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Related Experiment Videos

PGE(2)-mediated eNOS induction in prolonged hypercapnia.

Daniella Checchin1, Xin Hou, Pierre Hardy

  • 1Department of Pediatrics, Research Center, Hôpital Ste. Justine, 3175 Côte Ste. Catherine, Montreal, Québec H3T 1C5, Canada.

Investigative Ophthalmology & Visual Science
|May 1, 2002
PubMed
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Prolonged hypercapnia increases retinal blood flow via prostaglandins (PGs) and induced endothelial nitric oxide synthase (eNOS). This mechanism explains sustained retinal hyperemia during elevated CO2.

Area of Science:

  • Ophthalmology
  • Physiology
  • Cardiovascular Research

Background:

  • Prostaglandins (PGs) are known to cause hyperemia during acute hypercapnia.
  • The mechanism for sustained increases in retinal blood flow (RBF) during prolonged hypercapnia is not fully understood.

Purpose of the Study:

  • To investigate if prolonged hypercapnia causes sustained RBF increase via prostaglandin-dependent induction of endothelial nitric oxide synthase (eNOS).

Main Methods:

  • Piglet model exposed to hypercapnia (6% CO2) to measure RBF, PGE2, nitrite, and NOS protein.
  • Ex vivo eyecup preparations assessed PGE2, eNOS mRNA, NOS protein, and vasomotor responses.
  • Calcium (Ca2+) transients measured in neuroretinovascular endothelial cells.

Main Results:

Related Experiment Videos

  • Hypercapnia induced biphasic RBF increases (0.5h and 6-8h), pH normalization abolished these.
  • Early RBF increase linked to PGE2; late phase to nitrite and NOS protein.
  • Cyclooxygenase inhibition blocked both phases; NOS inhibition blocked only the late phase.
  • Hypercapnic acidosis increased retinal PGE2 and eNOS-dependent vasorelaxation ex vivo.
  • eNOS mRNA expression correlated with late RBF increase, blocked by transcription inhibitor and Ca2+ channel blocker.

Conclusions:

  • Sustained hypercapnia induces a novel mechanism for late retinal hyperemia.
  • This hyperemia is secondary to prostaglandin E2 (PGE2)-mediated induction of endothelial nitric oxide synthase (eNOS) expression.