[Show abstract][Hide abstract] ABSTRACT: Purpose:
The present study aimed to quantify retinal and choroidal blood flow (BF) during light, dark adaptation and flicker light stimulation using the microsphere technique.
Materials and methods:
Adult male Sprague-Dawley rats were anesthetized with isoflurane. Eyes were dark (Group I, n = 8), light (Group II, n = 8) adapted or stimulated with 10 Hz flicker light (Group III, n = 10). Retinal and choroidal BF were measured by a previously established method, using a mixture of 8 µm yellow-green and 10 µm red fluorescent microspheres. The microspheres were counted ex vivo in the dissected retina and choroid and in the reference arterial blood under a fluorescent microscope.
The choroidal BF was 64.8 ± 29 µl/min (mean ± SD) during dark adaptation, not significantly different from that during light adaptation (66.0 ± 17.8 µl/min). The retinal BF was 13.5 ± 3.2 µl/min during 10 Hz flickering light stimulation, significantly higher than that during dark adaptation in the control fellow eyes (9.9 ± 2.9 µl/min). The choroidal BF values were not statistically different between flicker stimulation and dark adaptation. Retinal BF was 11.6 ± 2.9 µl/min during light adaptation. Dark adaptation did not increase retinal BF (Group I, 8.2 ± 2.4 µl/min; Group II, 9.9 ± 2.9 µl/min).
These findings argue against a dark-induced or flicker-induced functional hyperemia in the choroid as a result of the demands of the outer retina. Retinal BF was not higher during dark adaptation. Our data support the conclusion that the inner retina has a higher energy demand in flicker conditions relative to dark.
No preview · Article · Jan 2013 · Current eye research
[Show abstract][Hide abstract] ABSTRACT: Purpose: We developed a rat model of acute hypertension by occluding the descending aorta and used cerebral blood flow (CBF) MRI to evaluate cerebral autoregulation (CA) under normocapnia and hypercanpia. This method avoids potential pharmaceutical complications and can be repeatedly applied in the scanner. The long term goal is to apply this approach to study CA in rat models of chronic hypertension, stroke and diabetes. Methods: 9 Long-Evans rats were used for MRI and blood-gas measurements. They were mechanically ventilated under normocapnia, and then hypercapnia. Blood pressure (BP) was modulated by a balloon catheter placed in the descending aorta near diaphragm. MRI studies were performed on an 11.7 T MRI using continuous arterial spin labeling. Modulation paradigm: OFF- ON(1min)-OFF. The mean CBF and BOLD (extracted from non-labeled images) signals of the cerebrum was reported. The changes of CBF, BP and BOLD (△CBF, △BP and △BOLD) from the baseline to the occlusion period were analyzed. Total 23 trials under normocapnia and 21 trails under hypercapnia were performed. Results: CBF, BOLD, BP, arterial pO2 and pH increased significantly during the occlusion under both hypercapnia and normocapnia. BP elevation was sustainable. After initial instant transient increase, CBF returned toward the baseline at a faster(p=0.047) rate under normocapnia than under hypercapnia(∼3x). Under normocapnia, ACBF was not linearly correlated to △BP(p=0.53). The absence of correlation and faster returning rate under normocapnia indicates CA. By contrast, under hypercapnia, ACBF increased linearly with ABP(p=0.002), which indicates autoregulation impairment. %△CBF vs. %△BOLD remained linearly correlated under both conditions. Conclusions: We developed a model of acute hypertension in rat for use in the MRI scanner. CBF MRI results indicated that there were apparent CA under normocapnia but was markedly impaired under hypercapnia. This approach sets the stage for study of CA in rat models of chronic hypertension, stroke and diabetes.