Retinal arteriolar diameter, blood velocity, and blood flow response to an isocapnic hyperoxic provocation

Abstract

Fisher. Retinal arteriolar diameter, blood velocity, and blood flow response to an isocapnic hyperoxic provocation. Am J Physiol Heart Circ Physiol 288: H2912-H2917, 2005. First published February 11, 2005 doi:10.1152/ajpheart.01037.2004.-The aim of this study was to simultaneously quantify the magnitude and response characteristics of retinal arteriolar diameter and blood velocity induced by an isocapnic hyperoxic provocation in a group of clinically normal subjects. The sample comprised 10 subjects (mean age, 25 yr; range, 21-40 yr). Subjects initially breathed air for 5-10 min, then breathed O 2 for 20 min, and then air for a final 10-min period via a sequential rebreathing circuit (Hi-Ox; Viasys) to maintain isocapnia. Retinal arteriolar diameter and blood velocity measurements were simultaneously acquired with a Canon laser blood flowmeter (CLBF-100). The response magnitude, time, and lag of diameter and velocity were calculated. In response to hyperoxic provocation, retinal diameter was reduced from control values of 111.6 (SD 13.1) to 99.8 (SD 10.6; P Ͻ 0.001) m and recovered after withdrawal of hyperoxia. Retinal blood velocity and flow concomitantly declined from control values of 32.2 (SD 6.4) mm/s and 9.4 (SD 2.5) l/min to 20.7 (SD 3.4) mm/s and 5.1 (SD 1.3) l/min, respectively (P Ͻ 0.001 for both velocity and flow), and recovered after withdrawal of hyperoxia. The response times and response lags were not significantly different for each parameter between effect and recovery or between diameter and velocity. We conclude that arteriolar retinal vascular reactivity to hyperoxic provocation is rapid with a maximal vasoconstrictive effect occurring within a maximum of 4 min. Although there was a trend for diameter to respond before velocity to the isocapnic hyperoxic provocation, the response characteristics were not significantly different between diameter and velocity. vascular reactivity; laser Doppler velocimetry; isocapnic hyperoxia THE BLOOD SUPPLY TO THE INNER retina is derived from the central retinal artery, whereas the choriocapillaris supplies the outer retina and photoreceptors. The retinal tissue is one of the most metabolically active in the body and, correspondingly, an uninterrupted nutrient supply is essential (50). The inner retinal blood vessels (i.e., past the lamina cribrosa) are thought to be unique due to the absence of an autonomic nerve supply to regulate vascular tone (53). Blood supply to the inner retina is regulated via local feedback signals that alter retinal perfusion in response to changes in systemic blood pressure or the concentration of certain metabolites (11,18). In particular, retinal blood flow is strongly dependent on the partial pressure of oxygen (PO 2 ; Refs. 14,25,31,42,48).The retinal vasculature can be noninvasively visualized and, consequently, its hemodynamic parameters quantified. Impairment of vascular reactivity has been demonstrated in the pathogenesis of various ocular diseases including diabetic retinopathy (13,20,25,32). Administration of O 2 has p...

Retinal Oxygen Metabolism During Normoxia and Hyperoxia in Healthy Subjects

“…Consistent with previous studies, [36][37][38][39][40][41][42] we observed a pronounced reduction in retinal vessel diameters, retinal blood velocities, and retinal blood flow during 100% oxygen breathing. We also observed an increase in SO 2 in both retinal arteries and retinal veins, with a more pronounced effect in the latter, which is again comparable to previous data.…”

Measurement of retinal blood flow in the rat by combining Doppler Fourier-domain optical coherence tomography with fundus imaging

“…Our data show a reduction of 50 to 60% in retinal blood flow, which is closer to the values obtained in humans. [41][42][43][44][45][46] Studying the response of retinal blood flow to hyperoxia is interesting, because it has been shown to be disturbed early in diabetes. 47 However, the mechanisms which lead to this reduced vasoconstrictor response to hyperoxia are poorly understood.…”

Similarities and Differences in Arterial Responses to Hypercapnia and Visual Stimulation

“…Given that capillary blood velocities are B0.1 cm/s or lower, as found in animal studies (Villringer et al, 1994;Kleinfeld et al, 1998;Hutchinson et al, 2006), the rationale is to use as low a velocity-encoding level as possible without losing too much detection power, especially with the typical ASL perfusionweighted signal change already being very small. At Venc = 3 cm/s, one is likely to be probing arterioles and perhaps small arteries in addition to capillaries as part of the microvascular compartment, because arterioles and small pial arteries of diameter < 200 mm appear to have flow velocities that range from 1 to 6 cm/s (Kobari et al, 1984;Gilmore et al, 2005;Kisilevsky et al, 2008). Decreasing the bipolar crushing gradients, or in other words, using higher levels of velocity encoding, such as 6 cm/s (b = 0.32 seconds/mm 2 ) and 9 cm/s (b = 0.14 seconds/ mm 2 ) would still exclude significant arterial signal, given that the large conductive arteries in the human brain are known to have flow velocities of 30 cm/s and beyond, as measured in the posterior, middle, and anterior cerebral arteries.…”