Increase in choroidal blood flow in rabbits with endothelin-1 induced transient complete obstruction of retinal vessels

Graefes Arch Clin Exp Ophthalmol. 1995 Jul;233(7):425-9. doi: 10.1007/BF00180946.

Abstract

Background: In a previous paper, we reported that retinal blood flow (RBF) ceased immediately after injection of 1 nmol endothelin-1 (ET-1) and no recovery of RBF was detected for at least 50 min. In this study, we confirmed the same duration of RBF cessation and measured choroidal blood flow (CBF) for 180 min.

Methods: We measured CBF in a rabbit model of transient complete obstruction of retinal vessels induced by intravitreal injection of a high dose of ET-1, using the hydrogen clearance method. We also investigated the effects of intravitreal injection of ET-1 on intraocular pressure (IOP), blood pressure, pulse rate and blood gases.

Results: CBF was significantly greater in the ET-1-injected eyes than in the control eyes 40-130 min after injection of ET-1 (P < 0.05). The maximal CBF ratio in the ET-1-injected eyes was 128 +/- 7.4% at 40 min. CBF decreased to the pre-injection level at 140 min after the injection of ET-1. There was no significant change in blood pressure, pulse rate and blood gases throughout this experiment, and there was no significant difference in IOP between ET-1-injected eyes and control eyes.

Conclusion: It seems likely that the increase in CBF resulted from some local mechanisms of control that compensated for the decrease in RBF induced by intravitreal injection of ET-1. This model may be useful for investigation of the regulatory system of intraocular circulation, including endothelin receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Flow Velocity / physiology
  • Blood Gas Analysis
  • Blood Pressure
  • Choroid / blood supply*
  • Endothelins
  • Female
  • Intraocular Pressure
  • Male
  • Pulse
  • Rabbits
  • Retinal Artery / drug effects
  • Retinal Artery Occlusion / chemically induced
  • Retinal Artery Occlusion / physiopathology*
  • Vasoconstriction / physiology

Substances

  • Endothelins