EVect of acute intraocular pressure changes on short posterior ciliary artery haemodynamics

Background/aims—Vascular insuYciency due to abnormal autoregulation has been proposed as a major factor in the development of glaucoma. The anterior optic nerve is primarily perfused by the short posterior ciliary arteries. The autoregulatory capacity of these vessels in response to acutely elevated intraocular pressure (IOP) was examined in normal human subjects. Methods—Colour Doppler imaging was performed on the short posterior ciliary arteries of 10 normal subjects at baseline and during four incremental IOP elevations. Using a scleral suction cup placed temporally, IOP was elevated to approximately 25, 30, 40, and 50 mm Hg. Additional measurements were performed immediately after pressure release. Systolic and diastolic flow velocities were measured and Pourcelot’s resistivity index was calculated. Results—Systolic and diastolic flow velocities decreased linearly with each incremental increase in IOP (p<0.001). Pourcelot’s resistivity index increased linearly with each incremental increase in IOP (p<0.001). Changes in end diastolic velocity, peak systolic velocity, and Pourcelot’s resistivity index were linearly related to changes in IOP. Conclusion—The normal healthy eye is not able to autoregulate to maintain PCA blood flow velocities in response to acute large elevations in IOP. (Br J Ophthalmol 1999;83:33–38) The pathogenesis of glaucomatous optic neuropathy remains incompletely understood. While elevated intraocular pressure (IOP) is a clear risk factor, vascular insuYciency and abnormal autoregulation of the optic nerve circulation have been hypothesised to play a significant role in the development and progression of glaucoma. It is possible that mechanical and vascular factors have a synergistic interaction. Experimentally, elevated IOPs have produced delayed circulation times, most notably in the peripapillary choroid. 6 Similar findings have been described in glaucoma patients. 8 Using colour Doppler imaging (CDI), abnormal blood flow velocities in the retrobulbar vessels of primary open angle and normal tension glaucoma patients have been measured. An increase in mean and end diastolic velocity and a decrease in resistance index have been noted in the central retinal and short posterior ciliary arteries of glaucoma patients after trabeculectomy. A recent CDI study of patients with nonischaemic optic atrophy failed to demonstrate a significant change in retrobulbar haemodynamics suggesting that optic atrophy itself does not alter orbital haemodynamics to the extent noted in glaucoma patients. These findings and the possible association of normal tension glaucoma with vasospastic angina, migraine headache, and Raynaud’s disease add further support to a vascular contribution to glaucomatous optic nerve damage. Colour Doppler imaging has recently been used to demonstrate the highly dependent relation between central retinal artery haemodynamics and acute changes in IOP. Acute incremental elevation of IOP in healthy human subjects resulted in a progressive drop in central retinal artery blood flow velocities implying a close link among mechanical and haemodynamic factors in this particular vascular bed. In contrast, ophthalmic artery flow velocities were found to be unaVected by acute IOP changes. Since the anterior optic nerve is supplied largely by the short posterior ciliary arteries, 22 the purpose of this study was to determine the relation between short posterior ciliary artery haemodynamics and acute changes in IOP. This was studied by using scleral suction to acutely alter IOP in healthy eyes and monitoring the short posterior ciliary arteries with non-invasive CDI. Materials and methods All subjects had normal eye examinations with the exception of refractive error. No subject had systemic vascular disease. Ten subjects, five men and five women, were studied. Their ages ranged from 26 to 56 years. All measurements were made on the left eye. This procedure was approved by the University of Miami Human Subjects Institutional Review Board. Informed consent was obtained from all subjects. All experimental procedures conformed to the tenets set out in the Declaration of Helsinki. All subjects were reclined at 120°. Drops of 0.5% proparacaine hydrochloride (proxymetacaine, Alcon Laboratories, Fort Worth, TX, USA) were placed into each subject’s left eye. Cotton swabs soaked in 4% lignocaine hydrochloride were applied to the temporal conjunctiva for 2 minutes. Brachial artery blood pressures were measured using sphygmomanometry and IOP was measured using a TonoPen XL tonometer (Mentor, Inc, Norwell, MA, USA). A Quantum 2000V (Siemans, Issaquah, Br J Ophthalmol 1999;83:33–38 33 Department of Ophthalmology and Visual Science, Vanderbilt University, Nashville, TN, USA K M Joos B E Steinwand Bascom Palmer Eye Institute, University of Miami, Miami, FL, USA K M Joos M D Kay L E Pillunat E K Gendron W J Feuer UniversitatsAugenklinik, Hamburg, Germany L E Pillunat Department of Ophthalmology and Physiology, Indiana University, Indianapolis, IN, USA A Harris Correspondence to: Dr K M Joos, Department of Ophthalmology and Visual Science, Vanderbilt University, 8017 MCE, Nashville, TN 37232-8808, USA. Accepted for publication 30 July 1998 group.bmj.com on October 15, 2017 Published by http://bjo.bmj.com/ Downloaded from