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Related Experiment Videos

Hypothesis: vasoconstriction contributes to amaurosis fugax.

J K Williams1, G L Baumbach, M L Armstrong

  • 1Department of Internal Medicine, VA Medical Center, Iowa City, Iowa.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|February 1, 1989
PubMed
Summary

Atherosclerosis potentiates serotonin-induced retinal vasoconstriction, impairing vision. This study reveals how platelet aggregation in atherosclerosis contributes to amaurosis fugax.

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Area of Science:

  • Ophthalmology
  • Vascular Biology
  • Cardiovascular Research

Background:

  • Platelets are implicated in amaurosis fugax pathophysiology.
  • Emboli and vasospasm are proposed mechanisms for amaurosis.
  • Serotonin release during platelet aggregation may affect retinal vessels.

Purpose of the Study:

  • To test if retinal vessel constrictor responses to serotonin are potentiated in experimental atherosclerosis.
  • To investigate the role of serotonin in amaurosis fugax pathogenesis.

Main Methods:

  • Measuring retinal blood flow in normal and atherosclerotic cynomolgus monkeys.
  • Infusing serotonin into the retinal circulation of both groups.
  • Assessing retinal function via light response.

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Main Results:

  • Serotonin infusion did not alter retinal blood flow in normal monkeys.
  • In atherosclerotic monkeys, serotonin reduced retinal blood flow significantly (66 to 5 mL/min/100g).
  • Serotonin abolished the light response in atherosclerotic monkeys' retinas.

Conclusions:

  • Atherosclerosis markedly potentiates serotonin-induced retinal vasoconstriction.
  • Altered platelet-derived vasoactive substance responses may contribute to amaurosis fugax.
  • The study demonstrates a profound, reversible impairment of retinal function due to serotonin in atherosclerosis.