Time course of changes in optic nerve head circulation after acute reduction in intraocular pressure.
OBJECTIVE
To study the time course of changes in circulation in the optic nerve head (ONH) after acute reduction in intraocular pressure (IOP) and to evaluate the effects of a calcium antagonist, a nitric oxide synthetase (NOS) inhibitor, indomethacin, and sympathetic nerve amputation on the changes in ONH circulation after reduction of IOP.


METHODS
In anesthetized albino rabbits, acute reduction of IOP (acute increase in ocular perfusion pressure [OPP]) was manometrically achieved and normalized blur (NB), a quantitative index of tissue blood velocity obtained with the laser speckle method, was serially monitored for 30 seconds and 60 minutes. The effects of systemic administration of 1 microg/kg per hour nilvadipine (a calcium antagonist), 300 microg/kg Nomega-nitro-l-arginine (l-NAME, a nonselective NOS inhibitor), and 5 mg/kg indomethacin or sympathetic nerve amputation on the changes in NB after reduction of IOP were studied.


RESULTS
During changes in IOP from 10 to 40 mm Hg and then back to 10 mm Hg, NB exhibited no significant change. During changes in IOP from 10 to 60 mm Hg and then back to 10 mm Hg, NB initially decreased with an increase in IOP to 60 mm Hg and then increased to baseline level when IOP was returned to 10 mm Hg. In the nilvadipine-treated rabbits, during changes in IOP from 10 to 40 mm Hg and back to 10 mm Hg and during the changes from 10 to 60 mm Hg and back to 10 mm Hg, NB decreased with increase in IOP to 40 or 60 mm Hg and then increased to slightly above the baseline when IOP returned to 10 mm Hg. l-NAME, indomethacin, and sympathetic nerve amputation each had little effect on the time course of change in NB.


CONCLUSIONS
ONH circulation was stably maintained after reduction of IOP from 40 to 10 mm Hg but not after that from 60 to 10 mm Hg. The changes in NB after reduction of IOP occurred quickly and were partially impaired with a calcium antagonist, but not with the NOS inhibitor, indomethacin, or sympathetic nerve amputation. These findings suggest the importance of vascular smooth muscle in maintaining stable ONH circulation against reduction of IOP in a fashion nearly independent of NO, endogenous prostaglandins, and the sympathetic nervous system.
Takayama
Jun
J
Eye Clinic, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan.
Tomidokoro
Atsuo
A
Tamaki
Yasuhiro
Y
Araie
Makoto
M
D000208:Acute Disease; D000818:Animals; D001775:Blood Circulation / Q000187:drug effects / Q000502:physiology; D001776:Blood Circulation Time; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007429:Intraocular Pressure; D017078:Laser-Doppler Flowmetry; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052247:Nitric Oxide Synthase Type II; D015814:Ocular Hypotension / Q000503:physiopathology*; D009898:Optic Disk / Q000098:blood supply*; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000502:physiology; D013997:Time Factors
D002121:Calcium Channel Blockers; D004791:Enzyme Inhibitors; C035100:nilvadipine; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D009543:Nifedipine; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin