CHOROIDAL MYOGENIC AUTOREGULATION AND INTRAOCULAR-PRESSURE

This study tests the hypothesis that choroidal myogenic autoregulation participates in the intraocular pressure (IOP) response to mean arterial pressure (MAP) by minimizing arterial-pressure-dependent changes in choroidal blood volume. To test this hypothesis, the IOP response to MAP was quantified before and after impairing choroidal autoregulation. In a previous study, the efficacy of choroidal myogenic autoregulation was inversely related to IOP. Therefore, in one series of experiments (n = 6), the relationship between MAP and IOP was determined at normal and elevated baseline IOP (i.e., 15 and 25 mmHg, respectively). In a second series of experiments (n = 6), the relationship between MAP and IOP was determined at the normal IOP (15 mmHg) before and after administering hydralazine, an arterial vasodilator. In both series, the MAP manipulations were kept brief to avoid the confounding effects of aqueous compensation. The experiments were performed in pentobarbital anesthetized rabbits with hydraulic occluders placed on the thoracic descending aorta and inferior vena cava to raise and lower MAP, respectively. MAP was measured via a central ear artery catheter. The right eye was cannulated with two 23 gauge needles; one cannula was used to set the IOP by varying the ocular volume and the other was used to measure the IOP. The protocol consisted of inflating the occluders to cause brief (1-1·5 min) ramp increases and decreases in MAP over a wide pressure range. Baseline IOP was set prior to each occlusion, but was otherwise uncontrolled. In the first series, the MAP range was 30 to 95 mmHg and IOP changed by 6 mmHg at the normal baseline IOP and by 18 mmHg at the elevated baseline IOP. The corresponding volume shifts were 7·7 and 14·5 μl, respectively. In the second series, the MAP range was 25 to 95 mmHg and IOP changed by 6 mmHg during control and by 14 mmHg after hydralazine. The corresponding volume shifts were 6·7 and 13·8 μl, respectively. In both series, the prompt return of IOP to baseline upon restoration of normal MAP indicated that the volume changes were due to changes in ocular blood volume. Additional experiments confirmed that elevating the baseline IOP and administering hydralazine impaired choroidal autoregulation but did not alter the cranial venous pressure response to varying MAP. Other experiments showed that during sustained increases in MAP the initial rise in IOP was small and IOP returned to baseline within 3-5 min under control conditions, but after hydralazine the initial rise in IOP was greater and required a longer period of time to return to baseline. These results are consistent with the hypothesis that myogenic autoregulation in the choroid normally minimizes MAP-dependent changes in ocular blood volume and the consequent fluctuations in IOP. © 1994 Academic Press. All rights reserved.