September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Effect of systemic blood pressure modification on ocular and cerebral blood vessels
Author Affiliations & Notes
  • Shajan Velaedan
    Optometry & Vision Sciences, Melbourne University, Melbourne, Victoria, Australia
  • Zheng He
    Optometry & Vision Sciences, Melbourne University, Melbourne, Victoria, Australia
  • Algis J Vingrys
    Optometry & Vision Sciences, Melbourne University, Melbourne, Victoria, Australia
  • Bang V Bui
    Optometry & Vision Sciences, Melbourne University, Melbourne, Victoria, Australia
  • Footnotes
    Commercial Relationships   Shajan Velaedan, None; Zheng He, None; Algis Vingrys, None; Bang Bui, None
  • Footnotes
    Support  NHMRC Project Grant 1046203, ARC Future Fellowship FT130100338
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 2207. doi:
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      Shajan Velaedan, Zheng He, Algis J Vingrys, Bang V Bui; Effect of systemic blood pressure modification on ocular and cerebral blood vessels. Invest. Ophthalmol. Vis. Sci. 2016;57(12):2207.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : The retinal vasculature is considered a useful surrogate for the brain blood vascular network. There has been no direct comparison of the capacity of vessels in the eye and brain to respond to changes in blood pressure. We compare autoregulatory capacity by quantifying change in arterial width in rat retina and brain across a wide range of blood pressures.

Methods : Sodium nitroprusside (1.25 mg/ml, 0.004 ml/min) and angiotensin II (0.0325 mg/ml, 0.005 ml/min) were injected via femoral veins of anesthetized (60:5 mg/kg ketamine:xylazine) adult Long-Evans rats (eye, n=8; brain, n=8) to induce transient hypo- and hypertension, respectively. An area of skull was thinned to image arteries on the cortical surface. Retinal and cortical arteries were imaged using an Andor Neo cMOS camera at 1700 frames/sec for 500 ms at each 5 mmHg change in mean arterial pressure (MAP range 40 – 180 mmHg). Changes in arterial width were quantified using ImageJ and expressed as percentage change from baseline and plotted as a function of MAP. A 3-line function was used to describe the data, with parameters compared using the 95% confidence limits returned by bootstrapping.

Results : Retinal and cerebral arteries (50-90 mm diameter) showed robust vasodilation (at -25 mmHg, eye 9.6 ± 3.9 %, brain 7.7 ± 3.7 %) and constriction (at +25 mmHg, eye -11.4 ± 2.0 %, brain -5.5 ± 3.0 %) as MAP decreased and increased, respectively. For MAP increases or decreases greater than 25 mmHg retinal arteries show no further change in diameter. The brain was similar to the eye with regards to high MAP induced vasoconstriction. However, with a blood pressure drop of as much as 60 mmHg below habitual MAP, arteries on the cortical surface can still vasodilate (maximal vasodilation eye 11.6 ± 6.3 %, brain 29.7 ± 8.6 %, p<0.05).

Conclusions : We show that measuring change in arterial diameter in response to blood pressure alteration is an excellent way to assess autoregulation in the eye and brain. Whilst retinal and surface cortical arteries showed similarities in vaso-responses to changes in blood pressure, there are distinct differences. In particular, cortical arteries had a greater capacity to compensate for drops in blood pressure. Such differences must be taken into account when using the retinal vessels as a surrogate for studying the cerebral vasculature.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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