Practice styles and preferences of Finnish cataract surgeons - 1998 survey.

PURPOSE: To collect information of current cataract surgery techniques in Finland. METHODS: A questionnaire of 36 multiple choice questions about practice styles and preferences in cataract surgery was sent to 153 ophthalmologists in Finland. In three weeks, 75 respondents returned the questionnaire (49%), and of these 68 (44%) reported doing cataract surgery. RESULTS AND CONCLUSIONS: Topical anesthesia, temporal approach for the incision, either clear corneal or frown scleral, no suture closure of the wound, continuous circular capsulorhexis, phacoemulsification technique and foldable IOLs are often preferred in Finland. It can be calculated that this survey represents roughly 70-80% of all performed cataract operations in Finland and thus these results may be regarded as a reliable picture of current cataract surgery techniques in Finland.

Compatibility of corticosteroids and antibiotics in combination.

PURPOSE: To study the compatibility of combinations of antibiotics and steroids commonly used in anterior segment surgery. SETTING: Research Laboratory, Helsinki University, Finland. METHODS: Aggregate production in vitro and in vivo was studied for three injectable antibiotics (cefotaxime sodium, tobramycin sulfate, and gentamicin) and four corticosteroids (triamcinolone acetonide, methylprednisolone sodium succinate, methylprednisolone acetate, and dexamethasone sodium phosphate) using conventional and dark-field microscopy. Aggregate formation on collagen shields and subconjunctival aggregate formation of tobramycin sulfate in combination with methylprednisolone acetate or dexamethasone sodium phosphate was also studied. RESULTS: Dexamethasone sodium phosphate (4 mg/mL) did not form aggregates with any of the three antibiotics tested. Cefotaxime sodium did not cause aggregates when 24 mg/mL of dexamethasone sodium phosphate was used both in vitro and in vivo or in association with collagen shields. CONCLUSIONS: To avoid undesired side effects, such as epithelial sloughing and corneal edema after collagen shield application, antibiotics and steroids must be carefully selected.

Intraocular effects of ruthenium red in responses to compound 48/80 and topical formaldehyde in rabbit.

We have previously shown the presence and localization of mast cells and the intraocular effects of compound 48/80 in the rabbit eye. In the present study we have evaluated the mechanism of action of compound 48/80 using ruthenium red as a blocker of sensory axon reflexes in the rabbit eye and by measuring the intraocular pressure (IOP), the pupil size, the blood pressure, the protein and cAMP content in the aqueous humour. Topical neutral formaldehyde was used as a topical inducer of neuronally mediated response in a separate series of experiment. Intracamerally-injected ruthenium red suppressed the compound 48/80-induced elevation intraocular pressure and prevented miosis, while having little if any effect on the breakdown of the blood-aqueous barrier and on the increase in the cAMP concentration in aqueous humour. Ruthenium red also inhibited the irritative response in eyes treated with topical 1% formaldehyde. As the blood-aqueous barrier in the rabbit is an extremely sensitive system higher doses of ruthenium red causes damage of the barrier in the ruthenium red treated eyes. The results demonstrate that compound 48/80 not only has a mast cell degranulating effect but also a sensory nerve- stimulating effect.

Systemic cyclosporin treatment for high-risk corneal transplantation.

The success rate for uncomplicated penetrating keratoplasty is very high. However, in high risk patients there is a significantly increased risk for immunologic graft failure and the success rate is relatively poor. Oral cyclosporin A treatment has dramatically decreased the rejection rate in solid organ transplantation. Its oral use in ophthalmology has so far been relatively limited and topical use restricted by poor penetration of the drug into ocular tissues. The favorable results of oral cyclosporin treatment to prevent corneal graft failure in high-risk patients is demonstrated in this study. High-risk corneal transplant patients were selected from the general population scheduled to undergo corneal transplantation. Twenty-two of 277 patients who were operated during a four-year period were regarded as high-risk keratoplasty patients. Systemic cyclosporin A treatment (5mg/kg/day) was given prophylactically to 14 of these patients who were considered to be at high-risk for keratoplasty rejection (CsA group). In addition the patients received a low dose of corticosteroids. Eight similar patients receiving high dose corticosteroids served as a control group (control group). In the CsA group graft survival was 78.6% compared with 37.5% in the control group at 1.5 years. The grafts of patients receiving CsA had a significantly better survival rate (p.o5) than those in control at one and 1.5 years. On the follow-up to four years graft survival in patients treated with CsA was, however, decreasing to 35.7%. The low graft survival in both high-risk groups is in great contrast to graft survival in all patients operated during the same period (93.1%). Systemic cyclosporin treatment when received at the time of the operation is effective in reducing failure from irreversible rejection in high-risk keratoplasty, but for maximal effect, a six-month period of treatment is too short. Subjective side effects were frequent but still acceptable. Blood tests did not reveal any pathological hepatic or renal laboratory values caused by system CsA administration. Careful and frequent follow-ups of the patients are however needed.

Corneal vascularization and opacification during long-term use of dipivefrin.

Dipivefrin hydrochloride is a lipophilic prodrug for epinephrine hydrochloride, allowing lower concentration of the drug to achieve the same intraocular pressure lowering effect and having also less harmful effects than epinephrine hydrochloride. However, harmful effects have been associated also with the use of dipivefrin and here we report of a case of corneal vascularization during long-term use of dipivefrin.

Effect of captopril on ocular irritative response to topical neutral formaldehyde and YAG-laser capsulotomy in the rabbit.

Angiotensin converting enzyme (ACE) -inhibitors inhibit degradation of inflammatory mediators substance P (SP) and bradykinin, which may further stimulate the synthesis of prostaglandins. The resulting increase in inflammatory mediators in tissues is suggested to be the reason for the dry cough, involving sensory C-fiber activation, among patients receiving ACE-inhibitor therapy. In the present study, the effect of an ACE-inhibitor, captopril, on ocular irritative responses was studied in the rabbit. Intravenous captopril decreased markedly the blood pressure and the intraocular pressure (IOP) modestly. Topical neutral formaldehyde elicits an irritative response in the eye mediated through sensory neuropeptides SP and calcitonin gene-related peptide (CGRP). Following topical neutral formaldehyde, the increase in IOP and breakdown of the blood-aqueous barrier were inhibited by captopril, while miosis was not affected. Cyclic AMP (cAMP) content in the aqueous humour was increased by captopril, and this increase was inhibited by indomethacin. Following YAG-laser anterior capsulotomy, captopril inhibited the increase in IOP, breakdown of the blood-aqueous barrier and miosis. The present study demonstrates that use of short-term administration of captopril prior to sensory nerve stimulation or YAG laser anterior capsulotomy does not enhance the ocular responses to these stimuli in the rabbit. In the present study, captopril inhibited these responses, at least partly by decreasing the blood pressure.

Characterization of binding sites and effects of calcitonin gene-related peptide (CGRP) and CGRP 8-37 on regional blood flow in rabbit salivary glands.

Calcitonin gene-related peptide (CGRP) is a neuropeptide present in nerve fibres of salivary glands in several species, including man. One of the major targets of these nerve fibres are blood vessels of the glands. The presence and distribution of specific binding sites for CGRP in the rabbit major salivary glands was here investigated autoradiographically. In order to determine the physiological role of CGRP, regional blood flow was measured after intravenous (i.v.) or intra-arterial (i.a.) administration of CGRP or the antagonist CGRP 8-37, using a microsphere technique. Specific binding sites for CGRP were found in the parotid, submandibular and sublingual glands, distributed mainly in the muscular and endothelial layers of the blood vessel walls. CGRP injected i.a. (10 pmol/kg) caused a significant increase in regional blood flow in all major salivary glands. However, i.v. infusion of CGRP (120 pmol/kg) decreased regional blood flow in the parotid and sublingual glands, due to a general decrease in peripheral resistance and redistribution of peripheral blood flow. CGRP 8-37 given i.a. together with CGRP significantly inhibited the blood-flow increase by CGRP alone. It is concluded that most of the CGRP receptors in the rabbit salivary glands are localized in vascular elements. The physiological data show that CGRP acts as a vasodilator in the major salivary glands of the rabbit in vivo, and that the effect of CGRP is inhibited by the CGRP antagonist CGRP 8-37.

Use of collagen shields in cataract surgery.

A randomized, prospective, multicenter study evaluated the efficacy and safety of using collagen shields to deliver drugs after cataract surgery. Collagen shields saturated with an antibiotic and a steroid were placed in 90 eyes postoperatively. A control group of 93 eyes received the same drugs through a peribulbar/retrobulbar injection. One day after surgery, the shield group had significantly less corneal edema, conjunctival hemorrhaging, and postoperative pain and fewer corneal opacities. All symptoms except the conjunctival hemorrhaging disappeared by day seven. Our study suggests that using collagen shields for drug delivery after cataract surgery decreases tissue damage and increases patient comfort without adverse side effects.

Early rehabilitation after small incision cataract surgery.

BACKGROUND: The use of smaller cataract incision is thought to induce less astigmatism, resulting in a more stable refraction and more stable wound. METHODS: We have analyzed the early astigmatic changes and rehabilitation in 20 eyes of 16 patients operated with advanced phacoemulsification techniques. The patients operated with small-incision surgery (incision 4.0 mm) were compared to those with large-incision surgery (incision 7.5 mm). Keratometric values and visual acuity data were evaluated up to 6 months postoperatively. RESULTS: Less initial induced astigmatism was demonstrated at day 7 postoperatively with a 4.0-millimeter incision (0.1 +/- 0.53 D) compared with a 7.5-millimeter incision (1.90 +/- 1.97). Similar but not statistically significant changes were seen at days 1 and 30 postoperatively. Visual rehabilitation was also faster in the small-incision group and 70% of the eyes gave uncorrected visual acuity of 20/40 or better in this group as early as the first postoperative day. Only 11% of the eyes showed that uncorrected visual acuity after large-incision surgery at first postoperative day. CONCLUSION: The low amount of induced cylinder, rapid stabilization of the wound, and faster visual rehabilitation confirms the advantage of small-incision cataract surgery to large-incision surgery.

Inhibitory effect of methysergide on calcitonin gene-related peptide-induced vasodilatation and ocular irritative changes in the rabbit.

1. Calcitonin gene-related peptide (CGRP) is involved in ocular neurogenic inflammation in the rabbit, causing vasodilatation in the anterior uvea, breakdown of the blood-aqueous barrier, increase in the intraocular pressure (IOP) and rise in the adenosine 3':5'-cyclic monophosphate (cyclic AMP) content in the aqueous humour. So far there is no means of preventing these CGRP-induced ocular effects. 2. In the present study, the effect of intravenous methysergide (1-10 mg kg-1, b.w.) on CGRP-induced changes in the IOP, blood-aqueous barrier and cyclic AMP content in the aqueous humour was studied in vivo. The effect of methysergide on CGRP-induced vasodilatation both in vivo and in vitro was also investigated. 3. Methysergide decreased intraocular pressure but had only a transient effect on blood pressure. Methysergide decreased the regional blood flow in ocular tissues by 53-65%, but did not have such a vasoconstrictor effect in most extra-ocular tissues studied. 4. Methysergide inhibited CGRP-induced vasodilatation, increase in the IOP, breakdown of the blood-aqueous barrier and increase in the cyclic AMP content in the aqueous humour in vivo. 5. In vitro, methysergide alone did not have effects on the vascular tone in isolated ophthalmic artery of rabbit. However, it potentiated noradrenaline (NA)-induced contraction. There were no differences in the IC50 values for CGRP on the NA-induced contraction in the presence and absence of methysergide, indicating that methysergide has no direct effect on the vasorelaxant effect of CGRP in vitro. 6. The present study demonstrates that in the rabbit eye methysergide inhibits CGRP-induced changes.One inhibitory mechanism of methysergide may be to enhance the effect of a vasoconstrictor (NA) to antagonize the vasodilator effect of CGRP. The present findings suggest that a methysergide-sensitive mechanism may be used to limit some pathophysiological conditions in the eye that involve neurogenic inflammation and the release of CGRP.

Ocular irritative response to YAG laser capsulotomy in rabbits: release of calcitonin gene-related peptide and effects of methysergide.

The Neodymium (Nd):YAG laser is commonly used in ophthalmology mainly for the posterior capsulotomy in patients with secondary cataract after extracapsular cataract extraction. A frequent side-effect following different kinds of YAG laser treatments is an acute increase in the intraocular pressure (IOP). The present study addresses the role of calcitonin gene-related peptide (CGRP) in the ocular irritative response following YAG laser anterior capsulotomy in rabbits. The YAG laser anterior capsulotomy caused an irritative response in the eye, which consisted of an increase in the IOP, miosis and breakdown of the blood-aqueous barrier. Following YAG laser capsulotomy, CGRP-immunoreactivity was found in the aqueous humour in different molecular weight forms as revealed by gel-permeation chromatography. One of the peaks coeluted with synthetic human CGRP. Methysergide attenuated the increase in the IOP and disruption of the blood-aqueous barrier, but not the miosis, following YAG laser anterior capsulotomy. The present study demonstrates the release of CGRP into the aqueous humour following YAG laser capsulotomy, and suggests that CGRP is partly causing the increase in IOP and disruption of the blood-aqueous barrier in this irritative response.

Mast cells in the anterior uvea of the rabbit. Intraocular effects of compound 48/80 in the rabbit.

In the present study, the presence and localization of mast cells and the intraocular effects of compound 48/80 have been studied in detail in the rabbit eye using histochemical and physiological methods. In histochemical studies mast cells were localized in the anterior uvea, especially in the ciliary and iridial processes. Intracamerally injected, compound 48/80 caused an increase in the intraocular pressure, disruption of the blood-aqueous barrier and an increase in the cAMP content in the aqueous humour. Miosis was observed only after higher doses of compound 48/80 (greater than 100 micrograms) and even then only one-half of the eyes responded. The intraocular effects, excluding miosis, of compound 48/80 resembled an on/off-type of response, where 20 micrograms caused only minor changes, if any, and 50 micrograms gave a maximal response. The ocular hypertensive reaction developed a tachyphylaxis so that the second and third consecutive dose of compound 48/80 (100 micrograms) produced no significant change in IOP. The results indicate that mast cells, which are present in the anterior uvea in an extent not known previously, might be involved in certain inflammatory reactions in the rabbit eye. The inconsistent and slight miosis after the intracameral application of compound 48/80 indicates that the mechanism is different from that caused by sensory nerve stimulation. The rapid development of tachyphylaxis after consecutive application of compound 48/80 suggests that mast cells are easily depleted which might be useful for further studies to evaluate the functional role of mast cells in different pathophysiological conditions in the rabbit eye.

Effect of topical and intracameral methysergide on calcitonin gene-related peptide-induced irritative changes in the rabbit eye.

Calcitonin gene-related peptide (CGRP) is a neuropeptide localized in the ocular sensory nerves. It is responsible for most of the irritative changes in the rabbit eye in neurogenic inflammation, namely vasodilation in the anterior uvea, breakdown of the blood-aqueous barrier and increase in the intraocular pressure. In the present study, intracameral methysergide inhibited the CGRP-induced irritative changes in the rabbit eye. Provided that sufficient concentration of methysergide could be reached in the anterior chamber after topical application, it might be possible to use locally administered methysergide to limit different pathophysiological conditions in the eye in which CGRP is involved.

Intraocular and cardiovascular effects of calcitonin gene-related peptide (CGRP)-I and -II in the rabbit.

Calcitonin gene-related peptide (CGRP) is a 37-amino acid neuropeptide localized in the eye in the sensory nerves. In this study, the physiological effects of the two naturally occurring forms of human CGRP, CGRP-I, and -II, which differ only in three amino acids, have been demonstrated in the rabbit eye and cardiovascular system. Intravenously administered CGRP-I caused a biphasic increase in the intraocular pressure (IOP), disruption of the blood-aqueous barrier, and increase in the cyclic adenosine 3',5'-monophosphate (cAMP) content in the aqueous humor. CGRP-II caused a monophasic increase in the IOP and disruption of the blood-aqueous barrier, but no increase in the cAMP content occurred. CGRP-I and -II decreased the blood pressure in a similar dose-dependent manner. The effects of intracamerally administered CGRP-I and -II were very similar in the eye. An increase in the IOP, breakdown of the blood-aqueous barrier, and an increase in the cAMP content in the aqueous humor occurred. The differences in the biological responses between CGRP-I and -II in the rabbit eye might be a result of the different affinities of the CGRP forms to a single receptor. Alternatively, different subtypes of receptors for CGRP-I and -II may exist in the rabbit.

Calcitonin gene-related peptide (CGRP) immunoreactive sensory nerves in the human and guinea pig uvea and cornea.

The presence of calcitonin gene-related peptide (CGRP) immunoreactive nerves in the uvea and cornea of human and guinea pig eyes was evaluated using immunohistochemical techniques. CGRP immunoreactivity was found in thin, varicose nerve fibers in both species. Most of the fibres were localized in the ciliary body, and were mainly associated with blood vessels. In the human ciliary body, a moderate number of CGRP immunoreactive nerves were also seen in the ciliary muscle. In the iris and cornea, CGRP immunoreactive fibres were relatively uncommon. In the iris, they were mostly found associated with blood vessels, while in the cornea they were seen sub-epithelially or as free nerve endings in the epithelium. In the trigeminal ganglion, small sized ganglion cells displayed CGRP immunoreactivity. About 40% of all ganglion cells were immunoreactive nerves in the guinea pig, while sympathetic denervation did not change the staining pattern of CGRP immunoreactivity. The present findings, together with previous physiological data, suggest that CGRP might play a role in the regulation of the blood flow, aqueous humour dynamics, and neurogenic inflammation, not only in experimental animals but also in man.

Platelets and polymorphonuclear leukocytes in experimental ocular inflammation in the rabbit eye.

Accumulation of 111indium-oxine (111In)-labelled platelets and the kinetics of 111In-labelled polymorphonuclear leukocytes (PMNLs) were studied in the anterior eye during neurogenic inflammation (induced by topical neutral formaldehyde) or after paracentesis in the rabbit, after formaldehyde irritation, 40 times more platelets were found in the aqueous humor 60 min later than in the control eyes and 400 times more after paracentesis. Platelets were found to be increased in the ciliary body, but not in the iris or choroid. Under light microscopy, some of the blood vessels in the ciliary processes were occluded and filled with red blood cells and platelets. The amount of PMNLs increased in the aqueous humor 15-20 h following formaldehyde irritation. After paracentesis, increased amounts of PMNLs were found in the iris and ciliary body 3-6 h later, while in the aqueous humor PMNLs were observed already 2 h. In the present study, increased amounts of 111In-labelled platelets and PMNLs were demonstrated in the anterior eye during experimental ocular inflammation. This method provides a useful tool for evaluating the accumulation of cells or the cell kinetics in ocular tissues during experimental inflammation.

CGRP in relation to neurogenic inflammation and cAMP in the rabbit eye.

The effects of topical application of neutral formaldehyde (1%) and intracameral administration of calcitonin gene-related peptide (CGRP, 0.5- or 2.0 micrograms) on the intraocular pressure (IOP), blood-aqueous barrier, pupil size, blood pressure and cyclic AMP (cAMP) content in the aqueous humour of a rabbit were studied. Topical chemical irritation with 1% formaldehyde caused a typical irritative response in the eye with a rise in the IOP, breakdown of the blood-aqueous barrier and miosis. The cAMP content in the aqueous humour was also increased (88.5 +/- 35.0 pmol ml-1, P less than 0.05) when compared with the control group (16.3 +/- 3.6 pmol ml-1). Intracameral administration of CGRP caused a rise in the IOP, breakdown of the blood-aqueous barrier and also systemic hypotension. Miosis was not observed after intracameral CGRP but an increase in the cAMP content in the aqueous humour was seen (130.5 +/- 30.3- and 158.7 +/- 48.1 pmol ml-1, both P less than 0.01, after 0.5 or 2.0 micrograms, respectively). The cAMP concentration in the aqueous humour after topical chemical irritation and intracameral CGRP correlated with the intensity of the breakdown of the blood-aqueous barrier. CGRP seems to cause most, but not all, of the ocular changes after sensory nerve stimulation elicited by topical neutral formaldehyde. Of these CGRP-induced changes, only the breakdown of the blood-aqueous barrier is related to an increase in the cAMP content in the aqueous humour. Contralateral responses after sensory nerve stimulation were similar to contralateral responses to intracameral CGRP.

Effect of neurogenic irritation and calcitonin gene-related peptide (CGRP) on ocular blood flow in the rabbit.

The effects of sensory nerve stimulation (topical neutral formaldehyde, 1%) and intracameral injection of calcitonin gene-related peptide (CGRP) on regional ocular blood flow, intraocular pressure (IOP), the blood-aqueous barrier, pupil size, and blood pressure were studied in the rabbit. Sensory nerve stimulation elicited a typical irritative response in the rabbit eye, with vasodilation in the ciliary body (from 128 +/- 31 to 363 +/- 105 mg/min, p less than 0.05) accompanied with a breakdown of the blood-aqueous barrier, rise in the IOP, and miosis. CGRP caused similar, but not identical, changes in the eye: vasodilation in the ciliary body (from 60 +/- 14 to 258 +/- 75 mg/min, p less than 0.05), breakdown of the blood-aqueous barrier and rise in the IOP, accompanied with systemic hypotension. Miosis was not observed after CGRP. In the present study, the vasodilatory action of CGRP on the rabbit eye has been shown. This makes our understanding of the mechanism of the ocular irritative response after sensory nerve stimulation more complete. Thus, CGRP through vasodilation disrupts the blood-aqueous barrier and raises the IOP. The more intense increase in the IOP after sensory nerve stimulation than after CGRP is probably caused by a CGRP-induced vasodilation and breakdown of the blood-aqueous barrier, enhanced by a miosis-induced pupillary block.

Effect of alpha-adrenergic and serotonergic blockers on the acute irritative response in the rabbit eye.

The effect of alpha-adrenergic and serotonergic (5-HT) blockers on the acute irritative response in the rabbit eye elicited by topical, neutral formaldehyde (1%), was studied. In the control animals, the peak rise in the intraocular pressure (delta IOP) after irritation was 29.5 +/- 5.7 mm Hg, and the perfusion pressure of the eye at 1 min after irritation was 50.1 +/- 2.8 mm Hg. The peak rise in the IOP was inhibited by phentolamine (alpha- and 5-HT-antagonist, delta IOP = 6.6 +/- 2.1 mm Hg, P less than 0.01), methysergide (5-HT-antagonist, delta IOP = 10.6 +/- 4.4 mm Hg, P less than 0.05), and prazosin (alpha 1-antagonist, delta IOP = 12.8 +/- 3.7 mm Hg, P less than 0.05). Perfusion pressures of the eyes were decreased after pretreatment with phentolamine or prazosin, and were 35.2 +/- 4.8 mm Hg (P less than 0.05) and 25.7 +/- 3.7 mm Hg (P less than 0.01), respectively. Perfusion pressure in the methysergide group remained unchanged (75.4 +/- 14.2 mm Hg). Yohimbine (alpha 2-antagonist) and ketanserin (5-HT2-antagonist) did not inhibit the IOP response. None of the antagonists could inhibit the miosis or disruption of the blood-aqueous barrier induced by topical neutral formaldehyde. In the contralateral eyes, the changes in the IOP, in the integrity of the blood-aqueous barrier, and also in the pupil size, were enhanced by ketanserin. The present study demonstrates the inhibitory actions of methysergide, phentolamine, and prazosin on the neurally mediated, acute irritative response in the rabbit eye. Methysergide seems to inhibit the response, probably acting via the 5-HT1-receptors. A part of the effect of phentolamine might be explained by an inhibitory action via 5-HT1-receptors. The effect of phentolamine and prazosin on the alpha 1-receptors seems to create an inhibitory action on the irritative response by lowering the perfusion pressure of the eye.

Effect of serotonin and its antagonist (ketanserin) on intraocular pressure in the rabbit.

The effects of topical and intracameral serotonin and topical, intracameral and intravenous selective (5-HT2) serotonin antagonist, ketanserin, on the intraocular pressure (IOP) were studied in the rabbit. The IOP was measured using a pneumotonometer or electromanometrically using intracameral needles. Topical 2% serotonin decreased the IOP by 4.0 +/- 0.9 mmHg (delta IOP, p less than 0.01) in normal eyes. This hypotensive effect was reduced after sympathetic denervation. Intracameral serotonin (4.0 micrograms), on the other hand, caused a rise in the IOP, and a breakdown of the blood-aqueous barrier, which were not inhibited by sympathectomy. Topical 2% ketanserin lowered the IOP in the ipsilateral eye by 4.1 +/- 0.4 mmHg (p less than 0.001). A decrease in the IOP of the contralateral eye was observed as well. After sympathectomy the hypotensive action of topical ketanserin on the IOP was inhibited. Intravenous ketanserin (0.5 mg/kg b.w.) lowered the IOP significantly and in the sympathectomized eyes a small decrease occurred, as well. In anesthetized animals topical, intravenous or intracameral ketanserin didn't cause a decrease in the IOP. The present study indicates the controlling effect of serotonin and ketanserin on the IOP. The hypotensive actions of topical serotonin and ketanserin on the IOP are at least partly dependent on the intact sympathetic innervation of the eye. However, the action of ketanserin seems to mediate also through central pathways.