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Li and colleagues explore the effects of acute arterial blood pressure and venous pressure changes on IOP in rats with unilateral experimental glaucoma using a micro bead model. Ocular pulse amplitude and IOP were recorded from the anterior chamber during hemodynamic challenge using either phenylephrine or rapid saline IV loading. At the end of eight weeks, IOP was elevated by 60% in the unilateral ocular hypertensive eye.
Phenylephrine infusion induced a significant increase in both arterial blood pressure and IOP. A significantly greater IOP increase and a larger ocular pulse amplitude were found in the experimental eye with the higher pressure. A sustained rise in IOP was similarly found following IV saline loading with a greater rise observed in the experimental eyes. Some limitations of this outflow obstruction model of glaucoma include: 1) micro bead obstruction is not representative of obstruction seen in human glaucoma; 2) pressure measurements may be confounded by general anesthesia; 3) techniques used to induce blood pressure elevation are not representative of physiologic responses.
However, this study reports several findings that may provide insights into mechanisms that contribute to the pathology observed in human glaucoma. Firstly, there is an exaggerated IOP response during acute elevations in blood pressure with a real time linear relationship. Secondly, during an acute increase in blood pressure there is an associated increase in the ocular pulse amplitude in the eyes with the experimental glaucoma. Thirdly, a sustained IOP elevation occurs in eyes with intravenous volume loading, with a greater response experienced in the eyes with experimental glaucoma. The current study also agrees with other investigators findings of a direct relationship between ocular pulse amplitude and IOP as well as a highly synchronous correlation of the ocular and cardiac pulse.