Studies of the ocular pulse in primates.

Ocular pulse amplitude (OPA) and intraocular pressure (IOP) were measured in groups of human subjects with primary open-angle glaucoma (POAG), ocular hypertension (OHT), low-tension glaucoma (LTG), retinal degenerations (RD), in OHT volunteers treated with single doses of 2% epinephrine, 4% pilocarpine, 0.5% timolol or 1% p-amino-clonidine, and in normal subjects before and after exercise. Compared to normal controls, OHT subjects showed significantly higher IOP and OPA, while OPA was significantly lower in ocular normotensive LTG and RD subjects groups. All drug treatments lowered IOP in OHT subjects, but did not change OPA significantly. Exercise in normal volunteers increased calculated ocular perfusion pressure by 22.5%, lowered IOP by 32%, but showed no significant change in OPA. When IOP was elevated > or = 5 mmHg in lasered monkey eyes peak pulse volume (PPV) was increased significantly in the unlasered eyes. Epinephrine 2% or 1% p-aminoclonidine lowered IOP moderately with no change in PPV, while treatment with 4% pilocarpine or 0.5% timolol reduced IOP and increased PPV significantly. The findings suggest that LTG may be associated with an ocular vascular abnormality. OPA in OHT or normal human subjects did not change when IOP was decreased by antiglaucoma drug treatments or exercise, respectively. These results indicate that OPA may be physiologically autoregulated in human subjects with IOPs in the 11-21 mmHg range. However, laser-induced glaucomatous monkey eyes with higher IOP (30-35 mmHg) did not autoregulate, but showed a low peak pulse volume, which increased when IOP was reduced 5 mmHg or more by means of antiglaucoma drug treatment.