Effects of nitric oxide synthase inhibition on ciliary blood flow, aqueous production and intraocular pressure

J. W. Kiel, H. A. Reitsamer, J. S. Walker, F. W. Kiel

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

A prior study found that inhibition of nitric oxide synthase with L-NAME causes a large, rapid decrease in IOP in anesthetized rabbits. In this follow-up study we sought to determine if this hypotensive effect was due to decreased aqueous production, possibly caused by ciliary vasoconstriction. Two protocols were performed in anesthetized rabbits. In the first protocol, mean arterial pressure (MAP) and IOP were measured by direct cannulation, and aqueous flow was measured by fluorophotometry, before and after L-NAME (5 mg kg-1, i.v., n = 7). In the second protocol, ciliary blood flow was measured transclerally by laser Doppler flowmetry while MAP was varied mechanically over a wide range before and after L-NAME (5 mg kg-1, i.v., n = 8). L-NAME caused a significant increase in MAP and decreases in IOP. ciliary blood flow and aqueous flow. L-NAME also caused a significant downward shift in the ciliary pressure-flow relation over the entire pressure range examined. The results indicate that L-NAME causes ciliary vasoconstriction and decreases aqueous production, suggesting that the L-NAME ocular hypotensive effect may be due in part to a blood flow-dependent decrease in aqueous production. However, assuming no uveoscleral outflow and constant episcleral venous pressure and outflow facility, the decrease in aqueous flow accounts for 66% of the drop in IOP, suggesting an additional effect of L-NAME on aqueous outflow.

Original languageEnglish (US)
Pages (from-to)355-364
Number of pages10
JournalExperimental Eye Research
Volume73
Issue number3
DOIs
StatePublished - 2001

Fingerprint

NG-Nitroarginine Methyl Ester
Intraocular Pressure
Nitric Oxide Synthase
Arterial Pressure
Vasoconstriction
Fluorophotometry
Rabbits
Pressure
Laser-Doppler Flowmetry
Venous Pressure
Catheterization

Keywords

  • Aqueous dynamics
  • Ciliary body
  • Fluorophotometry
  • Laser Doppler flowmetry
  • Nitric oxide
  • Regional blood flow

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Effects of nitric oxide synthase inhibition on ciliary blood flow, aqueous production and intraocular pressure. / Kiel, J. W.; Reitsamer, H. A.; Walker, J. S.; Kiel, F. W.

In: Experimental Eye Research, Vol. 73, No. 3, 2001, p. 355-364.

Research output: Contribution to journalArticle

Kiel, J. W. ; Reitsamer, H. A. ; Walker, J. S. ; Kiel, F. W. / Effects of nitric oxide synthase inhibition on ciliary blood flow, aqueous production and intraocular pressure. In: Experimental Eye Research. 2001 ; Vol. 73, No. 3. pp. 355-364.
@article{bfd825ac9a254bf5bce50fefffe3700b,
title = "Effects of nitric oxide synthase inhibition on ciliary blood flow, aqueous production and intraocular pressure",
abstract = "A prior study found that inhibition of nitric oxide synthase with L-NAME causes a large, rapid decrease in IOP in anesthetized rabbits. In this follow-up study we sought to determine if this hypotensive effect was due to decreased aqueous production, possibly caused by ciliary vasoconstriction. Two protocols were performed in anesthetized rabbits. In the first protocol, mean arterial pressure (MAP) and IOP were measured by direct cannulation, and aqueous flow was measured by fluorophotometry, before and after L-NAME (5 mg kg-1, i.v., n = 7). In the second protocol, ciliary blood flow was measured transclerally by laser Doppler flowmetry while MAP was varied mechanically over a wide range before and after L-NAME (5 mg kg-1, i.v., n = 8). L-NAME caused a significant increase in MAP and decreases in IOP. ciliary blood flow and aqueous flow. L-NAME also caused a significant downward shift in the ciliary pressure-flow relation over the entire pressure range examined. The results indicate that L-NAME causes ciliary vasoconstriction and decreases aqueous production, suggesting that the L-NAME ocular hypotensive effect may be due in part to a blood flow-dependent decrease in aqueous production. However, assuming no uveoscleral outflow and constant episcleral venous pressure and outflow facility, the decrease in aqueous flow accounts for 66{\%} of the drop in IOP, suggesting an additional effect of L-NAME on aqueous outflow.",
keywords = "Aqueous dynamics, Ciliary body, Fluorophotometry, Laser Doppler flowmetry, Nitric oxide, Regional blood flow",
author = "Kiel, {J. W.} and Reitsamer, {H. A.} and Walker, {J. S.} and Kiel, {F. W.}",
year = "2001",
doi = "10.1006/exer.2001.1050",
language = "English (US)",
volume = "73",
pages = "355--364",
journal = "Experimental Eye Research",
issn = "0014-4835",
publisher = "Academic Press Inc.",
number = "3",

}

TY - JOUR

T1 - Effects of nitric oxide synthase inhibition on ciliary blood flow, aqueous production and intraocular pressure

AU - Kiel, J. W.

AU - Reitsamer, H. A.

AU - Walker, J. S.

AU - Kiel, F. W.

PY - 2001

Y1 - 2001

N2 - A prior study found that inhibition of nitric oxide synthase with L-NAME causes a large, rapid decrease in IOP in anesthetized rabbits. In this follow-up study we sought to determine if this hypotensive effect was due to decreased aqueous production, possibly caused by ciliary vasoconstriction. Two protocols were performed in anesthetized rabbits. In the first protocol, mean arterial pressure (MAP) and IOP were measured by direct cannulation, and aqueous flow was measured by fluorophotometry, before and after L-NAME (5 mg kg-1, i.v., n = 7). In the second protocol, ciliary blood flow was measured transclerally by laser Doppler flowmetry while MAP was varied mechanically over a wide range before and after L-NAME (5 mg kg-1, i.v., n = 8). L-NAME caused a significant increase in MAP and decreases in IOP. ciliary blood flow and aqueous flow. L-NAME also caused a significant downward shift in the ciliary pressure-flow relation over the entire pressure range examined. The results indicate that L-NAME causes ciliary vasoconstriction and decreases aqueous production, suggesting that the L-NAME ocular hypotensive effect may be due in part to a blood flow-dependent decrease in aqueous production. However, assuming no uveoscleral outflow and constant episcleral venous pressure and outflow facility, the decrease in aqueous flow accounts for 66% of the drop in IOP, suggesting an additional effect of L-NAME on aqueous outflow.

AB - A prior study found that inhibition of nitric oxide synthase with L-NAME causes a large, rapid decrease in IOP in anesthetized rabbits. In this follow-up study we sought to determine if this hypotensive effect was due to decreased aqueous production, possibly caused by ciliary vasoconstriction. Two protocols were performed in anesthetized rabbits. In the first protocol, mean arterial pressure (MAP) and IOP were measured by direct cannulation, and aqueous flow was measured by fluorophotometry, before and after L-NAME (5 mg kg-1, i.v., n = 7). In the second protocol, ciliary blood flow was measured transclerally by laser Doppler flowmetry while MAP was varied mechanically over a wide range before and after L-NAME (5 mg kg-1, i.v., n = 8). L-NAME caused a significant increase in MAP and decreases in IOP. ciliary blood flow and aqueous flow. L-NAME also caused a significant downward shift in the ciliary pressure-flow relation over the entire pressure range examined. The results indicate that L-NAME causes ciliary vasoconstriction and decreases aqueous production, suggesting that the L-NAME ocular hypotensive effect may be due in part to a blood flow-dependent decrease in aqueous production. However, assuming no uveoscleral outflow and constant episcleral venous pressure and outflow facility, the decrease in aqueous flow accounts for 66% of the drop in IOP, suggesting an additional effect of L-NAME on aqueous outflow.

KW - Aqueous dynamics

KW - Ciliary body

KW - Fluorophotometry

KW - Laser Doppler flowmetry

KW - Nitric oxide

KW - Regional blood flow

UR - http://www.scopus.com/inward/record.url?scp=0034781310&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034781310&partnerID=8YFLogxK

U2 - 10.1006/exer.2001.1050

DO - 10.1006/exer.2001.1050

M3 - Article

C2 - 11520110

AN - SCOPUS:0034781310

VL - 73

SP - 355

EP - 364

JO - Experimental Eye Research

JF - Experimental Eye Research

SN - 0014-4835

IS - 3

ER -