AUTOREGULATION OF HUMAN OPTIC-NERVE HEAD BLOOD-FLOW IN RESPONSE TO ACUTE CHANGES IN OCULAR PERFUSION-PRESSURE

Citation
Ce. Riva et al., AUTOREGULATION OF HUMAN OPTIC-NERVE HEAD BLOOD-FLOW IN RESPONSE TO ACUTE CHANGES IN OCULAR PERFUSION-PRESSURE, Graefe's archive for clinical and experimental ophthalmology, 235(10), 1997, pp. 618-626
Citations number
19
Categorie Soggetti
Ophthalmology
ISSN journal
0721832X
Volume
235
Issue
10
Year of publication
1997
Pages
618 - 626
Database
ISI
SICI code
0721-832X(1997)235:10<618:AOHOHB>2.0.ZU;2-I
Abstract
Background: Studies in animals have demonstrated that optic nerve head (ONH) blood flow (F-onh) is autoregulated, but there is a lack of evi dence for such a process in humans. Therefore, we investigated the rel ationship between F-onh and mean ocular perfusion pressure (PPm) in no rmal volunteers when PPm is decreased through elevation of the intraoc ular pressure (IOP). Methods: Laser Doppler flowmetry (LDF) was used t o measure relative mean velocity (Vel(ohn)), volume (Vol(onh)) and F-o nh of blood at sites of the ONH away from visible vessels, while PPm w as decreased in two ways: (1) rapidly, by IOP increments of 15 a durat ion, and (2) slowly, by IOP increments of 2 min duration, both by scle ral suction cup in one eye of each of nine subjects. Results: A rapid and large decrease of PPm of more than 100% induced a decrease of more than 80% in F-onh. With the slower decrease in PPm, F-onh remained co nstant down to a PPm of approximate to 22 mm Hg (IOP = 40 mm Hg) and t hen decreased, predominatly due to a decrease in Vel(ohn). Immediately after removal of the suction cup, F-onh increased transiently by 44% above baseline. Conclusions: This study demonstrates efficient blood f low autoregulation in the OHN, which is probably brought about by an i ncrease in vascular capacitance. The magnitude of the reactive hyperae mia agrees with the compensatory decrease in ONH vascular resistance d uring IOP elevation. The time scale of the autoregulatory process and the dependence of the hyperaemia upon duration of IOP elevation sugges t a metabolic mechanism of autoregulation.