The locations of mitochondria in mammalian photoreceptors: relation to retinal vasculature.

Adult mammalian photoreceptors are elongated cells, and their mitochondria are sequestered to the ends of the cell, to the inner segments and (in some species) to axon terminals in the outer plexiform layer (OPL). We hypothesised that mitochondria migrate to these locations towards sources of oxygen, from the choroid and (in some species) from the deep capillaries of the retinal circulation. Six mammalian species were surveyed, using electron and light microscopy, including immunohistochemistry for the mitochondrial enzyme cytochrome oxidase (CO). In all 6 species, mitochondria were absent from photoreceptor somas and were numerous in inner segments. Mitochondria were prominent in axon terminals in 3 species (mouse, rat, human) with a retinal circulation and were absent from those terminals in 3 species (wallaby, rat, guinea pig) with avascular retinas. Further, in a human developmental series, it was evident that mitochondria migrate within rods and cones, towards and eventually past the outer limiting membrane (OLM), into the inner segment. In Müller and RPE cells also, mitochondria concentrated at the external surface of the cells. Neurones located in the inner layers of avascular retinas have mitochondria, but their expression of CO is low. Mitochondrial locations in photoreceptors, Müller and RPE cells are economically explained as the result of migration within the cell towards sources of oxygen. In photoreceptors, this migration results in a separation of mitochondria from the nuclear genome; this separation may be a factor in the vulnerability of photoreceptors to mutations, toxins and environmental stresses, which other retinal neurones survive.

A-type potassium current in retinal arteriolar smooth muscle cells.

PURPOSE: By their control of membrane potential and intracellular free Ca(2+) ([Ca(2+)](i)), K(+) currents are pivotal in the regulation of arterial smooth muscle tone. The goal of the present study was to identify and characterize the A-type K(+) current in retinal microvascular smooth muscle (MVSM) and to examine its role in modulating membrane potential and cellular contractility. METHODS: Whole-cell perforated patch-clamp recordings were made from MVSM cells within intact isolated arteriolar segments. Before patch-clamping, retinal arterioles were anchored in the physiological recording bath and perfused with an enzyme cocktail to remove surface basal lamina and to uncouple electrically the endothelial cells from the overlying MVSM cells. RESULTS: K(+) currents were activated by depolarizing steps from -80 to +100 mV in 20-mV increments. A dominant, noninactivating current was elicited by depolarization to potentials positive of -50 mV. Inhibition of this current by 100 nM of the Ca(2+)-activated K(+) channel blocker, Penitrem A, revealed a rapidly inactivating K(+) current that resembled an A-type current. The A-type current was insensitive to tetraethylammonium (TEA) at 1 mM, but was partially suppressed by higher concentrations (10 mM). 4-Aminopyridine (10 mM; 4-AP) completely blocked the A-type current. The 4-AP-sensitive transient current was activated at a potential of -60 mV with peak current densities averaging 29.7 +/- 5.68 pA/pF at +60 mV. The voltage of half-inactivation was -28.3 +/- 1.9 mV, and the time constant for recovery from inactivation at +60 mV was 118.7 +/- 7.9 ms. Under current-clamp conditions 4-AP depolarized the membrane potential by approximately 3 to 4 mV and triggered small contractions and relaxations of individual MVSM cells within the walls of the arterioles. CONCLUSIONS: A-type current is the major voltage-dependent K(+) current in retinal MVSM and appears to play a physiological role in suppressing cell excitability and contractility.

Ocular blood flow evaluation in injured and healthy fellow eyes.

PURPOSE: To assess if injured eyes develop ocular blood flow disturbances that may contribute to development of traumatic glaucoma. METHODS: Twenty-five eyes of 25 patients hospitalized from January 1997 to July 1999 for blunt (15) or penetrating (10) eye injury and elevated intraocular pressure (IOP) (>23 mm Hg) were controlled at least 24 months after the trauma and underwent visual field examination, pulsatile ocular blood flow (pOBF), and color Doppler imaging (CDI) analysis of ophthalmic artery, central retinal artery, nasal and temporal short posterior ciliary arteries. Uninjured healthy eye was used as control. RESULTS: IOP was significantly higher in injured eyes (15.1+/-3.3 vs 13.0+/-2.7 mmHg; p<0.01), but only 2 eyes (8%) were under medical treatment. pOBF values were significantly lower in injured eyes: 11.25+/-6.56 microL/sec in the trauma eyes and 15.40+/-7.29 in fellow eyes (p=0.002). Resistivity index of all investigated retrobulbar vessels was very significantly higher in injured eyes than in fellow eyes (p<0.0001). There is no significant correlation between IOP and ocular blood flow disturbance. CONCLUSIONS: Long-term follow-up (mean 39+/-12 months) of injured eyes shows, besides a slight but significant increase of IOP, a very significant impairment of ocular blood supply to injured eyes compared to healthy fellow eyes with reduction of pulsatile ocular blood flow and marked increase of resistance to flow in all retrobulbar vessels. These anomalies may be considered an independent risk factor to develop traumatic glaucoma.

Microvasculature of the rat optic nerve head.

PURPOSE: To describe the arterial blood supply, capillary bed, and venous drainage of the rat optic nerve head. METHODS: Ocular microvascular castings from 6 Wistar rats were prepared by injection of epoxy resin through the common carotid arteries. After polymerization, tissues were digested with 6 M KOH, and the castings washed, dried, and coated for scanning electron microscopy. RESULTS: Immediately posterior to the globe, the ophthalmic artery trifurcates into the central retinal artery and two posterior ciliary arteries. The central retinal artery directly provides capillaries to the nerve fiber layer and only contributes to capillary beds in the neck of the nerve head. The remainder is supplied by branches of the posterior ciliary arteries that are analogous to the primate circle of Zinn-Haller. Arterioles arising from these branches supply the capillaries of the transitional, or laminar, region of the optic nerve head. These capillaries are continuous with those of the neck and retrobulbar optic nerve head. All optic nerve head capillaries drain into the central retinal vein and veins of the optic nerve sheath. A flat choroidal sinus communicates with the central retinal vein, the choriocapillaris, and with large veins of the optic nerve sheath. CONCLUSIONS: The microvasculature of the rat optic nerve head bears several similarities to that of the primate, with a centripetal blood supply from posterior ciliary arteries and drainage into the central retinal and optic nerve sheath veins. Association of nerve sheath veins with the choroid represents an important difference from the primate.

Optic nerve head microvasculature of the rabbit eye.

Vascular luminal castings of rabbit eyes were microdissected and studied with scanning electron microscopy to elucidate the three-dimensional angioarchitecture of the optic nerve head. Using sequential microdissection, an incomplete arterial circle was identified as terminal branches of two to three short posterior ciliary arteries around the optic nerve head. Several recurrent branches from the arterial circle form a pial arterial network. This pial system supplies the optic nerve head microvasculature and receives numerous venules from them. The only large vessel to enter the optic nerve is a central retinal artery that has few branches within the optic nerve and provides several branches at the surface of the optic disc. Moderately numerous vessels connect the retinal and ciliary vascular layers within the optic nerve head. Few arterioles to the optic nerve head arise from the choroid; however, there are a small number of capillary and numerous venous connections between them. These results indicate that the principal blood supply of the rabbit optic nerve head is derived from the short posterior ciliary arteries by the arterial circle. The retinal arteries contribute to the surface vasculature of the optic nerve head. The pial system also plays a significant role in both supply and drainage of the rabbit optic nerve head.

Vasoactivity of intraluminal and extraluminal agonists in perfused retinal arteries.

PURPOSE: To evaluate the vasoactive response of isolated perfused arteries of the pig to K+ and adrenergic agonists and to compare the effects of intraluminal (IL) and extraluminal (EL) drug delivery. METHODS: A new microperfusion system was developed, in which short lengths of porcine retinal arteries (outer diameter 90.4 +/- 2.7 microns) were cannulated at both ends and perfused at a controlled rate (5 microliters/min) with outflow through a single side branch. The diameter of the vessel and the intraluminal pressure were monitored, and the effect of intraluminally and extraluminally applied agonists was determined. Endothelial cell function and the integrity of the blood retinal barrier was verified. RESULTS: Consistent vasoactive responses were obtained from most vessels. The resting diameter of the vessel was not greatly influenced by changes in flow rate or intraluminal pressure over the physiological range. Adrenaline and noradrenaline caused dose-dependent contractions, which were larger when applied intraluminally than they were when applied extraluminally. The largest contraction for adrenaline was 19.0% +/- 2.1% (n = 13) IL and 8.4% +/- 1.5% (n = 13) EL, and for noradrenaline, 17.8% +/- 1.9% (n = 13) IL and 6.8% +/- 1.1% (n = 13) EL. The IL contraction to 124-mM K+, 19.0% +/- 1.6% (n = 21), was also greater than that for EL application, 5.0% +/- 1.0% (n = 13). We found that the existence of myogenic contractions was restricted to the special case in which vessels with no branches were pressurized under zero flow conditions. CONCLUSIONS: Pig retinal arteries exhibited asymmetry in their responses to adrenergic agonists and K+, with contractions significantly larger when the drug was applied to the intraluminal surface rather than the extraluminal surface. This asymmetry may reflect an important property of retinal vessels. Microperfusion systems of this type may prove valuable in developing a better understanding of control mechanisms in retinal circulations.

Contractile responses of isolated bovine retinal microarteries to acetylcholine.

The contractile responses of isolated and activated bovine retinal microarteries (BRA) (diameter, 204 +/- 4 microns; n = 48) to acetylcholine (ACh) were studied. These responses depended on the nature of the activating agent. The ACh relaxed BRA activated by prostaglandin F2 alpha (PGF2 alpha) and circumferential stretching in a dose-dependent manner but had no significant effect on K(+)-activated BRA. The effects of ACh also depended on the degree of BRA activation: the stronger the PGF2 alpha-induced contractions, the weaker the relaxation produced by ACh. In equivalent PGF2 alpha-induced contractions, the ACh effects were reproducible. The muscarinic antagonist, atropine, reversed the relaxation caused by ACh of PGF2 alpha-activated BRA. Physostigmine, an inhibitor of acetylcholinesterase, did not potentiate or prolong the relaxant action of ACh. Selective removal of the BRA endothelium (by gassing the BRA lumen, checked by scanning electron microscopy) blocked the relaxation caused by ACh of PGF2 alpha-induced contractions and unmasked a constricting action of ACh. This suggests that, in BRA with functional endothelium, the direct constricting effects of ACh on smooth muscle are masked by the more potent dilating activity, mediated by endothelial muscarinic receptors. Acetylcholinesterase was not found in BRA.

Blood supply to the retina and the lens in the gerbil (Meriones unguiculatus).

The blood supply to the retina and the lens in 32 gerbils (Meriones unguiculatus) of both sexes from infancy to maturity was studied under light and stereoscopic microscopes, and a scanning electron microscope. Mercox (CL-2R; Dai Nippon Ink, Tokyo, Japan) was injected into the left ventricle of 30 animals in order to visualize the blood supply to the retina and the lens from the ophthalmic artery. The central retinal artery arises from the ophthalmic artery, passes through the papilla of the optic nerve together with the central retinal vein and penetrates the vitreous space (cavity of the eye) between the lens and the internal limiting membrane of the retina, where it divides into the central branches covering the lens and the parietal branches to supply the retina. The former passes through the hyaloid space after branching several arterioles and then covers the lens like a network from its medial and marginal sides. Different from small experimental animals, the parietal branches, just after separating from the central one, divides into the nasal, dorsal and temporal branches in the vitreous space, each of which then subdivides to distribute across the retina on the inner limiting membrane, then delineates the membrana vasculosa retinae. This basal pattern of vasculization 1 day after birth continues to death. Both the central and parietal branches of the central retinal artery correspond to the branches of the hyaloid artery in embryo and the latter is preserved in adult gerbils.

Amyloid beta(1-42) and its beta(25-35) fragment induce in vitro phosphatidylcholine hydrolysis in bovine retina capillary pericytes.

We describe the inhibitory effect of full-length Abeta(1-42) and Abeta(25-35) fragment of amyloid-beta peptide on phosphatidylcholine (PtdCho) metabolism in bovine retina capillary pericytes. Cell cultures were incubated with Abetas for 24 h. Peroxidation indices (malondialdehyde and lactate dehydrogenase release) significantly increased after 20-50 microM Abeta(1-42) or Abeta(25-35) treatment. In addition, [Me-3H]choline incorporation into PtdCho strongly decreased while either 3H-choline or 14C-arachidonic acid release from prelabeled cells increased, indicating PtdCho hydrolysis. The effect was very likely due to prooxidant action of both Abeta peptides. Reversed-sequence Abeta(35-25) peptide did not depress 3H-choline incorporation nor stimulate PtdCho breakdown. With addition of Abetas at low concentrations (2-20 microM) to pericytes, marked ultrastructural changes, well connected to metabolic alterations, emerged including shrinkage of cell bodies, retraction of processes, disruption of the intracellular actin network. Cells treated with higher concentrations (50-200 microM) displayed characteristics of necrotic cell death. The data suggest that: (a) Abeta(1-42) and Abeta(25-35) peptides may modulate phospholipid turnover in microvessel pericytes; (b) together with endothelial cells, pericytes could be the target of vascular damage during processes involving amyloid accumulation.

Microvasculature of the human optic nerve.

PURPOSE: Methyl methacrylate vascular corrosion casting techniques were used to examine the normal anterior optic nerve microvasculature in 18 human eye bank eyes. METHODS: Selective cannulation of the central retinal artery, the short posterior ciliary arteries, or both, allowed the methyl methacrylate to be injected into the anterior optic nerve circulation. Preflushing with tissue plasminogen activator greatly enhanced the filling of the fine microvasculature by dissolving the intraluminal clots. RESULTS: The superficial nerve fiber layer of the optic nerve received its primary blood supply from the central retinal artery. In 11 of 13 eyes injected with methyl methacrylate through the short posterior ciliary arteries, there was a perineural, circular arterial anastomosis (circle of Zinn-Haller) at the scleral level. Branches from this circle penetrated the optic nerve to supply the prelaminar and laminar regions and the peripapillary choroid. In the two eyes without this arterial circle, direct branches from the short posterior ciliary arteries supplied the anterior optic nerve. The venous drainage of the anterior optic nerve was almost entirely through the central retinal vein and its tributaries. CONCLUSIONS: This study demonstrates that the main arterial vascular supply to the anterior optic nerve is from the short posterior ciliary arteries. The contribution of the peripapillary choroid to the anterior optic nerve is minimal in comparison to the direct contribution from the short posterior ciliary arteries.

Histopathological abnormalities in ocular blood vessels of CADASIL patients.

PURPOSE: To assess histopathological findings in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). DESIGN: Case reports and histopathological evaluation of enucleated eyes. METHODS: Four eyes from two CADASIL patients were enucleated at autopsy and prepared for histopathological analysis using light and electron microscopy. RESULTS: Thickening of arterial walls with fibrosis, eosinophilic Periodic acid Schiff-positive basement membrane material and loss of vascular smooth muscle cells (VSMC) in the central retinal artery and its branches, the leptomeninges, the ocular adnexa, and the optic disk were observed. On electron microscopy, numerous deposits of granular, osmiophilic material in arterial walls as well as VSMC and pericyte degeneration were noted. In contrast to retinal vessels, the choroid was not affected. CONCLUSION: Our findings suggest a differential involvement of small blood vessels in CADASIL, depending on the angioarchitecture and support autopsy data of nervous tissue describing that loss of VSMCs is most pronounced in tissues depending on blood-tissue barriers.

Blood-flow velocities in the extraocular vessels in normal volunteers.

PURPOSE: To determine normal values of blood-flow velocities in extraocular vessels. METHODS: In one eye each in 189 healthy adult volunteers, blood-flow velocities in the ophthalmic artery (OA), central retinal artery (CRA), central retinal vein (CRV), short lateral posterior ciliary artery (LPCA), and short medial posterior ciliary artery (MPCA) were measured by color Doppler imaging. In the arteries, peak systolic velocity (PSV), end diastolic velocity (EDV), and resistivity index (RI) were calculated. In the CRV, maximal and minimal blood-flow velocities were measured. Influence of age, gender, blood pressure, and heart rate on blood-flow velocities and the resistivity index were analyzed. RESULTS: Mean outcomes +/- S.D. cm/sec were as follows: in the OA, PSV was 39.2 +/- 5.3, EDV was 9.1 +/- 2.5, and RI was 0.77 +/- 0.05. In the CRA, PSV was 11.0 +/- 1.8, EDV was 3.3 +/- 0.9, and RI was 0.71 +/- 0.05. In the short LPCA, PSV was 11.2 +/- 1.7, EDV was 3.7 +/- 1.0, and RI was 0.68 +/- 0.06. In the short MPCA, PSV was 11.2 +/- 11.7, EDV was 3.6 +/- 0.9, and RI was 0.68 +/- 0.05. In the CRV, mean maximal velocity was 4.5 +/- 0.9, and mean minimal velocity was 3.3 +/- 0.7. Age, gender, systolic blood pressure, diastolic blood pressure, and heart rate had no consistent statistically significant influence on the measured and calculated variables. CONCLUSION: Normal values for blood-flow velocities in the extraocular vessels serve as a basis in deciding whether a measured value of a patient is normal or abnormal.

Pathogenesis of hypertensive retinopathy. An experimental study in the monkey.

Retinal changes in accelerated hypertension were studied in seventeen monkeys with experimental hypertension by means of ophthalmoscopy and colour and flourescence photography during life, and by injection and digest preparations and light and electron microscopy after the animals had been killed. Cotton-wool spots developed in all but three monkeys. The arteries became tortuous and dilated and the light reflex decreased in those animals that became hypertensive. The earliest abnormality was a development of many points of fluorescein leakage on terminal arterioles or small arteries. Such leaking points were always present in relation to cotton-wool spots but were not confined to such areas. Focal narrowing of arteries was not observed but arteriolar occlusion and retrograde filling of the distal segment was present in three animals. Superficial linear haemorrhages were noted in five animals. Light microscopy revealed cotton-wool spots which were identical to those observed in man with a collection of swollen axons containing densely staining pseudonuclei. Study of the arterioles by electron microscopy showed findings ranging from normality to extensive necrosis. Many precapillary arteries were constricted and some were virtually occluded. Degenerative changes were present in smooth muscle cells in the wall of many of the constricted arterioles. Many arteries also showed insudation into their wall of plasma which had seeped into the muscular coat displacing and sometimes entirely replacing the smooth muscle cells. Except for arterioles with advanced necrosis, there was no indication of how plasma insudation occurred. Two arterioles with extensive necrosis showed a break within the endothelial cell cytoplasm through which penetration of plasma proteins had probably occurred. The extravascular tissues showed collections of amorphous material, sone of it with the typical banded configuration of fibrin. The sequence of events proposed to explain these features is as follows: (1) The arterioles constrict as the pressure rises, most likely as a result of vascular autoregulation. This may head to occlusion of the precapillary arterioles and is associated with necrosis of vascular smooth muscle. (2) Dilatation then occurs with insudation of plasma into the unsupported wall through a damaged endothelium. This stage probably corresponds to the autoregulatory break-point and is evidenced clinically by focal leakage of fluorescein. (3) Progressive plasma insudation into the vessel wall with further muscle necrosis results in secondary occlusion and the typical picture of advanced fibrinoid necrosis.

Immunogold staining of elastin in the wall of the retinal arteries in Macaca mulatta.

Elastin has been demonstrated in the wall of the retinal arteries in or immediately adjacent to the optic disc of adult Macaca mulatta using the immunogold labelling technique with delta-elastin antibody. Since elastin is thought to provide elasticity to the walls of these vessels, perhaps its presence in the retinal arteries plays a role in contractility and regulation of blood flow throughout the retinal vascular system.

Stereological estimation of Weibel-Palade bodies in the retinal vasculature of normal and diabetic dogs.

The absolute volume of Weibel-Palade (WP) bodies, the storage organelles of von Willebrand factor (vWF), was estimated by a stereological method in a known volume of central retina from normal and 5-year diabetic dogs. The results showed that the volume of WP bodies present in the endothelium of the retinal vasculature varies with blood vessel type and in diabetes. In both diabetic and normal dogs the endothelium of the retinal veins contained a higher volume of WP bodies than that of the retinal arteries. In dogs which had been diabetic for a duration of 5 years the volume of WP bodies present in the endothelium of retinal veins was significantly greater than in the endothelium of veins from the control animals. However, there was no significant difference in the volume of WP bodies present in the endothelium of retinal arteries or capillaries between the two groups of animals.

Electron microscopic studies of pipestem sheathed vessel in human retina.

Histopathology of a clinically observed pipestem sheathed vessel in the retina was studied by electron microscopy. This vessel was characterized by a marked increase and disarrangement of collagen fibrils in the media and adventitia, and invasion of the cytoplasmic processes of Müller cells into the adventitia. The lumen of the vessel was extremely narrow but was preserved with healthy endothelial cells. It is suggested that increased and disarranged collagen fibrils in the vessel wall is related mainly to the ophthalmoscopic appearance of the pipestem sheathing. The infiltration of glial cells in the vessel wall may be of less significance to the pipestem sheathing.

Sectorial blood supply to the monkey optic disc surface from the cilioretinal artery.

The cilioretinal artery in one monkey eye (left) was observed using fluorescein videoangiography and a scanning laser ophthalmoscope, and was further evaluated by scanning electron microscopy after microvascular corrosion casting. Following intravenous injection of fluorescent dye, a choroidal flush was observed at 5.7 seconds. Appearance of the dye in two cilioretinal arteries at the edge of the temporal optic disc was at 5.9 seconds, and the capillary phase of these arteries, at 6.4 seconds. The dye was first observed in the central retinal artery at 6.9 seconds. The cilioretinal arteries directly supplied the microcirculation of the temporal quadrant of the optic disc and the retinal vasculature in the disc-macular area. The vascular casting showed the entire course of the cilioretinal arteries in the retina. The cilioretinal arteries entered the temporal edge of the retrobulbar optic nerve head and branched to the prelaminar and the temporal edge of the optic disc.

Retinopathy in diabetic (KKA gamma) mice: diabetic microvascular changes to the retina in KKA gamma mice revealed by light and electron microscopy.

Pericytic changes in the retinal vessels of diabetic (KKA gamma) and control (C57BL) mice were studied by light and electron microscopy. An improved histochemical technique for alkaline phosphatase was used in the light microscopic study. In the control mice, a continuous pathway was identified extending from the retinal arterioles, via the superficial and deep retinal capillaries, to the retinal venules. The deep retinal capillaries formed networks and were localized within the deeper retinal layers; the retinal arterioles, superficial capillaries, and venules were present in the nerve fiber layer. Examination of KKA gamma mice, aged 16 to 28 weeks, revealed engorgement of the arterioles, hypertrophy of the pericytes (which contained numerous actin filaments) within the superficial retinal capillaries, and narrowing of the deep retinal capillaries. These microvascular changes indicate retinal hyperperfusion, local hypertension of the superficial retinal capillaries, adaptive hyperfunctional changes in the pericytes of these capillaries, and ischemia of the deep retinal capillaries. The pericytic changes observed in the diabetic capillaries contrasted sharply with previous reports; an explanation for this variance is suggested.

[Ultrastructural study on retinal arteriolar caliber irregularity in stroke-prone spontaneously hypertensive rats].

Ultrastructural changes in the arteriolar wall with caliber irregularity of spindle type, rosary type and diffuse dilatation type were studied in stroke-prone spontaneously hypertensive rats (SHRSP) aged 4, 6 and 10 months with systolic blood pressures of 210-240 mmHg by use of intravenously injected gelatin fluorescein preparation (IVGFP) and light and electron microscopy. Tridimensional graphic models were reconstructed from light micrographs of cross-sectioned serial preparations using a computerized micrograph-analyser. In the spindle type, I found markedly thickened media and smooth muscle cell necrosis at the narrowed portion of the arteriole central to the ampullar portion and a marked stretch and disappearance of the inner elastic lamina at the ampullar portion. These vascular changes of arteriolosclerosis were most advanced in the spindle type among three types of caliber irregularity. Tridimensional graphic models disclosed that there was no correlation between the wall thickening and luminal diameter of the arteriole. These results may explain the process of development of caliber irregularity in SHRSP.

[Optic nerve microcirculation. III. Lamina cribrosa]. / Mikrokrzenie w nerwie wzrokowym. III. Blaszka sitowa.

The architecture of the lamina cribrosa was investigated on the material of 160 optic nerves of people decreased at the age of 6 months to 80 years, free of pathological changes of circulation. The posterior segment of lamina cribrosa is supplied by arterial blood from: centripetal arterioles of the pia mater, ramifications from the secondary and tertiary posterior short ciliary arteries and from the longitudinal net of capillaries of the optic nerve. The central part of the lamina cribrosa is supplied by the twigs of the complete or incomplete vascular ring of Zinn-Haller or directly from secondary twigs of choroidal arteries. The anterior part of lamina cribrosa is vascularized by choroidal vessels and in a minor part by the vascular ring of Zinn-Haller. The circulation in the area of lamina cribrosa is integrally connected with the system of posterior short ciliary arteries and the arterioles of the internal vagina of the optic nerve. The central retinal artery does not give up any branches in this region. Similarly to other segments of the optic nerve there exists an individual variability in the system and course of the vessels in the lamina cribrosa. The vascular system of lamina cribrosa is connected anteriorly with the vessels of the paralaminar area of the optic disc which receive vascular branches from early ramifications of the central retinal artery (25 p.c. of cases).