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J. K. Adleman, S. Dorner, J. A. Fisher, T. Wong, G. E. Trope, C. Hudson; Retinal Vascular Reactivity Response to Hyperoxic Hypocapnia and Hypoxic Hypercapnia in Healthy Subjects. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5020.
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To determine the vascular reactivity capacity in response to vaso-constrictive and -dilatory provocation of retinal arterioles in healthy subjects.
One randomly chosen eye of 15 healthy subjects was studied (mean age 25, range 20-32 years). End-tidal gas concentrations were applied using a custom model-based prospective end-tidal targeting system (RespirActTM, TRI, Toronto). The vasoactive properties of O2 and CO2 were combined to administer a hyperoxic hypocapnic constrictor stimulus and two graded hypoxic hypercapnic dilatory stimuli in random order. A 15 minute interval was employed following hyperoxic hypocapnia to avoid any persistent effects of O2.Vascular reactivity was defined as change from a standardized baseline in arteriolar diameter, blood velocity and blood flow as assessed by the Canon Laser Blood Flowmeter. Three hemodynamic measurements were acquired in the superior temporal arteriole at approximately 1 disc diameter from the optic nerve head.
At baseline, the mean magnitude of flow was 9.8µL/min. Flow reduced by 22% during hyperoxic hypocapnia (p<0.01) and increased by 17% during the maximal hypoxic hypercapnia phase (p<0.04). In response to the two dilatory stimuli, diameter increased (p<0.04) to hypoxic hypercapnia but the diameter response to the more efficacious dilatory stimulus was not different when compared to the lower dilatory stimulus. Blood pressure and heart rate increased during the dilatory stimuli.
This study provides an estimation of the normal range of total vascular reactivity capacity to extreme constrictor and dilatory stimuli in the retina. During the second dilatory stimulus, diameter showed a subdued magnitude of dilation. We interpret this to represent a myogenic autoregulatory response, secondary to a rise in perfusion pressure, which superseded the metabolic response to inhaled gases.
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