Document Detail


Time course of the change in optic nerve head circulation after an acute increase in intraocular pressure.
MedLine Citation:
PMID:  12939318     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: To investigate the time course of changes in optic nerve head (ONH) circulation after an acute increase in intraocular pressure (IOP), by using the laser speckle method, and to evaluate the effects of a calcium antagonist, the nitric oxide synthetase inhibitor, indomethacin, or sympathetic nerve amputation on the response in ONH circulation after an acute increase in IOP. METHODS: In rabbits, the normalized blur (NB) level, a quantitative index of tissue blood velocity in the ONH, was monitored for 60 minutes after an increase in IOP from 20 mm Hg to 40, 50, or 60 mm Hg and for 25 seconds after increase in IOP from 20 mm Hg to 50 or 60 mm Hg with high time resolution. The effects of systemic administration of 1 micro g/kg per hour nilvadipine (a calcium antagonist), 30 mg/kg N(omega)-nitro-L-arginine (L-NAME), or 5 mg/kg indomethacin, or those of sympathetic nerve amputation on the time course of the changes in NB were studied. RESULTS: NB showed a quick recovery within several seconds after increase in IOP to 40 or 50 mm Hg, whereas no or little recovery occurred after an increase to 60 mm Hg. The nilvadipine treatment significantly increased NB at IOP of 20 mm Hg (baseline NB, P = 0.045) and apparently impaired the recovery of NB after the increase in IOP. After L-NAME administration, baseline NB significantly decreased (P = 0.028), and the NB recovery time was slightly but significantly prolonged (P = 0.012). Indomethacin showed no effects on baseline NB or NB recovery. Sympathetic nerve amputation increased baseline NB (P = 0.027), but did not influence NB recovery. CONCLUSIONS: The current results showed a quick recovery response in the ONH circulation after an acute increase in IOP in rabbits. A calcium antagonist impaired the response. Production of nitric oxide or prostaglandins or the sympathetic nervous system is probably not mainly responsible for the reaction.
Authors:
Jun Takayama; Atsuo Tomidokoro; Kiyoshi Ishii; Yasuhiro Tamaki; Yasuhiro Fukaya; Tomokazu Hosokawa; Makoto Araie
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  44     ISSN:  0146-0404     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-08-26     Completed Date:  2003-09-16     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3977-85     Citation Subset:  IM    
Affiliation:
Eye Clinic, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Circulation / drug effects,  physiology
Blood Flow Velocity / drug effects,  physiology
Calcium Channel Blockers / pharmacology
Indomethacin / pharmacology
Intraocular Pressure*
Laser-Doppler Flowmetry
NG-Nitroarginine Methyl Ester / pharmacology
Nifedipine / analogs & derivatives*,  pharmacology
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type II
Ocular Hypertension / physiopathology*
Optic Disk / blood supply*
Parasympathectomy
Rabbits
Time Factors
Chemical
Reg. No./Substance:
0/Calcium Channel Blockers; 21829-25-4/Nifedipine; 50903-99-6/NG-Nitroarginine Methyl Ester; 53-86-1/Indomethacin; 75530-68-6/nilvadipine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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