Effect of acute decreases of perfusion pressure on choroidal blood flow in humans.

PURPOSE To investigate the relationship between choroidal blood velocity (ChBVel), blood volume (ChBVol) and blood flow (ChBF) in the foveal region of the human ocular fundus and ocular perfusion pressure and to determine whether the choroidal circulation has some autoregulatory capacity. METHODS Measurements of ChBVel, ChBVol and ChBF were obtained by laser Doppler flowmetry in healthy subjects (age range, 21 to 57 years) with normal eye examination results. Measurements were performed at normal intraocular pressure (IOP) and during successive step increases in IOP induced by scleral suction. In experiment 1, in six eyes (five subjects), the IOP was increased rapidly, in steps of 50 to 100 mm Hg of suction pressure, which each lasted approximately 10 seconds to a level above diastolic ophthalmic artery blood pressure (IOP = approximately 72 mm Hg). In experiment 2, in 14 eyes (seven subjects), the IOP was increased slowly in four successive steps at 2-minute intervals to a level of approximately 42 mm Hg. We also determined the pulsatility of the flow parameters during the heart cycle, pulsatility = 1 - diast value/syst value. RESULTS For both rates of suction cup increase, the relationship between ChBFm (mean ChBF over the heart cycle) and mean perfusion pressure was not linear. At high pressure, ChBFm was less affected by decreases in the pressure than expected from a passive vascular system. In some cases, no change in ChBFm was detectable, although significant changes in PChBF occurred. Further decreases in perfusion pressure resulted in a proportional decrease in ChBFm. On release of suction, a significant increase in ChBFm over baseline value was detectable in experiment 1. CONCLUSIONS The relationship between ChBFm and ocular mean perfusion pressure appears to be bilinear and reveals some autoregulation for moderate step decreases in perfusion pressure. The temporal characteristics of the ChBFm-response suggest a neural or passive hemodynamical process rather than a myogenic or metabolic compensatory mechanism.