June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
Altered retinal hemodynamics and mean circulation time in spontaneously hypertensive rats
Author Affiliations & Notes
  • Norman R Harris
    Molecular & Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, United States
  • Wendy Leskova
    Molecular & Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, United States
  • Ravdeep Warar
    Molecular & Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, United States
  • Footnotes
    Commercial Relationships   Norman Harris, None; Wendy Leskova, None; Ravdeep Warar, None
  • Footnotes
    Support  NIH Grant EY025632
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 1335. doi:
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      Norman R Harris, Wendy Leskova, Ravdeep Warar; Altered retinal hemodynamics and mean circulation time in spontaneously hypertensive rats. Invest. Ophthalmol. Vis. Sci. 2020;61(7):1335.

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

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Abstract

Purpose : Although it is known that the retinal arteriolar vasculature is constricted in hypertensive individuals, the details of retinal hemodynamics and perfusion of the retinal vascular bed has yet to be adequately characterized.

Methods : Male and female spontaneously hypertensive rats (SHR; N=4) and Wistar-Kyoto controls (WKY; N=6) were anesthetized prior to measurements of mean arterial blood pressure and preparation for intravital microscopy of the retinal microcirculation. Retinal vascular velocities (V) were measured with the use of 1.9 μm diameter fluorescent microspheres, and diameters (D) and mean circulation times (MCT) were measured following the infusion of fluorescent dextran. Arteriolar and venular shear rates (SR) were calculated from the equation SR=8V/D.

Results : Mean arterial blood pressure was highly elevated in SHR vs WKY (138±11 vs 82±6 mmHg; p<0.01). Likely due to the increased pressure head, arteriolar velocities increased in SHR vs WKY by 34% (11.5±0.4 vs 8.6±0.4 mm/s; p<0.001). Venular velocities were not increased, indicating a loss of kinetic energy through the retinal circulation, with the force absorbed by the vessel wall in the form of highly elevated shear. Shear rates in SHR were increased by 63% in the arterioles (1396±72 vs 856±37 /s; p<0.0001) and by 39% in the venules (838±81 vs 604±44 /s; p<0.05). Possibly as a result of autoregulation, vascular diameters in the SHR decreased significantly to prevent a corresponding increase in blood flow in SHR vs WKY (260±29 vs 288±36 nl/s; p=0.6). Arteriolar diameters in SHR constricted by 20% (65.7±2.4 vs 81.8±2.7 μm; p<0.01) and venular diameters constricted by 18% (82.1±1.5 vs 99.6±3.4 μm; p<0.01). Finally, MCT decreased dramatically in SHR by 55% (0.206±0.024 vs 0.456±0.041 s; p<0.01).

Conclusions : The autoregulatory response in the SHR retina, while keeping flow (and possibly filtration pressure) at control levels, induced substantial vasoconstriction that resulted in highly elevated shear forces, which are known to increase vascular permeability and initiate several signal pathways in the vessel wall. The dramatic 55% decrease in MCT despite only 34% increases in arteriolar (and no change in venular) velocities is likely to be a consequence of altered flow distribution in the hypertensive retina, with flow possibly diverted towards shorter pathways, leaving areas of the retina underperfused.

This is a 2020 ARVO Annual Meeting abstract.

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