Measuring sexual harassment: development and validation of the Sexual Harassment Inventory

Recent studies have suggested that intravenous infusion of fenoldopam, a selective dopamine-1 receptor agonist, elevates intraocular pressure (IOP) in man. This study evaluated the effect of intravenous fenoldopam on IOP, aqueous humor outflow facility and gonioscopy in 12 healthy human subjects. Three doses (0.2, 0.5 and 1.0 microg/kg/min) were infused for 120 minutes in a double masked, placebo controlled, four-way crossover design. IOP was measured every 20 minutes in the supine position and every 40 minutes while sitting during the drug and placebo infusions. Tonography and gonioscopy were performed at baseline and after 120 minutes of infusion. Compared to placebo, IOP increased by 3.5 mm Hg (32%) for the lowest dose, 5.8 mm Hg (46%) for the intermediate dose, and 6.9 mm Hg (55%) for the highest dose (p<0.05 for all three doses). IOP returned to baseline within 30 minutes of stopping the infusion. The outflow facility decreased from baseline by 26% after 120 minutes of infusion for all drug doses. In contrast, outflow facility increased from baseline by 11% during placebo infusion. Compared to placebo, the fenoldopam induced changes in outflow were statistically significant (p<0.05). There was no change in the gonioscopic appearance of the anterior chamber angle during the infusion. This study shows that systemic administration of a selective dopamine-1 receptor agonist causes a significant dose-dependent increase in IOP that can be explained in part by diminished outflow facility. These results support a role for the dopamine-1 receptor in the modulation of IOP in general and suggest modulation of aqueous humor outflow by dopaminergic receptors.     

Effects of adenosine agonists on intraocular pressure and aqueous humor dynamics in cynomolgus monkeys

The effects of single or multiple topical doses of the relatively selective A1 adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N6-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20-250 micrograms) or CHA (20-500 micrograms) produced ocular hypertension (maximum rise = 4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall = 2.1 or 3.6 mmHg) from 2-6 hr. The relatively selective adenosine A2 antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 micrograms) inhibited the early hypertension, without influencing the hypotension. Neither 100 micrograms R-PIA nor 500 micrograms CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 micrograms R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A2 receptors, while the subsequent hypotension appears to be mediated by adenosine A1 receptors and results primarily from increased outflow facility.     

Aqueous humor dynamics in beagle dogs with caffeine-induced ocular hypertension

In order to investigate the possible mechanisms for caffeine-induced ocular hypertension, the intraocular pressure (IOP) and the outflow through the trabecular meshwork were measured in beagle dog eyes after dosing with intravenous caffeine (30 mg/kg) alone or in combination with the topical beta-blocker befunolol [applied as 100 microliters of a 1% (w/v) solution] which inhibits aqueous humor formation in the ciliary body. Intravenous injections of caffeine significantly increased the IOP at 0.25 and 1 hr after a single dose. The ocular hypertension recovered within 2 hr following dosing. Over time, there were no differences in the outflow between the caffeine and control groups. The instillation of befunolol lowered outflow and produced ocular hypotension. The levels of the IOP and outflow in dogs treated with caffeine and befunolol in combination were almost the same as those in dogs treated with befunolol alone. Single-dose and combination-dose studies demonstrate that intravenous caffeine increases the IOP in normal beagle dogs possibly by increasing aqueous humor formation and not by the inhibition of aqueous humor drainage through the trabecular meshwork.     

NaCl-preferring NZB/B1NJ mice and NaCl-avoiding CBA/J mice have similar amiloride inhibition of chorda tympani responses to NaCl

After intracameral injection calcitonin gene-related peptide has been demonstrated to break the blood aqueous barrier and increase intraocular pressure in rabbits. However in cats, calcitonin gene-related peptide decreases intraocular pressure by increasing the outflow facility of aqueous humor. In the present study, the effect of intracameral injection of calcitonin gene-related peptide on the outflow facility in rabbits has been investigated and the intraocular pressure and outflow facility were measured following intravitreal administration of calcitonin gene-related peptide. The results demonstrate that in spite of the apparent pseudofacility component caused by a breakdown of the blood aqueous barrier also the true trabecular outflow is probably increased in the rabbit eye after intracameral injection of calcitonin gene-related peptide. The intravitreal administration of calcitonin gene-related peptide leaves the blood aqueous barrier intact and causes an increase in the outflow facility of aqueous humor with a concomitant long-lasting decrease in intraocular pressure.     

Increase in aqueous humor production following D1 receptors activation by means of ibopamine

BACKGROUND: Topically administered 2% ibopamine (a dopaminergic agonist) induces a transitory ocular hypertension in 92% of patients with primary open-angle glaucoma and in 52% of patients with normal tension glaucoma. In normal eyes, ibopamine has no effect on IOP. PURPOSE: The aim of the present study was to verify, by means of fluorophotometric techniques, which hydrodynamic changes could be induced in normal and glaucomatous eyes, stimulating the D1 receptor with 2% ibopamine administered topically. In addiction, we wanted to evaluate if ibopamine could modify IOP before and after an experimentally induced outflow system impairment in rabbits. METHODS: In study 1 we performed a measurement of aqueous humor flow in 6 healthy volunteers and in 6 glaucomatous patients, before and after 2% ibopamine administration. In study 2 the alteration of outflow pathways was induced by means of Laminaria Digitata in 10 rabbits. RESULTS: After 2% ibopamine administration we found a significant increase in aqueous humor production, both in glaucomatous (P = 0.035) and normal eyes (P = 0.004). In rabbits, we found no significant change in IOP at basal conditions. After experimentally induced outflow system impairment by laminaria, we observed a marked increase in IOP (+ 13.5 mmHg SD 7.2; P < = 0.001) following ibopamine administration. CONCLUSIONS: These experimental data have a diagnostic value in glaucoma, since they show how an intraocular hypertensive response due to ibopamine in normotensive eyes is a sign of initial outflow impairment. Moreover, the possibility to increase the aqueous humor production sets new trends in the treatment of post surgical ocular hypotony.     

Effect of mitomycin C on aqueous humor flow, flare and intraocular pressure in eyes with glaucoma 2 years after trabeculectomy

BACKGROUND: The purpose of this study was to determine the intraocular pressure (IOP), aqueous humor flow, flare and ocular side effects in eyes with a history of hypotony after trabeculectomy with adjunctive mitomycin C (MMC). METHODS: Thirty-six eyes with primary or secondary open-angle glaucoma and IOP < or = 8 mmHg during the postoperative period were studied 745 +/- 315 days after surgery. MMC (0.2 or 0.5 mg/ml) was applied to the episclera with a cellular sponge. Flare was studied with the Kowa Laser Flare Meter 500. Aqueous humor flow was measured in the afternoon (Fluorotron Master II). IOP, visual fields and best corrected visual acuity were also examined. Twenty-two contralateral eyes without surgical intervention served as controls. RESULTS: The mean age of patients was 44.5 +/- 16.8 years. The mean IOP was significantly lower in the MMC group than in the control group: 9.6 +/- 6.4 mmHg vs 18.0 +/- 13.6 mmHg at 2 years (P < 0.001). Aqueous flow was significantly lower in subjects treated with MMC than in controls (P < 0.001). The flare values were significantly higher in the MMC-treated group, with a mean of 12.0 +/- 7.7 photon counts/ms, than in the control group, mean 7.9 +/- 4.6 photon counts/ms (P < 0.019). CONCLUSION: Our data suggest that MMC is a useful ocular hypotensive agent which seems to participate in a change in aqueous humor dynamics when applied topically as an aqueous solution.     

The effect of topically administered carbonic anhydrase inhibitors on aqueous humor dynamics in rabbits

Repeated topical administration of 2.5% trifluormethazolamide, a halogenated derivative of methazolamide, resulted in a unilateral decrease in intraocular pressure in rabbits. Mean (+/- S.E.M.) baseline intraocular pressure (19.8 +/- 2.1 mm Hg) was significantly (P less than .05) decreased 30 minutes (16.1 +/- 2.2 mm Hg) and 60 minutes (15.8 +/- 2.7 mm Hg) after drug administration. Trifluormethazolamide did not alter outflow facility. Aqueous humor flow calculated from the tonographic data was reduced 44% and flow measured by fluorophotometry was reduced 29%. Topical delivery of trifluormethazolamide decreased the level of carbon dioxide in the aqueous humor in the treated eye in a manner similar to that observed after systemic administration of carbonic anhydrase inhibitors. Topical administration of 10% acetazolamide did not decrease intraocular pressure. However, topical administration of either trifluormethazolamide or acetazolamide before oral administration of water resulted in a blunting of the water-induced ocular hypertensive response.     

Functional morphology of the trabecular meshwork in primate eyes

The trabecular meshwork forms most of the resistance to aqueous humor outflow needed for maintenance of a pressure gradient between intraocular pressure of approximately 17 mmHg and venous pressure of approximately 10 mmHg. The composition of the extracellular material in the subendothelial or cribriform layer seems to be mainly responsible for outflow resistance. The aqueous humor pathways through the subendothelial layer can be influenced by ciliary muscle contraction and presumably also by contractile elements recently found both in trabecular meshwork and scleral spur. Pharmacologically induced disconnection of inner wall and cribriform cells leads to wash out of extracellular material through breaks of the endothelial lining of Schlemm's canal and to increase of outflow facility. In glaucomatous eyes the resistance to aqueous humor outflow is increased due to an increase in different forms of extracellular material deposited within the cribriform layer. The amount of this newly developed extracellular material is correlated with loss of axons in the optic nerve, indicating that a common factor is responsible for both changes. To investigate the effect of various factors on the biology of trabecular cells monolayer cultures derived from cribriform and corneoscleral trabecular meshwork have been established. The two cell lines can be differentiated because cribriform cells in vivo as in vitro stain for alphabeta-crystallin whereas the corneoscleral cells remain unstained. The effect of TGFbeta, a growth factor increased in aqueous humor of glaucomatous eyes and glycocorticoids on trabecular meshwork cells show typical changes in formation of extracellular matrix components and of stress proteins. Dexamethasone and oxidative damage also lead to increase of trabecular meshwork inducible glucocorticoid response (TIGR) protein. A mutation of the TIGR-gene family has recently been found in families with juvenile and chronic simple glaucoma. Future research has to clarify the significance of these genetic factors for the pathophysiology of glaucoma and the role of trabecular cell activity in this respect.     

Effect of 8-iso prostaglandin E2 on aqueous humor dynamics in monkeys

OBJECTIVE: To evaluate the effects of 8-iso prostaglandin E2 (8-iso PGE2; prosta-5,13-dien-1-oic acid,11,15-dihydroxy-9-oxo-,[5Z,8beta-11X,13E,15 S]-) on the intraocular pressure (IOP), outflow facility, and aqueous humor flow rates in normal monkeys and monkeys with glaucoma. METHODS: The IOP was measured before and as long as 6 hours after the topical application of 8-iso PGE2 to 1 eye of 6 normal monkeys and to the glaucomatous eye of 8 monkeys with unilateral laser-induced glaucoma. The pupil diameter was measured at the same times as the IOP measurements in the normal monkeys. Tonographic outflow facility and fluorophotometric flow rates of aqueous humor were measured in 6 normal monkeys before and after drug treatment. RESULTS: In normal monkeys, a single dose of 0.1% 8-iso PGE2 reduced (P<.01) the IOP for 4 hours in the treated eyes with a maximum (mean +/- SEM) reduction of 3.2 +/- 0.2 mm Hg, compared with the contralateral control eyes. The pupil size was smaller (P<.01) in the treated eyes by as much as 1.0 +/- 0.2 mm for 4 hours. In 8 glaucomatous monkey eyes, the application of 0.05% and 0.1% 8-iso PGE2 reduced the IOP (P<.01) for as long as 2 and 5 hours, respectively. The maximum reduction in the IOP was 4.6 +/- 0.8 mm Hg (0.05%) and 6.0 +/- 0.8 mm Hg (0.1%) compared with baseline measurements. The magnitude and duration of the ocular hypotensive effect were enhanced with twice-a-day administration for 5 consecutive days. Outflow facility in normal monkey eyes was increased (P<.05) by 48% in the treated eyes, and aqueous humor flow was unchanged (P>.10), compared with vehicle-treated contralateral control eyes. Mild eyelid edema, conjunctival edema, hyperemia, and discharge appeared in some eyes treated with the 0.1% drug concentration. CONCLUSIONS: The use of 8-iso PGE2 reduces the IOP in both normal and glaucomatous monkey eyes. An increase in outflow facility appears to account for most of the IOP reduction in normal monkeys. Clinical Relevance: The application of 8-iso PGE2 may have potential for the treatment of glaucoma as an outflow facility-increasing drug.     

Acidosis, alkalosis, and aqueous humor dynamics in rabbits

Systemic acidosis induced by intravenous administration of hydrochloric acid lowered intraocular pressure in unanesthetized rabbits. Aqueous humor flow was reduced by approximately 50%, as measured by the iodide method and as calculated from tonographic data. Outflow facility, episcleral venous pressure, plasma osmolality, blood pressure, pulse, and body temperature were not altered by systemic acidosis. Systemic alkalosis induced by intravenously administered sodium bicarbonate was associated with an increased intraocular pressure. Aqueous humor flow following systemic alkalosis was increased by approximately 100%, as measured by the iodide method and as calculated from tonographic data. Alkalosis was not associated with alterations in outflow facility, episcleral venous pressure, plasma osmality, blood pressure, pulse, or rectal temperature.     

Intraocular pressure in rabbits by telemetry II: effects of animal handling and drugs

PURPOSE: To measure under carefully controlled conditions the effects in the rabbit eye of commonly used therapeutic agents for glaucoma. METHODS: Rabbits were outfitted in one eye with an implantable telemetric pressure transducer and monitored for several months under controlled conditions of light/ dark and handling. Effects of tonometry, handling, water drinking, and instillation of topical ophthalmic medications on intraocular pressure were recorded during each 24-hour day/night cycle. RESULTS: Pneumatonometry, animal handling, and water drinking all had an effect on intraocular pressure that in many instances was of the same magnitude as the effects of pharmacologic agents. Dorzolamide and timolol caused a sustained reduction of intraocular pressure during the nocturnal period. Epinephrine had a biphasic effect, causing an immediate pressure elevation followed by a prolonged depression. Apraclonidine, latanoprost, and pilocarpine had no measurable effect. CONCLUSIONS: Continuous telemetric measurement of intraocular pressure in rabbits permits the measurement of uncontrollable artifacts that occur with tonometric measurements and animal handling. If environmental conditions are rigidly controlled, this method is very sensitive for detecting therapeutic effects of candidates for ocular hypotensive drugs. When healthy animals are used, the method appears to be more sensitive for drugs that affect aqueous humor formation than for drugs that affect aqueous humor outflow resistance.     

Glaucoma after macular hole surgery

OBJECTIVE: The study aimed to report incidence and to assess risk factors of postoperative glaucoma in patients with stage 3 idiopathic macular hole treated with pars plana vitrectomy, removal of posterior hyaloid membrane, and perfluoropropane gas tamponade. DESIGN: The author performed a retrospective chart review and statistical analysis of risk factors of postoperative glaucoma by using chi-square statistics, Fisher's exact test, and logistic regression. PARTICIPANTS: Forty consecutive patients with stage 3 idiopathic macular hole who were operated on between January 1994 and December 1995 were studied. INTERVENTION: A pars plana vitrectomy, removal of posterior hyaloid membrane, and 14% perfluoropropane gas tamponade were done to all patients. MAIN OUTCOME MEASURES: Preoperative and postoperative intraocular pressure measurements were performed. RESULTS: Twenty-one (52%) of 40 patients experienced transient intraocular pressure elevation to more than 30 mmHg. Nine (22%) had pressure elevation within 2 to 4 hours, 6 (15%) in 24 hours, and 6 (15%) in 1 week after surgery. Three patients, including one with a history of preoperative ocular hypertension, required extended topical antiglaucoma medication. Factors of age, race, gender, lens status, preoperative intraocular pressure (all preoperative intraocular pressure were 25 mmHg or less), and success in closure of macular hole were not to any statistically significant degree associated with postoperative pressure elevation. CONCLUSION: Glaucoma is a significant complication after stage 3 macular hole surgery even without adjunctive therapy. Usually happening within the first postoperative week, elevation of intraocular pressure in most cases is transient and can be controlled by medication. However, extended medication might become necessary in some cases.     

Determination of the facility of aqueous humor outflow in the dog, comparing in vivo and in vitro tonographic and constant pressure perfusion techniques

The gross facility of aqueous humor outflow (C) was estimated in the normal in vivo and in vitro dog eye, using tonography and constant pressure perfusion. Tonographic C value for 36 normal eyes, with the dog anesthetized with ketamine hydrochloride and acetylpromazine maleate, was 0.21 (+/- 0.14, SD); the mean tonographic value in 35 eyes with the patient anesthetized with sodium pentobarbital was 0.15 (+/- 0.09). Constant pressure perfusion of the in vivo normal dog eyes at 20 mm of Hg intraocular pressure yielded a mean C value of 0.13 (+/- 0.07) and at 30 mm of Hg 0.18 (+/- 0.13). As intraocular pressure increased from 10 to 50 mm of Hg, the rate of outflow, as determined by constant pressure perfusion, increased. The C values from in vitro constant pressure perfusion were greater than those in the in vivo eyes and deceased in most eyes as intraocular pressure was increased as compared with the in vivo preparation.     

Effects of Al3+ and Be2+ ions combined with NaF on ciliary process adenylyl cyclase activity and aqueous humor dynamics in the rabbit eye

PURPOSE: The activity of Al3+, Ga3+, and Be2+ ions in the presence of NaF to directly activate G-proteins was investigated by their potentiative effect on forskolin (FSK)-activated adenylyl cyclase in rabbit ciliary process membranes and their effects on aqueous humor dynamics in vivo. METHODS: Adenylyl cyclase (AC) was determined by radiometric conversion of ATP to cAMP by the particulate fraction of rabbit ciliary processes. Intravitreal injections of sterile solutions of analytical grade salts were made into the center of the vitreous in a volume of 20 microliters. Intraocular pressure, aqueous humor flow, and uveoscleral outflow measurements were made by pneumatonometry, fluorophotometry, and fluorescein-dextran method, respectively. Outflow facility was determined by tonography in the intact eyes and by two-level constant pressure perfusion in cannulated eyes. RESULTS: Both Al3+ (EC50, 40 mumol/l) and Be2+ (EC50, 11 mumol/l) in the presence of 0.5-2 mM NaF activated the stimulatory G-protein Gs. Ga3+ was ineffective and did not antagonize the activation by Al3+. Intravitreal injections of Al3+ (1 mumol/eye) or Be2+ (0.5 or 1 mumol/eye) had no significant intraocular pressure (IOP) effect, nor did 1.5 or 3 mumol/eye of NaF, but when either cation was injected together with NaF, IOP decreased by up to 40% for up to 140 hr. At the time of maximum IOP effect (72 hr) aqueous humor flow determined by fluorophotometry was decreased in BeCl2+ NaF-treated eyes by 40% relative to BeCl2-treated eyes; however, tonographic facility of outflow was unaffected. Uveoscleral flow was also decreased by 38% in BeCl2+ NaF treated eyes. CONCLUSIONS: These findings support the hypothesis that Gs activation of ciliary process adenylyl cyclase decreases aqueous humor formation rate in rabbit eyes, and that activation of G-proteins mediates contraction of ciliary muscles causing a decrease of aqueous humor outflow via the uveoscleral route. The results suggest that G-proteins putatively involved in trabecular facility changes are less sensitive to activation by BeF3- than are other parameters of aqueous humor dynamics.     

Effects of topical nipradilol, a beta-blocking agent with alpha-blocking and nitroglycerin-like activities, on aqueous humor dynamics and fundus circulation

PURPOSE: To study the effects of nipradilol, a nonselective beta-blocker with alpha 1-blocking activity and nitroglycerin-like activity, on aqueous humor dynamics and optic nerve head (ONH) circulation in albino rabbits. METHODS: Experiments were carried out during the dark phase, in conscious rabbits conditioned to a schedule of alternating 12-hour periods of light and dark. The blood-aqueous barrier permeability and the aqueous flow rate were determined fluorophotometrically. The effect on outflow to general blood circulation and uveoscleral outflow were determined by using the fluorophotometric Diamox technique, and the effect on the uveoscleral outflow was further assessed by using the anterior chamber perfusion method. The ONH circulation was estimated by using the laser speckle method. RESULTS: Unilateral topical administration of 0.25% nipradilol solution lowered intraocular pressure (IOP) with relatively weak contralateral effects in a dose-dependent manner with a maximum reduction of 6 mm Hg and an effect duration of 6 hours. Twice-daily instillation for 14 days showed no attenuation of the effects. Single instillation of 0.25% nipradilol showed no significant effect on blood-aqueous barrier permeability and decreased aqueous flow rate in the treated eye (17%; P < 0.01) and in the contralateral eye (9%, P < 0.05). Nipradilol produced no significant effect on outflow facility to general blood circulation, whereas it substantially increased uveoscleral outflow. Twice-daily 0.25% nipradilol instillation increased ONH tissue blood velocity by 13% (P < 0.01), which was probably attributable to locally penetrating drug. CONCLUSIONS: Because of its ability to lower IOP and to increase uveoscleral outflow and optic nerve head circulation in rabbits, further studies are warranted to determine whether nipradilol has potential as an antiglaucoma agent in humans.     

Acute renal failure complicating nonfulminant hepatitis A

PURPOSE: To compare the orbital blood flow velocities of patients with long-standing ocular hypertension and patients with primary open-angle glaucoma. METHODS: Twenty patients with ocular hypertension were recruited from our clinic and underwent color Doppler imaging evaluation of their retrobulbar vessels. The blood flow velocities and resistance index of their central retinal artery, temporal short posterior ciliary artery, and ophthalmic artery were compared with those of 20 glaucoma patients individually matched for age and level of the highest untreated intraocular pressure ever recorded. RESULTS: Glaucoma patients had significantly lower peak systolic velocity and end-diastolic velocity than did patients with ocular hypertension in their central retinal artery (p < 0.001). No significant difference between the groups was observed in the other vessels studied. CONCLUSIONS: Glaucoma patients had lower blood flow velocity in the central retinal artery compared with that of ocular hypertension patients of similar age and level of untreated intraocular pressure. This might be important in the development of glaucomatous damage in those patients.     

Comparison of the efficacy of apraclonidine and brimonidine as aqueous suppressants in humans

OBJECTIVE: To measure and compare the effect of apraclonidine hydrochloride and brimonidine tartrate on the rate of aqueous humor flow in human subjects. SUBJECTS AND METHODS: Forty normal human subjects were given apraclonidine or brimonidine by topical instillation. Aqueous humor flow was measured by the rate of disappearance of topically applied fluorescein. Intraocular pressure was measured by applanation tonometry. RESULTS: Apraclonidine suppressed aqueous humor flow between 39% and 44% and lowered intraocular pressure between 20% and 23%. Brimonidine suppressed aqueous humor flow between 44% and 48% and lowered intraocular pressure between 19% and 22%. CONCLUSION: No statistically significant differences were found between the effects of the 2 drugs on aqueous humor dynamics in normal subjects.     

Perfusion of the juxtapapillary retina and optic nerve head in acute ocular hypertension

Chronically elevated intraocular pressure (IOP) is often associated with glaucomatous optic nerve atrophy. Impaired blood flow may play a role in the pathogenesis of this disease. We present data concerning juxtapapillary retinal and optic nerve-head blood flow during acute increases in IOP. With the combination of a laser Doppler flowmeter and a scanning-laser system (Scanning Laser Doppler Flowmeter, SLDF; Heidelberg Engineering) the perfusion of the retina and the optic nerve head was quantified and visualized. Juxtapapillary retinal and optic nerve-head blood flow was measured simultaneously by SLDF during variations in IOP induced by a suction cup in nine healthy volunteers. The ocular pressure was increased for 2 min to IOP +15 mmHg, then to IOP +30 mmHg, and finally, to IOP +45 mmHg. Ocular perfusion pressure (PP) was calculated as the mean arterial blood pressure minus the IOP. The declines in juxtapapillary retinal flow as expressed in present per 10-mmHg IOP elevation ranged from 3.6% to 14.1% (median 7.4%). Over all measurements we found a significant linear relationship between juxtapapillary retinal blood flow and PP (r = 0.55, P < 0.0001). The observed decrease in optic nerve-head blood flow with increasing IOP was significantly greater as compared with the retinal blood flow decrease (8.4%/10 mmHg versus 7.4%/10 mmHg, P < 0.05). SLDF enables the quantification and visualization of perfused capillaries of the retina and the optic nerve head in high resolution. Acute elevations of IOP led to a decreases in juxtapapillary retinal and optic nerve-head blood flow of 7.4% and 8.4%/ 10-mmHg IOP increase, respectively.     

Effects of changes in intraocular pressure on human ocular haemodynamics

PURPOSE: Myogenic autoregulation is the ability of a vascular bed to maintain blood flow despite changes in perfusion pressure. Ocular perfusion pressure is defined as the difference between ocular arterial pressure and ocular venous pressure, the latter dependent on intraocular pressure (IOP). The aim of the present study was to investigate the effect of moderate increases in IOP on ocular haemodynamics. METHODS: Changes in IOP (+ 10 mmHg, +20 mmHg) were induced by a suction cup in 10 healthy subjects. Ocular fundus pulsations in the macula and the optic disc were measured by laser interferometry; blood flow velocities in the central retinal artery (CRA) and in the ophthalmic artery (OA) were measured by Doppler sonography. RESULTS: Changes in IOP caused a significant reduction in fundus pulsations, which was more pronounced in the macula (at +10 mmHg: -9 +/- 2%, p < 0.01; at +20 mmHg: -19 +/- 3%, p < 0.001) than in the optic disc (at +10 mmHg: -5 +/- 2% (ns); at +20 mmHg: -9 +/- 3%, p < 0.01). Mean flow velocity in the CRA was reduced by -5 +/- 3% at +10 mmHg (ns) and by -14 +/- 5% at +20 mmHg (p < 0.005), resistive index was increased by +4 +/- 1% at +10 mmHg (p < 0.05) and by +6 +/- 2% at +20 mmHg (p < 0.01). In contrast, a rise in IOP did not affect blood flow parameters in the OA. CONCLUSIONS: Our results from fundus pulsation measurements indicate that choroidal blood flow decreases when IOP is increased. The Doppler sonographic findings in the CRA indicate reduced blood flow velocity in this artery during raised IOP.     

Impact of antibiotic resistance on chemotherapy for pneumococcal infections

PURPOSE: To detect the mechanism of intraocular pressure elevation during hemodialysis. METHODS: We measured intraocular pressure, as well as serum osmolality and plasma CO2 pressure, every 30 min during hemodialysis, in 5 eyes with severely compromised aqueous outflow facility (Group A) from 4 renal failure patients. The same measurements were repeated on the same eyes using intravenous hyperosmotic Glyceol to prevent a rapid change in serum osmolality. We also measured the same parameters on 8 eyes with normal aqueous outflow facility (Group B) from 5 patients. The mean +/- SE of percent changes in each parameter was used for the statistical analysis. RESULTS: In Group A, the mean percent change of intraocular pressure increased significantly after 90 min, with the exception of the change at 180 min. The mean percent change of serum osmolality decreased significantly after starting dialysis. A negative correlation in the mean percent change of intraocular pressure with serum osmolality was detected (r = -0.759, r < 0.0001). The administration of intravenous hyperosmotic agent prevented significant changes in not only serum osmolality but also intraocular pressure. In Group B, the mean percent change in intraocular pressure showed no significant difference at any time, although the change in serum osmolality decreased significantly. CONCLUSION: A remarkable rise in intraocular pressure occurs during hemodialysis in eyes with an impaired aqueous outflow, when serum osmolality decreases rapidly.