Effects of intraocular pressure on pH outside rod photoreceptors in the cat retina

Abstract

Double-barreled H(+)-selective microelectrodes were used to study the effect of raising intraocular pressure (ocular hypertension) on intraretinal pH in the cat. A surprising alkalinizing response was observed in the subretinal space on the first experimental day in seven of 11 experiments. Of the three retinal regions studied, the alkalinizing response was present in the area centralis and in the adjoining near-discal region, but was absent in the superior temporal periphery. The alkalinizing response was relatively fragile, diminishing and then extinguishing with repetition of episodes of ocular hypertension. It was also never observed on the second experimental day. The alkalinizing response had a relatively low threshold, appearing with 10 mmHg elevations of intraocular pressure, i.e. when the perfusion pressure was still relatively high, but was also present across a wide range of perfusion pressures. It was maximal in amplitude in the most distal portion of the subretinal space and consisted of two components, an 'on' alkalinization during the episode of ocular hypertension, and an 'off' alkalinization following it. When the alkalinizing response was present in the subretinal space, it also could be recorded with placement of the microelectrode in the choroid. Elevations of systemic arterial blood pressure with epinephrine (intravenous), by raising perfusion pressure, also alkalinized the subretinal space, indicating that an increase in choroidal blood flow can produce this type of pH response. While pH recordings do not directly monitor blood flow, we tentatively interpreted the alkalinizing response with ocular hypertension as originating from a regional increase in choroidal blood flow, but we cannot rule out other explanations. Acidification of the subretinal space in response to ocular hypertension replaced the alkalinizing response when the latter extinguished, or acidification was the sole response in the absence of an alkalinization. The acidification also had a low threshold, was maximal in the most distal portion of the subretinal space, and increased in size with decreases in perfusion pressure. The acidification was reduced in amplitude by breathing 100% oxygen (hyperoxia). This was interpreted as suppression of the component of acidification that originated from an increase in glycolysis by the rod photoreceptors during ocular hypertension.