[Ultrastructural features of vascular iridociliary system after biopuncture by antihomotoxic medicine].

OBJECTIVE: To reveal ultrastructural features of iridociliary vessels after biopuncture with antihomotoxic medicine. METHODS: Myopia model was created on 10 rabbits by injecting all trans-retinoic acid in catheter Vasofix Certo 24G in left internal carotid artery until we got low myopia. After six months of daily injections all rabbits had myopia from -2,0 to 3,0 D. Animals were separated into two groups: 5 rabbits with daily intradermal injection in three points of upper eye lid without medicine during 10 days and 5 rabbits with daily intradermal injection in three points of upper eye lid with Cerebrum Compositum N during 10 days. Morphology of iridociliary system was explored. RESULTS: Biopuncture in myopia model increases level of metabolic reactions in iridociliary system, supplies adaptive reserves by the hemodynamic enrichment of ciliary body vessels and balance of autonomic nervous system impulsation.

Amlodipine and benazeprilat differently affect the responses to endothelin-1 and bradykinin in porcine ciliary arteries: effects of a low and high dose combination.

PURPOSE: Visual field defects caused by vasospasm are often encountered in ophthalmology as a feature of glaucoma with poor response to conventional treatment. Combination therapy with drugs acting via different mechanisms might be more effective. Therefore, the effects of the calcium antagonist amlodipine and the angiotensin converting enzyme (ACE) inhibitor benazeprilat at low and high dose combination on contractions to endothelin-1 and endothelium-dependent relaxations to bradykinin were examined in porcine ciliary arteries. METHODS: Segments of the arteries were suspended in myographs for isometric tension recording. RESULTS: Pretreatment of the vessels with either amlodipine, the low or high dose combination significantly reduced the sensitivity to endothelin-1 as compared to control (concentration shift 18.3-fold, 14.2-fold, 23.3-fold respectively; p < 0.05), while benazeprilat was ineffective. The maximal response to endothelin-1 (10(-7) M) was most inhibited by the high dose combination which reduced the contractions by 49% as compared to control (p < 0.05). The low dose combination and amlodipine alone were less effective (reduction: 25%; p < 0.05 and 20%; n.s., respectively). On the other hand, benazeprilat enhanced the sensitivity (concentration shift 73-fold; p < 0.05) and maximal relaxation to bradykinin (by 27%; p < 0.01), whereas amlodipine or the low or high dose combination were ineffective. CONCLUSIONS: These findings indicate that amlodipine and benazeprilat differently affect vascular function of ciliary arteries. A high dose combination of both substances was most effective in inhibiting contractions to endothelin-1, suggesting a potentiating effect of the two compounds. In contrast, endothelium-dependent relaxations to bradykinin were enhanced by benazeprilat alone, but not when combined with amlodipine.

Effect of oral nifedipine on ocular blood flow in patients with low tension glaucoma.

AIM: To investigate the effect of oral nifedipine on ocular blood flow in patients with low tension glaucoma (LTG). METHODS: In this prospective study we examined the effects of 3 weeks of treatment with oral nifedipine 30 mg/day in 11 patients with LTG, by using colour Doppler ultrasound imaging to measure haemodynamic variables in the central retinal (CRA), short posterior ciliary (SPCA), and ophthalmic (OA) arteries. Intraocular pressure (IOP) and blood pressures were also evaluated. RESULTS: Nifedipine failed to alter IOP nor did it change peak systolic velocity, end diastolic velocity,or the resistance index in any of the three ocular vessels studied (p > 0.05). However systolic and diastolic systemic arterial blood pressure measurements varied significantly after nifedipine treatment compared with baseline (p < 0.05). CONCLUSION: Our study failed to demonstrate a significant effect of nifedipine on retrobulbar circulation of patients with LTG.

Photodynamic therapy (PDT) of the ciliary body with silicon naphthalocyanine (SINc) in rabbits.

BACKGROUND AND OBJECTIVE: To investigate silicone naphthalocyanine (SINc; 0.5 mg/kg) for photodynamic therapy (PDT) of the ciliary body in pigmented rabbits. STUDY DESIGN/MATERIALS AND METHODS: SINc was dissolved in canola oil by heating, emulsified with Tween-80, and given by ear vein. Pharmacokinetics were studied in frozen sections by fluorescence microscopy using a CCD camera-based, low light detection system with digital image processing at 1 hr and 24 hr (12 rabbits, 24 eyes total). A Ti:Sapphire laser delivered light at 770 nm by contact fiberoptic (1,000 microns; 80 mW/cm2;20,40 and 80 J/cm2). Controls (5 rabbits), received laser light at 770 nm without SINc. For comparison, eyes received continuous wave Nd:YAG laser by fiberoptic contact (0.8-1.2 J). RESULTS: Localization studies showed intravascular distribution shifting to a ciliary body distribution at 24 hr. PDT at 1 hr and 24 hr postinjection showed a more selective destruction of the ciliary body at 24 hr. Ciliary processes treated at 24 hr showed infarction and marked edema with sparing of iris. Tissue thermal damage was minimal in PDT controls. Eyes treated with the Nd:YAG laser exhibited full-thickness thermal necrosis of iris, ciliary processes, and a fibrinous iridocyclitis. In contrast, eyes treated by PDT were quiet with thrombosis of superficial blood vessels. CONCLUSION: Tissue photon penetration is good at 770 nm and thermal effects from the exciting laser alone were minimal. The ciliary processes of pigmented rabbits exhibit a selective retention of SINc and on that basis can be selectively destroyed with a minimum on thermal damage to nontarget tissues.

[Ocular circulatory changes caused by retrobulbar anesthesia with and without added adrenaline]. / Okuläre Kreislaufveränderungen durch Retrobulbäranästhesie mit und ohne Adrenalinzusatz.

UNLABELLED: In 80 patients, retrobulbar anesthesia (RBA; 5 ml of a lidocaine-bupivacaine mixture with hyaluronidase) with or without addition of adrenaline (after-mixing concentration 1:500,000) was performed preoperatively. In 2 examination series, the acute and medium-term effects of RBA on the following ocular circulatory variables were investigated: ocular pulsation volume (PVoc), systolic ciliary and retinal perfusion pressures or blood pressures, respectively (method: oculo-oscillo-dynamography). RESULTS: RBA with adrenaline: Directly after injection, PVoc was reduced by an average of 49%, the ocular perfusion and blood pressures were lowered by averages of 8.0 and 4.3 mmHg, respectively, and the intraocular pressure (Pio; hand-applanation tonometer) was elevated by 3.5 mmHg. 15 min after injection, PVoc and the ocular perfusion and blood pressures were even slightly more reduced, whereas Pio had reassumed its pre-injection level. RBA without adrenaline: During both time periods after injection, the reduction of PVoc averaged 10% less compared to RBA with adrenaline. The changes in ocular perfusion and blood pressures and in Pio, however, were not significantly different from RBA with adrenaline. CONCLUSIONS: The lowering of PVoc--which variable is determined mainly by the pulsatile choroidal blood flow--in concert with the lowered ciliary perfusion and blood pressures is indicative of a reduced ciliary blood flow during RBA. Because of the decreased retinal perfusion and blood pressures, there is also a higher risk of reduced blood supply to the retina. Only to some degree, the observed inhibitory RBA effects on ocular circulation can be explained by adrenaline, and to an even smaller degree by the only transient Pio elevation.

Anisodamine increases blood flow to the retina-choroid and protects retinal and pancreatic cells against lipid peroxidation.

This study investigated the effect of anisodamine (2 and 5 mg/kg i.v.) on ocular and systemic blood flow distribution in awake lambs using the radioactive microsphere technique. In separate in vitro studies, the effects of anisodamine (at final concentrations of 0.01 to 2.5 mg/ml) were determined on arachidonic acid, alloxan and ultraviolet radiation-induced lipid peroxidation of isolated retinal cells from rabbits and on alloxan-induced lipid peroxidation of hamster pancreatic islet beta cells. Malondialdehyde production was used as an index of lipid peroxidation and measured by the thiobarbituric acid method. Anisodamine preferentially increased blood flow and oxygen delivery to the retina-choroid and iris-ciliary body of the eye by 50-100%. Anisodamine significantly attenuated lipid peroxidation in retinal cells induced by ultraviolet radiation, alloxan and arachidonic acid by 17-50% and protected pancreatic beta cells against alloxan-induced lipid peroxidation. These properties may, in part, account for the beneficial effect of anisodamine in certain patients with diabetes.

[Intraocular pressure and ocular hemodynamics following oculopression with and without added retrobulbar anesthesia]. / Augeninnendruck und okuläre Hämodynamik nach Okulopression mit und ohne zusätzliche Retrobulbäranästhesie.

Two series of experiments were performed prior to cataract surgery. In series 1, in 30 patients oculopression was performed for 15 min (30, 40 or 50 mmHg). Directly after oculopression the intraocular pressure (Pio) was found to be reduced by an average of 10.7 mmHg. Systolic retinal and ciliary perfusion pressures (measured by means of oculo-oscillodynamography according to Ulrich) were found to be increased by an average of 5.4 mmHg, and the ocular pulsation volume (PVoc) was unchanged. In series 2, we injected 5 ml of anesthetic plus adrenaline behind the eye in 20 patients, followed by 15 min of oculopression (30 or 40 mmHg). Directly after the injection, Pio was found to have increased by 3.7 mmHg, and the perfusion pressures and PVoc were reduced by an average of 8 mmHg and 51%, respectively. Directly after oculopression (15 min after injection), Pio was lower by 10.1 mmHg, but the perfusion pressures and PVoc also remained lower. The changes observed in series 1 and 2 did not depend on the amount of oculopression. We conclude that a reduction in Pio after oculopression has a beneficial effect on the ocular circulation (increased perfusion pressures), whereas retrobulbar anesthesia has an inhibitory effect (reduction of perfusion pressures and PVoc). The hemodynamic effects of oculopression are largely suppressed by additional retrobulbar anesthesia.

Cilioretinal arteries in large optic disks.

The cilioretinal arteries form a physiologic bypass between the ciliary and retinal circulation. The evaluation of photographs of 163 normal optic nerve heads revealed a significant (p less than 0.001) correlation between the number of cilioretinal arteries and the optic disk and cup size: the larger the disk and cup the more vessels. The vessels' prevalence in all optic disks was 27.0%. It increased from 0% in disks smaller than 2.00 mm2 to 50.0% in optic nerve heads larger than 4.1 mm2. No correlations existed between cilioretinal arteries and refraction, axial length, side, sex and age, according to the missing correlations between these parameters and optic disk and cup area. The presence of two or three cilioretinal arteries indicates a congenitally large optic disk and cup in normal eyes, and can be helpful in the differentiation of physiologic macrocups in macrodisks from glaucomatous cupping.

Morphology of tight junctions in the ciliary epithelium of rabbits during arachidonic acid-induced breakdown of the blood-aqueous barrier.

A reversible breakdown of the blood-aqueous barrier in the iridial processes of rabbits has been induced by arachidonic acid as demonstrated by the passage of horseradish peroxidase at places through the tight junctions. Freeze-fracture images reveal very discontinuous P-face ridges. However, the analysis of complementary replicas demonstrates that discontinuities of P-face ridges are always complemented by particles or short bars found in the E-face furrows. Though the problem exists of correlating freeze-fracture images of the junctional structure to the focal passage of horseradish peroxidase, the data suggest that the discontinuities of P-face ridges cannot be the structural counterpart of the passage of horseradish peroxidase. Alternative pathways of horseradish peroxidase are discussed in context with the offset bifibrillary model of the junction.

Possible significance of cilioretinal arteries in open-angle glaucoma.

To study the possible prognostic significance of the cilioretinal artery in open-angle glaucoma, the disc stereophotographs of one hundred consecutive patients with bilateral open-angle glaucoma were reviewed for the presence of cilioretinal arteries. The charts of 20 patients with unilateral cilioretinal arteries were then studied for the extent of the optic disc cupping and visual field damage. Despite the absence of a significant difference in the intraocular pressure between the two groups, eyes with cilioretinal arteries showed larger cup/disc ratios and more visual field damage when compared to the contralateral eyes without cilioretinal arteries in the same patients.

The effect of interruption of the short posterior ciliary arteries on slow axoplasmic transport and histology within the optic nerve of the rhesus monkey.

Tritiated leucine was injected into the vitreous of rhesus monkey eyes to make it available for protein synthesis by the ganglion cells. The short posterior ciliary arteries were cut three hours later or several weeks prior to the leucine injection. A reduction of labeled protein within the retrolaminar optic nerve was seen in all eyes so treated. Autoradiography revealed a diffuse reduction of axoplasmic transport into these optic nerve heads. There was consistent evidence of focal obstruction of labeled protein at the interface between the lamina scleralis and retrolaminar optic nerve. Vacuoles appeared in the most severely affected areas. These histologic changes were followed by gliosis in the areas of ischemic damage. Glaucomatous cupping of the optic nerve head was not seen within six weeks following the induced ischemia.