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Abstract #9730 Published in IGR 5-3
Time course of the change in optic nerve head circulation after an acute increase in intraocular pressure
Takayama J; Tomidokoro A; Ishii K; Tamaki Y; Fukaya Y; Hosokawa T; Araie MInvestigative Ophthalmology and Visual Science 2003; 44: 3977-3985
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 of from 20 mmHg to 40, 50, or 60 mmHg, and for 25 seconds after increase in IOP of from 20 mmHg to 50 or 60 mmHg with high time resolution. The effects of systemic administration of 1 μg/kg per hour nilvadipine (a calcium antagonist), 30 mg/kg NΩ-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 mmHg, whereas no or little recovery occurred after an increase to 60 mmHg. The nilvadipine treatment significantly increased NB at IOP of 20 mmHg (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.
Dr. J. Takayama, Eye Clinic, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan
Classification:
5 Experimental glaucoma; animal models
6.11 Bloodflow measurements (Part of: 6 Clinical examination methods)
11.8 Neuroprotection (Part of: 11 Medical treatment)
