Time course of the change in optic nerve head circulation after an acute increase in intraocular pressure.
OBJECTIVE
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.
Takayama
Jun
J
Eye Clinic, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan.
Tomidokoro
Atsuo
A
Ishii
Kiyoshi
K
Tamaki
Yasuhiro
Y
Fukaya
Yasuhiro
Y
Hosokawa
Tomokazu
T
Araie
Makoto
M
D000818:Animals; D001775:Blood Circulation / Q000187:drug effects / Q000502:physiology; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007429:Intraocular Pressure; D017078:Laser-Doppler Flowmetry; 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; D009798:Ocular Hypertension / Q000503:physiopathology*; D009898:Optic Disk / Q000098:blood supply*; D017764:Parasympathectomy; D011817:Rabbits; D013997:Time Factors
D002121:Calcium Channel Blockers; C035100:nilvadipine; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D009543:Nifedipine; D019331:NG-Nitroarginine Methyl Ester; D007213:Indomethacin