Comparison of retinal arteriolar and venular variability in healthy subjects

Rose, Patricia A.; Hudson, Chris

doi:10.1016/j.mvr.2006.10.001

Cited by 11 publications

(10 citation statements)

References 15 publications

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“…In post-capillary venule segments that demonstrated a definite response (colored symbols, Figs 1B and C and 3A and B), the constriction of −6% during isocapnic hyperoxia (Table 3) was smaller than the −14% constriction previously reported in larger venules 30 , whilst the 8% dilation following isoxic hypercapnia (Table 3) was comparable to the +6% reported in larger venules 34 .…”

Section: Discussionmentioning

confidence: 61%

Reactivity in the human retinal microvasculature measured during acute gas breathing provocations

Duan

Bedggood

Metha

et al. 2017

Sci Rep

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Although changes in vessel diameter following gas perturbation have been documented in retinal arterioles and venules, these responses have yet to be quantified in the smallest vessels of the human retina. Here, using in vivo adaptive optics, we imaged 3–25 µm diameter vessels of the human inner retinal circulation and monitored the effects of altered gas-breathing conditions. During isocapnic hyperoxia, definite constrictions were seen in 51% of vessel segments (mean ± SD for pre-capillary arterioles −9.5 ± 3.0%; capillaries −11.8 ± 3.3%; post-capillary venules −6.3 ± 2.8%); these are comparable with responses previously reported in larger vessels. During isoxic hypercapnia, definite dilations were seen in 47% of vessel segments (mean ± SD for pre-capillary arterioles +9.8 ± 1.5%; capillaries +13.7 ± 3.8%; post-capillary venules +7.5 ± 4.2%); these are proportionally greater than responses previously reported in larger vessels. The magnitude of these proportional changes implies that the capillary beds themselves play an important role in the retinal response to changes in carbon dioxide levels. Interestingly, the distribution of microvascular responses shown here differs from our previously reported responses to flicker stimulation, suggesting differences in the way blood supply is coordinated following gas perturbation and altered neural activity.

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Section: Discussionmentioning

confidence: 61%

Reactivity in the human retinal microvasculature measured during acute gas breathing provocations

Duan

Bedggood

Metha

et al. 2017

Sci Rep

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“…Studies investigating the diameter of arterioles and venules during breathing of a hyperoxic (100% O 2 ) gas mixture have also noted a difference in the reactivity of the vessels; the venular constriction is much greater than that observed in the arterioles. [24][25][26] These findings are not equivocal. 27,28 A likely explanation is the compliance of the venular wall, which is much greater than that of the arteriolar wall, which has a strongly developed smooth muscle cell layer.…”

Section: Discussionmentioning

confidence: 99%

Separate and Combined Effects of Hypoxia and Horizontal Bed Rest on Retinal Blood Vessel Diameters

Louwies

Mekjavič

Cox

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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Citation: Louwies T, Jaki Mekjavic P, Cox B, et al. Separate and combined effects of hypoxia and horizontal bed rest on retinal blood vessel diameters. Invest Ophthalmol Vis Sci. 2016;57:4927-4932. DOI:10.1167/ iovs.16-19968 PURPOSE. To assess the separate and combined effects of exposure to prolonged and sustained recumbency (bed rest) and hypoxia on retinal microcirculation. METHODS.Eleven healthy male subjects (mean 6 SD age ¼ 27 6 6 years; body mass index [BMI] ¼ 23.7 6 3.0 kg m À2 ) participated in a repeated-measures crossover design study comprising three 21-day interventions: normoxic bed rest (NBR; partial pressure of inspired O 2 , P i O 2 ¼ 133.1 6 0.3 mm Hg); hypoxic ambulation (HAMB; P i O 2 ¼ 90.0 6 0.4 mm Hg), and hypoxic bed rest (HBR; P i O 2 ¼ 90.0 6 0.4 mm Hg). Central retinal arteriolar (CRAE) and venular (CRVE) equivalents were measured at baseline and at regular intervals during each 21-day intervention.RESULTS. Normoxic bed rest caused a progressive reduction in CRAE, with the change in CRAE relative to baseline being highest on day 15 (DCRAE ¼ À7.5 lm; 95% confidence interval [CI]: À10.8 to À4.2; P < 0.0001). Hypoxic ambulation resulted in a persistent 21-day increase in CRAE, reaching a maximum on day 4 (DCRAE ¼ 9.4 lm; 95% CI: 6.0-12.7; P < 0.0001). During HBR, the increase in CRAE was highest on day 3 (DCRAE ¼ 4.5 lm; 95% CI: 1.2-7.8; P ¼ 0.007), but CRAE returned to baseline levels thereafter. Central retinal venular equivalent decreased during NBR and increased during HAMB and HBR. The reduction in CRVE during NBR was highest on day 1 (DCRVE ¼ À7.9 lm; 95 CI: À13.3 to À2.5), and the maximum DCRVE during HAMB (24.6 lm; 95% CI: 18.9-30.3) and HBR (15.2 lm; 95% CI: 9.8-20.5) was observed on days 10 and 3, respectively.CONCLUSIONS. The diameters of retinal blood vessels exhibited a dynamic response to hypoxia and bed rest, such that retinal vasodilation was smaller during combined bed rest and hypoxia than during hypoxic exposure.

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“…; Kagemann et al. ; Rose & Hudson ). This study, however, offered an explanation for the large intra‐individual variation as approximately half of the day‐to‐day variation in perfusion velocities could be ascribed to changes in blood glucose.…”

Section: Discussionmentioning

confidence: 99%

“…In the retina, hyperoxia has been shown to constrict major arterioles and venules by 5.6–14.0% and 5.8–15.0%, respectively (Hickam & Frayser ; Pakola & Grunwald ; Gilmore et al. ; Rose & Hudson ; Lott et al. ).…”

Section: Discussionmentioning

confidence: 99%

Retinal hemodynamic oxygen reactivity assessed by perfusion velocity, blood oximetry and vessel diameter measurements

Klefter

Lauritsen

Larsen

2014

Acta Ophthalmologica

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ABSTRACT.Purpose: To test the oxygen reactivity of a fundus photographic method of measuring macular perfusion velocity and to integrate macular perfusion velocities with measurements of retinal vessel diameters and blood oxygen saturation. Methods: Sixteen eyes in 16 healthy volunteers were studied at two examination sessions using motion-contrast velocimetry and retinal oximetry with vessel diameter corrections. To test oxygen reactivity, participants were examined during normoxia, after 15 min of hyperoxia and finally after 45 min of normoxia. Repeatability was assessed by intraclass correlation coefficients (ICC) and limits of agreement. Results: Fifteen minutes of hyperoxia was accompanied by mean reductions in arterial and venous perfusion velocities of 14% and 16%, respectively (p = 0.0080; p = 0.0019), constriction of major arteries and veins by 5.5% and 8.2%, respectively (p < 0.0001), increased retinal arterial oxygen saturation from 95.1 AE 5.0% to 96.6 AE 6.4% (p = 0.038) and increased retinal venous oxygen saturation from 62.9 AE 6.7% to 70.3 AE 7.8% (p = 0.0010). Parameters returned to baseline levels after subsequent normoxia. Saturation and vessel diameter ICCs were 0.88-0.98 (range). For perfusion velocities, short-term ICCs were 0.79-0.82 and long-term ICCs were 0.06-0.11. Intersession increases in blood glucose were associated with reductions in perfusion velocities (arterial p = 0.0067; venous p = 0.018). Conclusion: Oxygen reactivity testing supported that motion-contrast velocimetry is a valid method for assessing macular perfusion. Results were consistent with previous observations of hyperoxic blood flow reduction using blue field entoptic and laser Doppler velocimetry. Retinal perfusion seemed to be regulated around individual set points according to blood glucose levels. Multimodal measurements may provide comprehensive information about retinal metabolism.

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Comparison of retinal arteriolar and venular variability in healthy subjects

Cited by 11 publications

References 15 publications

Reactivity in the human retinal microvasculature measured during acute gas breathing provocations

Reactivity in the human retinal microvasculature measured during acute gas breathing provocations

Separate and Combined Effects of Hypoxia and Horizontal Bed Rest on Retinal Blood Vessel Diameters

Retinal hemodynamic oxygen reactivity assessed by perfusion velocity, blood oximetry and vessel diameter measurements

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