Abstract
The effect of decreased ocular mean perfusion pressure (PPm), defined as mean arterial blood pressure minus intraocular pressure (IOP), on optic nerve head blood flow (Fonh) and on the response of this flow (RFonh) to diffuse luminance flicker was investigated in 19 anesthetized cats using laser Doppler flowmetry. PPmwas decreased by increasing the IOP. The flicker stimulus consisted of 20-msec flashes delivered at 10 Hz for 30–60 sec. It illuminated a 30° diameter area of the fundus, centered at the optic disk. Decreasing PPmby 10–35% from its resting value resulted in a 23% increase in RFonh(supranormal RFonh). With further decreases in PPm, RFonhdecreased, reaching zero at a PPmbelow 20 mmHg. Fonhremained constant until PPmwas <40 mmHg and then decreased thereafter. When PPmwas brought back to resting value after having been decreased for ≈45 min, Fonhfirst increased by ≈380% and then returned to its value at rest within ≈4.5 min. At low PPm, hyperoxia decreased Fonhby 23% and restored the attenuated RFonhback to the value at resting PPmand hypoxia did not increase Fonh, as it did at normal PPm. This study confirms that the optic nerve head circulation is autoregulated over a wide range of PPmand reveals, for the first time, a hyperemic response to a prolonged decrease in PPm. It suggests that hypoxia plays a role in abolishing RFonhat low PPmand that the supranormal RFonhat moderately decreased PPmis due to an increase in the flicker-induced ganglion cell activity.
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