Changes In Ocular Perfusion Pressure Research Articles

Choroidal Blood Flow Regulation after Posture Change or Isometric Exercise in Men with Obstructive Sleep Apnea Syndrome

Obstructive sleep apnea (OSA) syndrome generates hypertension, atherosclerosis, and endothelial and autonomic dysfunction, which may mutually interact with ocular vascular regulation. Exercise and posture changes can be used to manipulate blood pressure, ocular perfusion pressure (OPP), or both. It was hypothesized that choroidal vascular reactivity in response to isometric exercise and posture changes could be altered in OSA patients. Healthy men were matched 1:1 for body mass index, sex, and age with patients with newly diagnosed OSA without cardiovascular comorbidities. All subjects underwent sleep studies and cardiovascular phenotyping (24-hour blood pressure monitoring, arterial stiffness measurements, and cardiac and carotid echography). Choroidal reactivity was assessed by laser Doppler flowmetry, which measured subfoveal choroidal blood flow. During exercise, blood pressure parameters increased significantly within the same range, with a similar profile over time in OSA patients and control subjects. A significant linear relationship (P = 0.0003) was noted between choroidal vascular resistance and the OPP changes during exercise in OSA patients and control subjects. From the sitting to the supine position, a significant decrease in mean arterial pressure occurred in both groups (10.9%-13.4%; P < 0.001). In both populations, no significant change in choroidal blood flow or vascular resistance was found during the posture change. Choroidal blood flow responses to exercise and posture changes were unchanged after 6 to 9 months of continuous positive airway pressure treatment. This study strongly suggests that the regulation of choroidal blood flow, which depends on the orthosympathetic and parasympathetic systems, is unaltered in men with OSA who have no comorbidities.

The impact of cataract on the quantitative, non-invasive assessment of retinal blood Flow

The aim of the study was to determine the impact of cataract on the quantitative, non-invasive assessment of retinal blood flow assessed by bidirectional laser Doppler flowmetry and simultaneous vessel densitometry. Ten patients scheduled for extracapsular cataract extraction using phacoemulsification and intraocular lens implantation between the ages of 61 and 84 (mean age 73 years, SD ± 8) were prospectively recruited. Two visits were required to complete the study; one visit prior to extracapsular cataract extraction and one at least 6 weeks after the surgery to allow for sufficient postoperative recovery. The severity of cataract was documented using the Lens Opacity Classification System (LOCS, III) at the first visit. Retinal arteriolar hemodynamics were measured at both visits using the high-intensity setting of the Canon Laser Blood Flowmeter. All eyes showed no clinical signs of postoperative intraocular inflammation. The quantitative assessment of retinal arteriolar diameter and blood flow were reduced following extracapsular cataract extraction (Wilcoxon signed-rank test, p = 0.022 and p=0.028, respectively); however, centreline blood velocity was not significantly changed (Wilcoxon signed-rank test, p=0.074). Intraocular pressure was unchanged pre- and postcataract extraction. Retinal vessel densitometry assessment in the presence of cataract results in the erroneous elevation of the diameter measurement and thereby the calculation of blood flow. The bidirectional Doppler assessment of blood velocity appears to be more robust to light scatter induced by cataract. Care needs to be exercised in the interpretation of studies of retinal vessel diameter or blood flow that utilize similar densitometry techniques.

Vascular Reacitivty in Glaucoma

AbstractToday, several lines of evidence indicate that beside the classical risk factors such as increased intraocular pressure or family history, decreased ocular perfusion may contribute to the pathogenesis of the disease. In particular, a decrease in ocular blood flow may lead to ischemic events, which in turn may trigger ganglion cell loss and subsequent detoriation of visual field. Recent studies have indicated that instabilities of perfusion rather than a continuous decline of ocular perfusion may be an important factor in the pathogenesis of the disease. In healthy subjects, changes in ocular perfusion pressure are compensated for by an autoregulatory response of the ocular vasculature, in order to keep blood flow constant. This mechanism may be impaired in patients with glaucoma. Indeed several studies indicate that glaucoma patients show reduced vascular reactivity as induced for example by changes in ocular perfusion pressure or by increased metabolic demands. This talk aims to summarize different techniques to test vascular reactivity in humans and the data currently available for patients with glaucoma. In addition, possible pathomechanisms of impaired vascular reactivity will be discussed.

The Vascular Aspect of Glaucoma ‐ What should we look at?

AbstractPurpose Glaucoma is an optic neuropathy of unknown origin. Increased intraocular pressure is the most important risk factor for the disease. In addition, reduced ocular perfusion pressure has been identified as a risk factor for glaucomatous optic neuropathy.Methods In a variety of studies we have focused on the complex interaction between intraocular pressure, mean arterial blood pressure, ocular perfusion pressure and ocular blood flow. In these studies various strategies were used to manipulate intraocular pressure, mean arterial blood pressure and ocular perfusion pressure and choroidal and optic nerve head blood flow were measured.Results In vivo the capacity of choroidal and optic nerve head blood flow to regulate its vascular tone during changes in ocular perfusion pressure strongly depends on the way how perfusion pressure is manipulated. Generally ocular vascular beds regulate better during changes in blood pressure than during changes in intraocular pressure.Conclusion With the improved understanding of ocular blood flow regulation in humans our understanding of perfusion abnormalities in glaucoma has also increased. Most importantly these studies show that any reduction in intraocular pressure has a strong impact on ocular blood flow regulation.

The role of oxygen in ocular blood flow regulation

AbstractThe normal function of the retina is crucially dependent on an adequate perfusion and oxygenation of the tissue. Thus, it does not come as a surprise that ocular blood flow is very well autoregulated. It is known for a long time that the retinal circulation, and to some extent also the chorodial circulation can compensate for changes in ocular perfusion pressure in order to keep blood flow constant. This is usually referred to as an autoregulatory response of these vascular beds. However, the ocular circulation also responds to changes in oxygen tension. For example, breathing of pure oxygen leads to a pronounced vasoconstriction of the retinal vessel, indicating that the ocular circulation also adapts to changes in oxygen tension. This talk aims to summarize our current evidence of the role of oxygen in ocular blood flow regulation and how this may relate to ocular pathologies such as glaucoma or diabetic retinopathy.

Role of Adenosine in the Control of Choroidal Blood Flow during Changes in Ocular Perfusion Pressure

The purpose of the present study was to investigate whether the nucleoside adenosine is involved in the regulatory processes of choroidal blood flow (ChBF) during an experimental decrease in ocular perfusion pressure (OPP). In this randomized, double-masked, placebo-controlled, two-way crossover study, 14 subjects received either intravenous adenosine or placebo on two different study days. The suction cup method was used for a stepwise increase in intraocular pressure (IOP). Subfoveal ChBF was measured by laser Doppler flowmetry. Mean arterial pressure (MAP) and IOP were measured noninvasively. Ocular perfusion pressure was calculated as OPP = 2/3MAP - IOP. Adenosine increased ChBF significantly versus placebo before application of the suction cup (P < 0.05). When the suction cup was applied, a significant decrease in OPP was observed. This effect was comparable on all study days. The decrease in OPP was paralleled by a significant decrease in ChBF (maximum between -43% and -52%) which was less pronounced than the decrease in OPP (maximum between -62% and -64%). Neither placebo nor adenosine influenced the ChBF increase during suction cup-induced changes in OPP. The data of the present study confirm that the human choroid shows some regulatory capacity during a decrease in OPP. Adenosine influences basal vascular tone in the choroid but is not involved in the regulatory mechanisms during an increase in IOP. (ClinicalTrials.gov number, NCT00712764.).

Effect of Latanoprost on Choroidal Blood Flow Regulation in Healthy Subjects

The present study tested the hypothesis that human choroidal blood flow (ChBF) regulation in the face of changes in ocular perfusion pressure (OPP) may be modified by a drug-induced decrease in intraocular pressure (IOP). This hypothesis was tested in a double-masked, randomized, placebo-controlled, parallel-group trial in 24 healthy volunteers. OPP was manipulated by 6 minutes of squatting and a subsequent period of artificial increase in IOP induced with a suction cup. These interventions were repeated after 14 days of treatment with either latanoprost or placebo. ChBF was measured continuously with a portable laser Doppler flowmeter. As expected, latanoprost significantly reduced IOP compared with placebo (P = 0.008). The relative increases in OPP during squatting (P = 0.97) and an artificial IOP increase (P = 0.75), however, were comparable after placebo and latanoprost. The response of ChBF was, in contrast, different between the two treatment groups. During the squatting-induced elevation of OPP, ChBF increased less after latanoprost than after placebo treatment (P = 0.049). During the suction cup-induced increase in IOP, the decrease in ChBF was less pronounced after latanoprost than after placebo (P = 0.026). Latanoprost, however, did not modify baseline ChBF at rest (P = 0.30). The data indicate that latanoprost improves ChBF regulation during both an increase and a decrease in OPP. Since latanoprost did not affect baseline ChBF, the authors assume that this effect is related to the decrease in IOP. This finding has important implications for understanding the relation between IOP and vascular factors in glaucoma, because it indicates that a reduction in IOP itself improves ChBF regulation.

Intraocular pressure and ocular perfusion during hemodialysis

To evaluate the intraocular pressure and ocular perfusion pressure during a hemodialysis. Sixty-seven eyes from thirty-five patients were evaluated at the beggining of hemodialysis, 2 hours and 4 hours after initiation. Intraocular pressure was evaluated using a Tonopen. Systolic and diastolic arterial pressures were measured with a manual sphygmomanometer. The ocular perfusion pressure was estimated by measuring the difference between 2/3 of the mean arterial pressure and the intraocular pressure values. Generalized estimating equations were used to evaluate the difference between the repeated measurements using the appropriate correction for inter-eye dependency. There was no statistically significant difference in ocular perfusion pressure, in intraocular pressure (p=0.93) and in systolic arterial pressure (p=0.92) at the three time points (p=0.69). But, when analyzing the extreme values, some patients exhibited lower diastolic perfusion pressures at all time points. Our results did not support the view that significant changes in ocular perfusion pressure and intraocular pressure occur during hemodialysis session. However, we observed that some patients exhibited lower diastolic perfusion pressures, which could be a poor prognostic factor for glaucoma patients.

The complex interaction between ocular perfusion pressure and ocular blood flow – Relevance for glaucoma

Glaucoma is an optic neuropathy of unknown origin. The most important risk factor for the disease is an increased intraocular pressure (IOP). Reducing IOP is associated with reduced progression in glaucoma. Several recent large scale trials have indicated that low ocular perfusion pressure (OPP) is a risk factor for the incidence, prevalence and progression of the disease. This is a strong indicator that vascular factors are involved in the pathogenesis of the disease, a hypothesis that was formulated 150 years ago. The relation between OPP and blood flow to the posterior pole of the eye is, however, complex, because of a phenomenon called autoregulation. Autoregulatory processes attempt to keep blood flow constant despite changes in OPP. Although autoregulation has been observed in many experiments in the ocular vasculature the mechanisms underlying the vasodilator and vasoconstrictor responses in face of changes in OPP remain largely unknown. There is, however, recent evidence that the human choroid regulates its blood flow better during changes in blood pressure induced by isometric exercise than during changes in IOP induced by a suction cup. This may have consequences for our understanding of glaucoma, because it indicates that blood flow regulation is strongly dependent not only on OPP, but also on the level of IOP itself. Indeed there is data indicating that reduction of IOP by pharmacological intervention improves optic nerve head blood flow regulation independently of an ocular vasodilator effect.

Ropivacaine in Peribulbar Anesthesia – Vasoconstrictive Properties

Peribulbar anesthesia can reduce ocular blood flow (OBF) by increasing intraocular pressure (IOP) or due to the action of drugs. Ropivacaine has low toxicity and intrinsic vasoconstrictive properties, yet to be proven on the ocular vasculature. Measurements of ocular pulse amplitude (OPA) allow the indirect evaluation of the OBF. The objective of the present study was to evaluate through the OBF the vasoconstrictive properties of ropivacaine in peribulbar anesthesia. Forty eyes undergoing peribulbar anesthesia with 7 mL of anesthetic solution without vasoconstrictor were randomly divided into two groups: ropivacaine (n = 20) and bupivacaine (n = 20). The IOP, ocular perfusion pressure (OPP), OPA, hemodynamic parameters, and the degree of akinesia before and 5 and 10 minutes after the blockade were evaluated. A dynamic contour tonometer was used to evaluate ocular parameters. Sedation was similar in both groups. A significant variation in hemodynamic parameters and intensity of the motor blockade was not observed between groups. Differences in IOP, OPP, and OPA (p < 0.05) were observed between both groups at 5 and 10 minutes. The variation of IOP at 5 and 10 minutes was -0.88% and -4.54%, respectively with ropivacaine, and 17.61% and 16.56% with bupivacaine. The change in OPP after 5 and 10 minutes was 1.5% and 4.2% with ropivacaine, and -7% and -6% with bupivacaine. Ocular pulse amplitude varied -55.59% and -59.67% with ropivacaine at 5 and 10 minutes, and -34.71% and -28.82% with bupivacaine. Ropivacaine reduced more intensely the ocular pulse amplitude despite little changes in IOP and OPP. The reduction in ocular blood flow caused by ropivacaine can be attributed to its vasoconstrictive effect.

Effect of acute postural variation on diabetic macular oedema

This study aimed to study the pathophysiology of diabetic macular oedema (DMO) by analysis of concomitant changes in macular volume (MV), mean arterial blood pressure (MABP), intraocular pressure (IOP), and retinal artery and vein diameters in response to acute postural changes in patients with DMO and healthy subjects. Thirteen patients with DMO (13 eyes) and five healthy subjects (five eyes) were examined after resting in a chair for 15 mins using optical coherence tomography to measure MV and fundus photography to assess retinal vessel diameters. The patients then lay down for 60 mins, during which they were examined repeatedly before they were reseated and examined again. Intraocular pressure was measured using pulse-air tonometry, arterial blood pressure by sphygomanometry and fluid columns using rulers and a spirit level. In healthy subjects, retinal artery (p = 0.02) and vein (p = 0.001) diameters decreased when subjects lay down, whereas MV remained stable. In patients with DMO, no orthostatic variation in retinal vessel diameters could be demonstrated, whereas MV had increased by 2.4 +/- 0.6% (mean +/- standard error of the mean; p = 0.006) 50 mins after assuming a recumbent position. In both healthy subjects and DMO patients, MABP decreased and IOP increased in a recumbent position, with no significant difference between the groups. The increase in MV that occurs in DMO when changing from a seated to a recumbent position is associated with a failure of retinal artery contraction, a response seen in healthy subjects that appears to counter-regulate the increase in ocular perfusion pressure caused by assuming a recumbent position.

Autoregulation in the choroid

Abstract Purpose To compare subfoveal choroidal blood flow (ChBF) in sitting and supine position in normal volunteers. Methods ChBF was measured with laser Doppler flowmetry in 22 healthy volunteers (mean age ± SD: 24 ± 5 years). Six independent measurements of choroidal blood flow were obtained in one randomly selected eye of each subject. Subsequently, the subjects assumed a supine position for 30 minutes and a new series of 6 measurements was obtained. Parallel hereto, systemic blood pressure and intraocular pressure were measured. Ocular perfusion pressure (OPP) was calculated based on formulas derived from ophthalmodynamometric studies. The influence of changing OPP on the change in ChBF was assessed in a linear regression analysis. Results The coefficient of variation for ChBF was 10.28% and 9.58% in the sitting and the supine position respectively. ChBF decreased by 6.6% (p=0.0017) in the supine position. The estimate for ophthalmic blood pressure in the supine position was adjusted to obtain a result of no change in OPP for no change in ChBF, yielding an average decrease for the estimate of OPP of 6.7% (p=0.0002). Change in OPP correlated significantly with change in ChBF (R2: 0.20; p=0.036) with a slope for the regression line of 1.04. Conclusion The comparable degree of change in ChBF and OPP and the linear relationship between the two parameters suggest a passive response of the choroidal circulation to the posture change. In contrast, the OPP estimates suggest a marked buffering of the change in perfusion pressure by the carotid system, compatible with a close control of the gradient in perfusion pressure between the heart and its branches within the carotid system.

Ocular blood flow autoregulation and the clinical implications of its alteration

AbstractAutoregulation is commonly defined as the ability of a vascular bed to adapt blood flow to changes in ocular perfusion pressure (pressure autoregulation) or to adapt to changes in metabolic need (metabolic autoregulation). Considering the high metabolic turnover of the eye, its intact function is strongly dependent on a stable blood supply, assured by an intact vascular autoregulation. However, it has been shown that in the recent years that several ocular diseases such as glaucoma, diabetic retinopathy or age related macula degeneration are associated with an impaired autoregulation. This vascular dysregulation may lead to an under‐ or overperfusion of the tissue and in turn to ischemia and/or oxidative stress. This talk seeks to summarize our current knowledge of autoregulation in the ocular vascular beds. Furthermore, the possible reasons of impaired autoregulation and how this may relate to ocular pathologies will be discussed.

Retinal Blood Flow Response to Posture Change in Glaucoma Patients Compared with Healthy Subjects

To characterize the retinal vascular autoregulatory response to ocular perfusion pressure (OPP) changes in patients with glaucoma and in healthy control subjects. Observational cohort study. Eighteen patients with open-angle glaucoma (OAG) and 8 control subjects, all females ages 40 to 60 years, were studied. Only subjects with known maximum intraocular pressure less than 22 mmHg in both eyes were included. Arterial diameter and blood speed in the inferior temporal retinal artery of the left eye were measured simultaneously at baseline while sitting, while reclining for approximately 30 minutes, and once again sitting using a retinal laser Doppler instrument. Blood flow rate was computed automatically. Brachial artery blood pressure and heart rate also were measured. Change in blood flow rate while reclining for approximately 30 minutes compared with baseline blood flow rate measured while seated. In control subjects, arterial diameter decreased by 7.5+/-3.4% (P = 0.0003) and blood speed increased by 24.6+/-10.8% (P = 0.004) while reclining compared with baseline. The concomitant change in the blood flow rate (6.5+/-12.0%; P = 0.15) compared with baseline was not statistically significant. In contrast, OAG patients showed a much broader range of blood flow changes in response to posture change (14.9+/-37.7%; P = 0.086) compared with baseline. Although there were no significant differences in the flow changes compared with baseline in either group, there was a significant difference in the variance of the blood flow changes in the OAG patients compared with the controls (P = 0.0025). Division of the OAG patients into subgroups revealed a significant (P = 0.031) association between baseline OPP and the retinal blood flow response to posture change. The authors describe the hemodynamic details of retinal vascular autoregulation in response to posture-induced changes in OPP in healthy subjects and document the lack of such autoregulation in a selected group of patients with OAG.

Effects of Moderate Changes in Intraocular Pressure on Ocular Hemodynamics in Patients with Primary Open-Angle Glaucoma and Healthy Controls

There is some indirect evidence for altered autoregulation in patients with glaucoma, but only a few studies have measured ocular blood flow directly during changes in ocular perfusion pressure. The present study was designed to compare pulsatile choroidal blood flow and optic nerve head (ONH) blood flow during moderate increases in intraocular pressure (IOP) in patients with primary open-angle glaucoma (POAG) and normal controls. Two nonrandomized studies comparing blood flow responses in glaucoma patients and controls in an open design. Sixteen patients with POAG glaucoma and 16 healthy gender-matched and age-matched controls were included in the choroidal blood flow experiments. The ONH blood flow experiment was performed in 14 POAG patients and 14 healthy gender-matched and age-matched controls. In the first study, pulsatile choroidal blood flow was assessed by laser interferometric measurement of fundus pulsation amplitude (FPA). In the second study, ONH blood flow was measured using laser Doppler flowmetry. In both cohorts, the IOP was increased stepwise by 10 and 20 mmHg using a suction cup. Fundus pulsation amplitude and ONH blood flow. The baseline values of FPA and ONH blood flow were lower in glaucoma patients as compared with age-matched and gender-matched healthy controls. In patients with POAG, FPA decreased by -4.5+/-5.8% and -11.3+/-4.9% during elevation of IOP of 10 and 20 mmHg, respectively. These results were not different from the results in healthy controls, where FPA decreased by -5.1+/-3.4% and -12.2+/-4.9% at the 2 pressure levels (P = 0.23 between groups). Optic nerve head blood flow showed no changes during the increase of IOP of 10 and 20 mmHg in either of the 2 groups (glaucoma patients, +2.1+/-14.7% and -0.8+/-15.2%; healthy controls, +4.3+/-12.0% and +0.2+/-14.2%; P = 0.83 between groups). The present study does not provide evidence for altered autoregulation in patients with POAG during a moderate increase in IOP. However, these results do not necessarily contradict the concept of vascular dysregulation in glaucoma.

Role of Endothelin-1 in Choroidal Blood Flow Regulation during Isometric Exercise in Healthy Humans

There is evidence that the choroid has some autoregulatory capacity in response to changes in ocular perfusion pressure (OPP). The mediators of this response are hitherto unidentified. The hypothesis for the current study was that endothelin (ET)-1 and/or angiotensin (ANF)-II may be involved in choroidal vasoconstriction during an increase in OPP. To test this hypothesis a randomized, double-masked, placebo-controlled, three way crossover study was performed in 12 healthy male volunteers. Subjects received on different study days intravenous infusions of the specific ET(A) receptor antagonist BQ-123, the angiotensin converting enzyme inhibitor enalapril or placebo. During these infusion periods subjects were asked to squat for 6 minutes. Choroidal blood flow was measured using a confocal laser Doppler flowmeter and ocular perfusion pressure (OPP) was calculated from mean arterial pressure and intraocular pressure. BQ-123 and enalapril had no effect on basal blood pressure, pulse rate, intraocular pressure, or choroidal blood flow. During isometric exercise, a pronounced increase in mean arterial pressure paralleled by an increase in OPP was observed. Although choroidal blood flow slightly increased during squatting, the increase was much less pronounced than the increase in OPP, indicating some regulatory potential of the choroid. Enalapril did not alter the choroidal pressure-flow relationship during isometric exercise, but BQ-123 induced a significant leftward shift of the pressure-flow curve (P < 0.001). The present data indicate that ET-1, but not ANG II, plays a role in choroidal blood flow regulation during isometric exercise in healthy humans. Hence, impaired choroidal autoregulation in patients with ocular vascular diseases may arise from an altered endothelin system. Further studies in such patients are warranted to verify this hypothesis.

Simultaneous management of blood flow and IOP in glaucoma.

Factors other than intraocular pressure (IOP) elevation must be involved in initiation and progression of glaucoma. An additional element in disease causation may be ischemia in the retina and optic nerve head. Ischemic damage to neurons in the CNS is similar mechanistically and histopathologically to changes seen in glaucoma. Further, glaucoma patients with normal IOP show clear evidence for cerebral and ocular ischemia. Aging and atherosclerosis reduce the ability of the eye to autoregulate blood flow when ocular perfusion pressure changes: the dependence of blood flow on perfusion pressure links ischemia to IOP. Consequently, neuroprotective treatments for glaucoma should be designed to both reduce IOP and improve ocular nutrient delivery.

The effect of nipradilol, an a-ß blocker, on retinal blood flow in healthy volunteers

Purpose. To study the effects of topically applied nipradilol, an a-ß blocker recently developed in Japan as an ocular hypotensive drug, on retinal blood flow (RBF) in healthy volunteers. Methods. Seven healthy volunteers (mean age, 33 years) underwent measurement of RBF using a newly developed stabilized laser Doppler velocimetry system. In a double-blind trial, retinal arterial blood flow, intraocular pressure (IOP), and blood pressure (BP) were measured before and after the instillation of nipradilol or saline every hour for 5 hours. Results. Retinal arterial blood flow and the diameter of the retinal artery significantly (p < 0.05) increased at 4 hours after instillation in nipradilol-treated eyes. Retinal blood velocity did not change significantly. Nipradilol evoked a significant (p < 0.05) bilateral decrease in IOP. Mean BP decreased significantly (p < 0.05) 3 hours after instillation. Ocular perfusion pressure (OPP), calculated from the mean BP and IOP, did not change significantly during the study. Conclusion. Topical nipradilol significantly increased retinal arterial blood flow in healthy volunteers, not through a secondary effect dependent on a change in OPP, but likely through the vasodilatory action of the drug.

Autoregulation of human optic nerve head blood flow in response to acute changes in ocular perfusion pressure.

Studies in animals have demonstrated that optic nerve head (ONH) blood flow (F(onh)) is autoregulated, but there is a lack of evidence for such a process in humans. Therefore, we investigated the relationship between F(onh) and mean ocular perfusion pressure (PPm) in normal volunteers when PPm is decreased through elevation of the intraocular pressure (IOP). Laser Doppler flowmetry (LDF) was used to measure relative mean velocity (Velohn), volume (Volonh) and F(onh) of blood at sites of the ONH away from visible vessels, while PPm was decreased in two ways: (1) rapidly, by IOP increments of 15 s duration, and (2) slowly, by IOP increments of 2 min duration, both by scleral suction cup in one eye of each of nine subjects. A rapid and large decrease of PPm of more than 100% induced a decrease of more than 80% in F(onh). With the slower decrease in PPm, F(onh) remained constant down to a PPm of approximately 22 mm Hg (IOP = 40 mm Hg) and then decreased, predominantly due to a decrease in Velohn. Immediately after removal of the suction cup, F(onh) increased transiently by 44% above baseline. This study demonstrates efficient blood flow autoregulation in the OHN, which is probably brought about by an increase in vascular capacitance. The magnitude of the reactive hyperaemia agrees with the compensatory decrease in ONH vascular resistance during IOP elevation. The time scale of the autoregulatory process and the dependence of the hyperaemia upon duration of IOP elevation suggest a metabolic mechanism of autoregulation.

Effect of changes in ocular perfusion pressure on choroid ischemia in man

The effect of changes in ocular perfusion pressure (PPm) on the choroidal blood flow (ChBF) in man was studied with the laser Doppler flowmetry (LDF) technique. We changed the PPm by increasing the intraocular pressure (IOP) or by increasing the blood pressure (BP) with isometric exercises. We observed that a) ChBF was not significantly different from baseline up to an IOP of 27 mm Hg and b) ChBF remained constant even if PPm increased by as much as 72%. Our results suggest that ChBF is autoregulated in response to an increase in IOP up to about 27 mm Hg. ChBF remains also constant in spite of an increase in systemic BP, probably due to a vasoconstriction induced by increased sympathetic activity.