酸血症在MCA中诱导的血管舒张大于RA,但MCA血流速度不受P(ET)O(2)增加的影响。

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