Increase In Choroidal Blood Flow Research Articles

Role of the superior salivatory nucleus in parasympathetic control of choroidal blood flow and in maintenance of retinal health

The vasodilatory pterygopalatine ganglion (PPG) innervation of the choroid is under the control of preganglionic input from the superior salivatory nucleus (SSN), the parasympathetic portion of the facial motor nucleus. We sought to confirm that choroidal SSN drives a choroid-wide vasodilation and determine if such control is important for retinal health. To the former end, we found, using transscleral laser Doppler flowmetry, that electrical activation of choroidal SSN significantly increased choroidal blood flow (ChBF), at a variety of choroidal sites that included more posterior as well as more anterior ones. We further found that the increases in ChBF were significantly reduced by inhibition of neuronal nitric oxide synthase (nNOS), thus implicating nitrergic PPG terminals in the SSN-elicited ChBF increases. To evaluate the role of parasympathetic control of ChBF in maintaining retinal health, some rats received unilateral lesions of SSN, and were evaluated functionally and histologically. In eyes ipsilateral to choroidal SSN destruction, we found that the flash-evoked scotopic electroretinogram a-wave and b-wave peak amplitudes were both significantly reduced by 10 weeks post lesion. Choroidal baroregulation was evaluated in some of these rats, and found to be impaired in the low systemic arterial blood pressure (ABP) range where vasodilation normally serves to maintain stable ChBF. In retina ipsilateral to SSN destruction, the abundance of Müller cell processes immunolabeled for glial fibrillary acidic protein (GFAP) and GFAP message were significantly upregulated. Our studies indicate that the SSN-PPG circuit mediates parasympathetic vasodilation of choroid, which appears to contribute to ChBF baroregulation during low ABP. Our results further indicate that impairment in this adaptive mechanism results in retinal dysfunction and pathology within months of the ChBF disturbance, indicating its importance for retinal health.

Assessment of choroidal blood flow using laser speckle flowgraphy

Background/aimsThere is considerable interest in novel techniques to quantify choroidal blood flow (CBF) in humans. In the present study, we investigated a novel technique to measure CBF based on laser...

Stimulation of Baroresponsive Parts of the Nucleus of the Solitary Tract Produces Nitric Oxide-mediated Choroidal Vasodilation in Rat Eye.

Preganglionic parasympathetic neurons of the ventromedial part of the superior salivatory nucleus (SSN) mediate vasodilation of orbital and choroidal blood vessels, via their projection to the nitrergic pterygopalatine ganglion (PPG) neurons that innervate these vessels. We recently showed that the baroresponsive part of the nucleus of the solitary tract (NTS) innervates choroidal control parasympathetic preganglionic neurons of SSN in rats. As this projection provides a means by which blood pressure (BP) signals may modulate choroidal blood flow (ChBF), we investigated if activation of baroresponsive NTS evokes ChBF increases in rat eye, using Laser Doppler Flowmetry (LDF) to measure ChBF transclerally. We found that electrical activation of ipsilateral baroresponsive NTS and its efferent fiber pathway to choroidal SSN increased mean ChBF by about 40–80% above baseline, depending on current level. The ChBF responses obtained with stimulation of baroresponsive NTS were driven by increases in both choroidal blood volume (ChBVol; i.e., vasodilation) and choroidal blood velocity (ChBVel; possibly due to orbital vessel dilation). Stimulation of baroresponsive NTS, by contrast, yielded no significant mean increases in systemic arterial blood pressure (ABP). We further found that the increases in ChBF with NTS stimulation were significantly reduced by administration of the neuronal nitric oxide (NO) synthase inhibitor Nω-propyl-l-arginine (NPA), thus implicating nitrergic PPG terminals in the NTS-elicited ChBF increases. Our results show that the NTS neurons projecting to choroidal SSN do mediate increase in ChBF, and thus suggest a role of baroresponsive NTS in the BP-dependent regulation of ChBF.

Type-specific photoreceptor loss in pigeons after disruption of parasympathetic control of choroidal blood flow by the medial subdivision of the nucleus of Edinger-Westphal.

The medial part of the nucleus of Edinger-Westphal (EWM) in birds mediates light-regulated adaptive increases in choroidal blood flow (ChBF). We sought to characterize the effect of loss of EWM-mediated ChBF regulation on photoreceptor health in pigeons housed in either moderate intensity diurnal or constant light (CL). Photoreceptor abundance following complete EWM destruction was compared to that following a lesion in the pupil control circuit (as a control for spread of EWM lesions to the nearby pupil-controlling lateral EW) or following no EW damage. Birds were housed post-lesion in a 12 h 400 lux light/12 h dark light cycle for up to 16.5 months, or in constant 400 lux light for up to 3 weeks. Paraformaldehyde-glutaraldehyde fixed eyes were embedded in plastic, sectioned, slide-mounted, and stained with toluidine blue/azure II. Blinded analysis of photoreceptor outer segment abundance was performed, with outer segment types distinguished by oil droplet tint and laminar position. Brains were examined histologically to assess lesion accuracy. Disruption of pupil control had no adverse effect on photoreceptor outer segment abundance in either diurnal light or CL, but EWM destruction led to 50-60% loss of blue/violet cone outer segments in both light conditions, and a 42% loss of principal cone outer segments in CL. The findings indicate that adaptive regulation of ChBF by the EWM circuit plays a role in maintaining photoreceptor health and mitigates the harmful effect of light on photoreceptors, especially short wavelength-sensitive cone photoreceptors.

Reversible Increase of Central Choroidal Thickness During High-Altitude Exposure.

This study aimed to quantify the impact of high altitude on choroidal thickness and relate changes of altered choroidal blood flow to clinical parameters and acute mountain sickness (AMS). This work is related to the Tübingen High Altitude Ophthalmology (THAO) study. Enhanced depth imaging spectral-domain optical coherence tomography was used to quantify macular choroidal layer thickness. Peripheral oxygen saturation, heart rate, and AMS scores were assessed in eight healthy subjects at baseline (altitude, 341 m) and at altitude (4559 m) for respective correlations. Longitudinal analysis revealed a significant (P = 0.011, ANOVA) increase in central choroidal thickness (CCT) during altitude exposure (CCT baseline = 271 ± 9 μm; CCT altitude = 288 ± 9 μm) due to an increased choroidal blood flow. Incidence of AMS at altitude was 50%, peripheral oxygen saturation decreased by 25%, and heart rate increased by 39%. All changes were completely reversible after descent to low altitudes. A small but significant increase in choroidal thickness was observed upon acute altitude exposure to 4559 m. This increase in choroidal blood flow was not related to AMS and was fully reversible after return to low altitude.

Alterations of choroidal blood flow regulation in young healthy subjects with complement factor H polymorphism.

A common polymorphism in the complement factor H gene (rs1061170, Y402H) is associated with a high risk of age-related macular degeneration (AMD). In the present study we hypothesized that healthy young subjects homozygous for the high-risk haplotype (CC) show abnormal choroidal blood flow (ChBF) regulation decades before potentially developing the disease. A total of 100 healthy young subjects were included in the present study, of which 4 subjects were excluded due to problems with genotyping or blood flow measurements. ChBF was measured continuously using laser Doppler flowmetry while the subjects performed isometric exercise (squatting) for 6 minutes. The increase in ChBF was less pronounced than the response in ocular perfusion pressure (OPP), indicating for some degree of choroidal blood flow regulation. Eighteen subjects were homozygous for C, 47 subjects were homozygous for T and 31 subjects were heterozygous (CT). The increase in OPP during isometric exercise was not different between groups. By contrast the increase in ChBF was more pronounced in subjects homozygous for the high risk C allele (p = 0.041). This was also evident from the pressure/flow relationship, where the increase in ChBF in homozygous C carriers started at lower OPPs as compared to the other groups. Our data indicate that the regulation of ChBF is abnormal in rs1061170 CC carriers. So far this polymorphism has been linked to age related macular degeneration (AMD) mainly via inflammatory pathways associated with the complement system dysfunction. Our results indicate that it could also be related to vascular factors that have been implicated in AMD pathogenesis.

Effects of orally administered moxaverine on ocular blood flow in healthy subjects

To investigate the effect of orally administered moxaverine (Kollateral forte®) on ocular blood flow in young healthy subjects. Sixteen healthy subjects (eight male/eight female) aged between 20 and 32 years were included in this placebo-controlled, double-masked, two-way crossover study. Volunteers received 900 mg moxaverine-hydrochloride administered orally in three equal doses or placebo identical in appearance on 2 study days. Outcome variables were measured at baseline and 5 h after first drug administration. Laser Doppler flowmetry was used to assess choroidal and optic nerve head blood flow. Blood velocities in the retrobulbar vessels were measured with color Doppler imaging. Neither moxaverine nor placebo changed mean arterial pressure or intraocular pressure. Neither moxaverine nor placebo had an effect on choroidal (moxaverine: by 9.5 ± 17.2 %, placebo 3.8 ± 18.8 %, p = 0.54 between groups) or optic nerve head blood flow (moxaverine: 4.8 ± 10.4 %, placebo: 1.8 ± 10.9 %, p = 0.52 between groups). Similarly, administration of moxaverine did not change blood flow velocities or calculated resistance index in the retrobulbar vessels compared to placebo. The data of the present study indicate that orally administered moxaverine does not increase ocular blood flow. This is in contrast to previous findings, where parenteral administration of moxaverine lead to a significant increase in choroidal blood flow and blood flow velocities in the retrobulbar vessels. The reason for these differing results is unclear, but may be related to the low bioavailability after oral administration.

Effect of Nifedipine on Choroidal Blood Flow Regulation during Isometric Exercise

To determine whether nifedipine, an L-type calcium channel blocker, alters choroidal blood flow (ChBF) regulation during isometric exercise in healthy subjects. The study was carried out in a randomized, placebo-controlled, double-masked, two-way crossover design. Fifteen healthy male subjects were randomly assigned to receive either placebo or nifedipine on two different study days. Subfoveal ChBF was measured with laser Doppler flowmetry while the study participants performed isometric exercise (squatting). This was performed before drug administration and during infusion of nifedipine and placebo, respectively. Mean arterial pressure (MAP) and intraocular pressure (IOP) were measured noninvasively, and ocular perfusion pressure (OPP) was calculated as &frac23; MAP-IOP. MAP and OPP increased significantly during all squatting periods (P < 0.01). The increase in ChBF was less pronounced than the increase in OPP during isometric exercise. Nifedipine did not alter the OPP increase in response to isometric exercise, but it significantly augmented the exercise-induced increase in ChBF (P < 0.001 vs. placebo). Although ChBF increased by a maximum of 14.2% ± 9.2% during the squatting period when placebo was administered, the maximum increase during administration of nifedipine was 23.2% ± 7.2%. In conclusion, the data of the present study suggest that nifedipine augments the ChBF response to an experimental increase in OPP. In addition, it confirms that the choroidal vasculature has a significant regulatory capacity over wide ranges of OPPs during isometric exercise. (ClinicalTrials.gov number, NCT00280462.).

Choroidal Blood Flow Response to Isometric Exercise in Glaucoma Patients and Patients with Ocular Hypertension

To analyze submacular choroidal blood flow (ChBF) response to isometric exercise in untreated patients with glaucoma and ocular hypertension. ChBF was examined by means of confocal laser Doppler flowmetry during 5 minutes of baseline, during 90 seconds of isometric exercise with a Martin's vigorimeter and during 15 minutes of recovery. Values from one randomly chosen eye of 45 healthy subjects, the eye with more advanced damage in 45 primary open-angle glaucoma (POAG) patients, and the eye with higher native intraocular pressure in 45 patients with ocular hypertension (OHT) were acquired, and parameters of ChBF as well as blood pressure response were analyzed. Healthy eyes demonstrated higher ChBF at baseline than did the eyes in both the other groups (5126 ± 1487, 4186 ± 1011, and 4437 ± 1372 arbitrary units, ANOVA P = 0.003). Both mean and diastolic arterial blood pressures at baseline were lower in POAG patients than in those with OHT and healthy controls (P < 0.03); however, the response of mean blood pressure to isometric exercise was comparable across groups (P = 0.79). The ChBF response to exercise was stronger in the POAG group (ANOVA P = 0.02), it was twice as high as in the controls (+8.1% ± 8.0% vs. +3.7% ± 6.7%; P = 0.007) and borderline higher than in the OHT patients (+5.0% ± 8.0%; P = 0.051). Baseline ChBF was lower in both the POAG and the OHT patients, compared with that in the controls. The stronger increase in ChBF in POAG patients in the face of an exercise-induced blood pressure increase indicates less active regulatory capacity in glaucoma patients.

Effect of systemic moxaverine on ocular blood flow in humans

A number of common eye diseases are associated with ocular perfusion abnormalities. The present study aimed to investigate whether systemically administered moxaverine improves ocular blood flow. Sixteen healthy volunteers were studied in this randomized, double-masked, placebo-controlled, two-way crossover study. Moxaverine in a dose of 150 mg was administered i.v. Ocular haemodynamic parameters were measured before and after drug administration. Retinal arterial and venous diameters were measured with a retinal vessel analyser. Retinal blood velocity was assessed using laser Doppler velocimetry and choroidal and optic nerve head blood flow was measured with laser Doppler flowmetry. Moxaverine increased choroidal blood flow (22.6 ± 27.9%), an effect which was significant versus placebo (p = 0.015). Red blood cell velocity in retinal veins tended to increase by 13.6 ± 13.3% after infusion of moxaverine, but this effect was not significant compared with placebo (p = 0.25). In the optic nerve head moxaverine also tended to increase blood flow (11.8 ± 12.7%), but, again, this effect was not significant versus placebo (p = 0.12). Neither moxaverine nor placebo had an effect on retinal arterial diameters. In retinal veins moxaverine tended to induce vasodilation (2.6 ± 2.8%) and to increase blood flow (19.6 ± 16.5%), but these effects were not significant (both p = 0.12). The present study indicates an increase in choroidal blood flow after systemic infusion of a single dose of moxaverine in healthy subjects. Further studies are warranted to investigate whether these effects are also seen after longterm treatment in patients with ocular vascular disease.

Choroidal blood flow response to hyperoxia and hypercapnia in patients with obstructive sleep apnea syndrome

Abstract Purpose Obstructive sleep apnea syndrome (OSA) is associated with ischemic and glaucomatous optic neuropathy. The physiopathology of these diseases includes an abnormal regulation in the optic nerve head vasculature. The aim of our study was to characterize the choroidal vascular reactivity to hyperoxia and 8% CO2 breathing in OSA patients, as compared with matched healthy control subjects. Methods Eighteen newly diagnosed OSA patients were included in this prospective study. Control subjects were matched with OSA patients for body mass index (BMI), gender and age. At the screening visit, each subject underwent a general exam, cardiovascular, neurologic and ophthalmological examinations, and underwent complete overnight polysomnography. The LDF instrument used in this study to measure subfoveal choroidal blood flow (ChBF) measured the following parameters: ChBVel (kHz); volume, ChBVol (in arbitrary units, AU) and the relative flow, ChBF = ChBVel ? ChBVol (in AU). Vascular choroidal reactivity was tested during hyperoxia and hypercapnia (8% CO2) inhalation. Results OSA patients exhibited a similar choroidal reactivity during hyperoxia (stability of choroidal blood flow) and hypercapnia (1.5% increase in choroidal blood flow per 1 mmHg PtCO2) than controls. Conclusion This prospective comparative study explored for the first time the choroidal blood flow of OSA patients and results showed that subfoveal ChBF reactivity to gas in OSA patients is similar to healthy control subjects. These preliminary results suggest that choroidal vasculature is protected against the inbalance between the vasodilation (NO) and vasoconstriction (endothelin) system.

Choroidal perfusion in eyes with untreated choroidal melanoma

Previous studies indicate that ocular blood flow is altered in eyes with choroidal melanoma. In the present study pulsatile ocular blood flow (POBF) was assessed to investigate whether there exists a correlation between tumour size and ocular blood flow parameters. Twenty-two patients with unilateral untreated choroidal melanoma were studied using two measurement techniques: POBF was measured with a pneumotonometer and local foveal fundus pulsation amplitude (FPA) by laser interferometry, and results were correlated. Tumour volume was calculated using the ellipsoidal solid model and was correlated to POBF and FPA. Levels of POBF and FPAs tended to be higher in tumour eyes compared with unaffected eyes, but the differences did not reach the level of significance. Both methods showed a high degree of correlation in unaffected eyes. In tumour eyes the correlation was slightly less pronounced. There was no correlation between tumour and POBF or FPA. Our results do not indicate choroidal hyperperfusion in patients with choroidal melanoma. The clinical usefulness of measuring POBF in tumour patients may be limited.

The effect of sildenafil on ocular blood flow

Sildenafil is a potent phosphodiesterase (PDE) 5 inhibitor that is used for patients with erectile dysfunction. Sildenafil induces vasodilation in selected smooth muscle via increased levels of guanosine 3′, 5′...

Effects of Topical Clonidine versus Brimonidine on Choroidal Blood Flow and Intraocular Pressure during Squatting

Clonidine and brimonidine, two alpha-2 agonists, have been shown to reduce intraocular pressure (IOP) in patients with glaucoma. Little is known, however, about the exact role of alpha receptors in the control of ocular blood flow in the posterior pole of the eye. Hence, the study was conducted to investigate the effects of topical clonidine versus topical brimonidine on choroidal blood flow and intraocular pressure during squatting. This was a randomized, double-masked, controlled, two-way crossover study. Twelve healthy male nonsmoking volunteers, aged between 19 and 35 years were included in the study. Two drops of clonidine or brimonidine were administered in the subjects' study eyes. Continuous measurement using the compact laser Doppler flowmeter was performed during a 6-minute squatting period, to assess choroidal blood flow regulation during an increase in ocular perfusion pressure. Both substances induced a pronounced but comparable (P = 0.8) decrease in IOP. Squatting increased mean arterial pressure (MAP) and ocular perfusion pressure (P < 0.01). This increase was comparable between the clonidine and the brimonidine study day (P = 0.88). Squatting induced an increase in choroidal blood flow that was less pronounced than the increase in ocular perfusion pressure. Compared with baseline the alpha-2 agonists decreased choroidal blood flow during squatting (P = 0.0026) to a comparable degree (P = 0.86). Vascular resistance increased at baseline and during squatting after administration of the alpha-2 agonists (P < 0.01) in both groups to a comparable degree (P = 0.56). Topical alpha-2 agonists may induce changes in choroidal blood flow, even after a single administration. Long-term studies are needed to study potential effects of brimonidine and clonidine in the clinical setting.

Long-Term Effect of Laser Treatment for Dry Age-Related Macular Degeneration on Choroidal Hemodynamics

To determine whether laser treatment applied according to the complications of age-related macular degeneration prevention trial (CAPT) has an effect on the choroidal circulation. Randomized controlled trial. This study included 30 CAPT patients with bilateral drusen. Laser Doppler flowmetry was used to measure relative choroidal blood flow (Ch(flow)) in the fovea. Measurements were obtained through dilated pupils in both eyes of each patient before photocoagulation was applied in one eye. Measurements were repeated at three months (30 patients) and 28 months (23 patients). Average Ch(flow) at baseline, three months, and 28 months was 7.2 +/- 2.1 (+/-1 SD), 7.3 +/- 2.5, and 6.8 +/- 2.7 arbitrary units (AU) in the control eyes and 6.6 +/- 1.6, 7.0 +/- 2.3, and 7.8 +/- 3.0 AU in the treated eyes. In comparison to control eyes, there was no significant change in Ch(flow) in the treated eyes at three months after treatment. At 28 months, however, there was a 5.6% drop in Ch(flow) in control eyes and an 18.2% increase in Ch(flow) in treated eyes from baseline. The average difference of 23.8% between the percentage changes in Ch(flow) observed in the control and treated eyes was statistically significant (paired two-tailed Student t test; P = .05). Our results suggest an increase in choroidal blood flow 28 months after laser treatment according to the CAPT protocol. This increase may play a role in the mechanism leading to the disappearance of drusen after photocoagulation. Whether removal of drusen after photocoagulation is beneficial to the patients is not known at this time.

Intravenous Administration of Diphenhydramine Reduces Histamine-Induced Vasodilator Effects in the Retina and Choroid

Intravenous administration of histamine causes an increase in choroidal blood flow (ChBF) and retinal vessel diameters in healthy subjects. The receptor mediating this response has not yet been identified. The present study was undertaken to clarify whether H1 receptor blockade with diphenhydramine affects the hemodynamic response of histamine in the choroid and the retina. A randomized, double-masked, placebo-controlled, two-way crossover study was performed in 18 healthy, male, nonsmoking subjects. Histamine (0.32 microg/kg per minute over 30 minutes) was infused intravenously in the absence (NaCl as placebo) or presence of the H1 blocker diphenhydramine (1.0 mg/min over 50 minutes). Ocular hemodynamic parameters, blood pressure, and intraocular pressure were measured before drug administration, after infusion of diphenhydramine or placebo, and after co-infusion of histamine. Subfoveal ChBF and fundus pulsation amplitude (FPA) were measured with laser Doppler flowmetry and laser interferometry, respectively. Retinal arterial and venous diameters were measured with a retinal vessel analyzer. Retinal blood velocity was assessed with bidirectional laser Doppler velocimetry. Administration of histamine caused a decrease in mean arterial pressure by -4% +/- 9% (ANOVA P = 0.01). This effect was blunted by coadministration of diphenhydramine (ANOVA, P = 0.04). Histamine significantly increased FPA and subfoveal ChBF. Coadministration of diphenhydramine significantly reduced this effect (ANOVA; FPA P = 0.001, ChBF P = 0.049). Histamine significantly increased retinal arterial diameter by +3.5% +/- 4.5% and retinal venous diameter by +3.7% +/- 2.8%. Again, coadministration of diphenhydramine significantly reduced the vasodilative effect to +0.3% +/- 5.5% in retinal arteries (ANOVA, P = 0.00006) and to +0.9% +/- 2.5% in retinal veins (ANOVA, P = 0.004). The present data confirm that histamine increases ChBF and retinal vessel diameters in healthy subjects. Administration of the H1 receptor blocker diphenhydramine significantly reduced histamine-induced changes in ocular perfusion parameters. These results strongly indicate that in the retina and choroid, H1 receptors are involved in the histamine-mediated hemodynamic effects in vivo.

Effect of histamine and cimetidine on retinal and choroidal blood flow in humans

Intravenous administration of histamine causes an increase in choroidal blood flow and retinal vessel diameter in healthy subjects. The mechanism underlying this effect remains to be elucidated. In the present study, we hypothesized that H2 receptor blockade alters hemodynamic effects of histamine in the choroid and retina. Eighteen healthy male nonsmoking volunteers were included in this randomized, double-masked, placebo-controlled two-way crossover study. Histamine (0.32 microg.kg(-1).min(-1) over 30 min) was infused intravenously in the absence (NaCl as placebo) or presence of the H2 blocker cimetidine (2.3 mg/min over 50 min). Ocular hemodynamic parameters, blood pressure, and intraocular pressure were measured before drug administration, after infusion of cimetidine or placebo, and after coinfusion of histamine. Subfoveal choroidal blood flow and fundus pulsation amplitude were measured with laser-Doppler flowmetry and laser interferometry, respectively. Retinal arterial and venous diameters were measured with a retinal vessel analyzer. Retinal blood velocity was assessed with bidirectional laser-Doppler velocimetry. Histamine increased subfoveal choroidal blood flow (+14 +/- 15%, P < 0.001), fundus pulsation amplitude (+11 +/- 5%, P < 0.001), retinal venous diameter (+3.0 +/- 3.6%, P = 0.002), and retinal arterial diameter (+2.8 +/- 4.2%, P < 0.01) but did not change retinal blood velocity. The H2 antagonist cimetidine had no significant effect on ocular hemodynamic parameters. In addition, cimetidine did not modify effects of histamine on choroidal blood flow, fundus pulsation amplitude, retinal venous diameter, and retinal arterial diameter compared with placebo. The present data confirm that histamine increases choroidal blood flow and retinal vessel diameters in healthy subjects. This ocular vasodilator effect of histamine is, however, not altered by administration of an H2 blocker. Whether the increase in blood flow is mediated via H1 receptors or other hitherto unidentified mechanisms remains to be elucidated.

Anatomical and functional evidence for progressive age-related decline in parasympathetic control of choroidal blood flow in pigeons

The choroid receives extensive parasympathetic innervation, which in birds arises largely from the ciliary ganglion (CG). Since age-related changes in parasympathetic regulation of choroidal blood flow (ChBF) could contribute to age-related retinal decline, we used anatomical and functional methods to determine if ChBF control by the CG shows age-related decline in pigeons. The efficacy of the choroidal vasodilatory response to activation of the CG preganglionic input from the medial subdivision of the nucleus of Edinger-Westphal (EWM) was assessed using laser Doppler flowmetry (LDF). The EWM receives bisynaptic retinal input, and electrical stimulation of EWM or light stimulation of the retina in young animals produces dramatic choroidal vasodilation. Transcleral LDF was therefore used to measure both basal ChBF and the increases in ChBF elicited by electrical stimulation of EWM or by retinal illumination in 0.5–18 year old pigeons. Fixed cryostat sections of the eye from 0.5 to 22 year old pigeons were immunolabeled for the 3A10 neurofilament-associated antigen to determine if intrachoroidal nerve fibers arising from CG exhibited age-related loss. We focused on superior choroid, since it is the primary target for CG nerve fibers. There was a marked age-related loss in the ChBF vasodilatory response elicited by either EWM stimulation or retinal illumination, as was also true for basal ChBF. A progressive decrease in choroidal nerve fibers of CG origin, to 17% of youthful abundance by 22 years of age, was also observed. The evoked ChBF increase, and basal ChBF, achieved 50% of their age-related decline between the ages of 3 and 4 years, while half the loss in CG innervation of choroid was later, occurring by 10 years. Age-related loss of choroidal nerve fibers occurs in parallel with but more slowly than the reduction in basal ChBF and the choroidal vasodilation that can be elicited via natural (light) or electrical activation of the central neural input to CG choroidal neurons. The prominent age-related decline in parasympathetic control of ChBF early in the pigeon life span could contribute to the age-related retinal decline observed in pigeons.

Posture changes and subfoveal choroidal blood flow.

To evaluate the effect of posture change on subfoveal choroidal blood flow (ChBF) in normal volunteers. The pulsatile, nonpulsatile, and mean ChBF were measured with laser Doppler flowmetry in 11 healthy volunteers with a mean age of 32 +/- 13 (SD) years. The posture of the subjects was changed from standing (90 degrees ), to supine (-8 degrees ), and back to standing, with a mechanically driven table. During the whole experimental procedure, ChBF and heart rate (HR) were continuously recorded. After 30 seconds in standing position, the subjects were tilted to supine during approximately 30 seconds. They remained in this position for approximately 2 minutes, after which they were tilted back to the standing position (recovery), where they remained for another approximately 2 minutes. Systemic brachial artery blood pressure (BP) was measured in the baseline, supine, and recovery positions. This procedure was repeated to measure the intraocular pressure (IOP) at the different postures. Mean BP did not change significantly throughout the experimental procedure. As the body was tilted from standing to supine, HR decreased by 16% (P < 0.0004), IOP increased by 29% (P < 0.001), and mean ChBF increased by 11% (P < 0.01). The increase in ChBF was primarily due to an increase in the nonpulsatile component of the blood velocity. Based on previously reported experimental data that indicate that the ocular perfusion pressure increases less than predicted by purely hydrostatic considerations when the body is tilted from the standing to the supine position, the observed increase in ChBF suggests a passive response of the choroidal circulation to the posture change.

Choroidal blood flow and arterial blood pressure.

Untreated hypertension is associated with ocular complications and is a risk factor for the development and progression of vascular ocular pathologies. We set out to investigate the association between systemic blood pressure and choroidal blood flow. All subjects were male non-smokers, who did not receive any medication and had normal or slightly elevated blood pressure (systolic blood pressure < or = 160 mmHg; diastolic blood pressure < or = 100 mmHg). The association between systemic blood pressure and fundus pulsation amplitude, a measure of pulsatile choroidal blood flow, was investigated in 318 volunteers. In addition, the association between systemic blood pressure and blood flow velocities in the posterior ciliary arteries supplying the choroid was investigated in these subjects. Ocular fundus pulsation amplitude (r = 0.252; P < 0.001) and mean flow velocity in the posterior ciliary arteries (r = 0.346, P < 0.001) were significantly associated with mean arterial pressure. The correlation of ocular haemodynamic variables with systolic and diastolic blood pressure was in the same range. Our data indicate a small, but significant increase in choroidal blood flow with increasing blood pressure.