Clinical & Experimental OphthalmologyVolume 40, Issue 3 p. 323-325 Ultrasound biomicroscopy of congenital iris flocculi Saman Kiumehr MD, Saman Kiumehr MD Einhorn Clinical Research Center, New York Eye and, Ear InfirmarySearch for more papers by this authorKenneth S Schor MD, Kenneth S Schor MD Einhorn Clinical Research Center, New York Eye and, Ear InfirmarySearch for more papers by this authorCarlos Gustavo V De Moraes MD, Carlos Gustavo V De Moraes MD Einhorn Clinical Research Center, New York Eye and, Ear Infirmary Department of Ophthalmology, New York University Medical Center, New YorkSearch for more papers by this authorJeffrey M Liebmann MD, Jeffrey M Liebmann MD Einhorn Clinical Research Center, New York Eye and, Ear Infirmary Department of Ophthalmology, New York University Medical Center, New YorkSearch for more papers by this authorRobert Ritch MD, Robert Ritch MD Einhorn Clinical Research Center, New York Eye and, Ear Infirmary Department of Ophthalmology, New York Medical College, Valhalla, New York, USASearch for more papers by this author Saman Kiumehr MD, Saman Kiumehr MD Einhorn Clinical Research Center, New York Eye and, Ear InfirmarySearch for more papers by this authorKenneth S Schor MD, Kenneth S Schor MD Einhorn Clinical Research Center, New York Eye and, Ear InfirmarySearch for more papers by this authorCarlos Gustavo V De Moraes MD, Carlos Gustavo V De Moraes MD Einhorn Clinical Research Center, New York Eye and, Ear Infirmary Department of Ophthalmology, New York University Medical Center, New YorkSearch for more papers by this authorJeffrey M Liebmann MD, Jeffrey M Liebmann MD Einhorn Clinical Research Center, New York Eye and, Ear Infirmary Department of Ophthalmology, New York University Medical Center, New YorkSearch for more papers by this authorRobert Ritch MD, Robert Ritch MD Einhorn Clinical Research Center, New York Eye and, Ear Infirmary Department of Ophthalmology, New York Medical College, Valhalla, New York, USASearch for more papers by this author First published: 17 May 2011 https://doi.org/10.1111/j.1442-9071.2011.02600.x Conflict/competing interest: None. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume40, Issue3April 2012Pages 323-325 RelatedInformation

PURPOSE:To assess the general morphology and position of the lamina cribrosa (LC) in healthy subjects using enhanced depth imaging-optical coherence tomography (EDI-OCT).METHODS:Serial horizontal and vertical B-scans of the optic nerve head (interval between images, approximately 30 μm) were prospectively obtained using EDI-OCT for both eyes of each healthy subject. After delineation of the anterior laminar surface, mean and maximum LC depths were measured in 11 equally spaced horizontal B-scans, and the depth of the anterior LC insertion was measured at 32 points along its circumference (reference plane, Bruch's membrane edges) for one randomly selected eye of each subject. Three-dimensional (3D) images of the anterior laminar surface and the peripapillary sclera were reconstructed from serial horizontal EDI-OCT B-scans to assess the 3D morphology of the anterior laminar surface.RESULTS:Among the 61 eyes (61 subjects) enrolled, 31 were excluded because of poor LC image quality, and 30 were included for analysis (mean age, 40 ± 18 [range, 21-78] years). Both mean and maximum LC depth profiles showed an elevation in the central area and a depression in the superior and inferior midperiphery of the LC. The anterior LC insertion was more posteriorly located in the superior and inferior than in the nasal and temporal regions. Three-dimensional LC images showed a bowtie-shaped horizontal central ridge of the LC.CONCLUSIONS:The LC has a central ridge ranging from the temporal to the nasal insertion areas and inserts more posteriorly in the superior and inferior than in the nasal and temporal regions. Further investigation is needed to elucidate the significance of these findings in the pathophysiology of glaucoma.

Objectives To assess focal lamina cribrosa (LC) defects in glaucoma using enhanced depth imaging optical coherence tomography and to investigate their spatial relationships with neuroretinal rim and visual field loss. Methods Serial horizontal and vertical enhanced depth imaging optical coherence tomographic images of the optic nerve head were obtained from healthy subjects and those with glaucoma. Focal LC defects defined as anterior laminar surface irregularity (diameter, >100 μm; depth, >30 μm) that violates the normal smooth curvilinear contour were investigated regarding their configurations and locations. Spatial consistency was evaluated among focal LC defects, neuroretinal rim thinning/notching, and visual field defects. Results Forty-six healthy subjects (92 eyes) and 31 subjects with glaucoma (45 eyes) were included. Ninety-eight focal LC defects representing various patterns and severity of laminar tissue loss were found in 34 eyes with glaucoma vs none in the healthy eyes. Seven of 11 eyes with glaucoma with no visible focal LC defect had a deeply excavated optic disc with poor LC visibility. Eleven focal LC defects presented clinically as an acquired pit of the optic nerve, and the others as neuroretinal rim thinning/notching. Focal LC defects preferably occurred in the inferior/inferotemporal far periphery of the LC including its insertion. Eyes with focal LC defects limited to the inferior half of the optic disc had greater sensitivity loss in the superior visual hemifield and vice versa. Conclusions Mechanisms of LC deformation in glaucoma include focal loss of laminar beams, which may cause an acquired pit of the optic nerve in extreme cases. Focal LC defects occur in tandem with neuroretinal rim and visual field loss.

Purpose: To evaluate the effects of memantine on improving visual function in patients with acute nonarteritic anterior ischemic optic neuropathy (NAION)Methods: This was a prospective, double masked, randomized, clinical trial. The study involved 47 subjects with unilateral NAION of less than 8 weeks duration. Eligible patients were randomly allocated to take either memantine tablets (5 mg daily during the first week and then 10 mg daily for the next two weeks, 25 subjects) or placebo tablets (22 subjects). Baseline visual acuity (VA) tests, pattern visual evoked potential (VEP) and automated perimetry (SITA-standard 24-2) were performed. VA tests were repeated 3 weeks, 3 months and 6 months after initial visit. VEP and automated perimetry were repeated 3 months after initial visit.Results: At baseline there was no significant difference between the two groups in terms of clinical and laboratory characteristics. After 3 weeks, 3 months and 6 months of treatment, best corrected visual acuity (BCVA) improved by -0.31 +/- 0.39, -0.49 +/- 0.47 and -0.53 +/- 0.48 logMAR in the memantine group respectively and -0.02 +/- 0.41, -0.09 +/- 0.60 and -0.05 +/- 0.67 logMAR in the placebo group respectively (P=0.024, P=0.025 and P=0.017). VEP results demonstrated a reduction of implicit time of -8.32 +/- 17.18 ms in the memantine group after 3 months, whereas in the placebo group it increased +5.7 +/- 21.60 ms (P=0.043). The change in VEP amplitude was not significantly different between the memantine and placebo groups (P=0.083). The effect of the memantine on mean deviation (MD) and pattern standard deviation (PSD) changes was not significantly different from that of the placebo (P=0.428 and 0.863 respectively).Conclusion: Treatment of patients who experience acute NAION with memantine may result in significant improvement in BCVA compared with no treatment. The VEP changes seen at 3 months may indicate improved transmission of impulses through the optic nerve.

Background: To evaluate and compare the effect of different doses of subconjunctival bevacizumab with betamethasone on the development of corneal major new vessels in a rat model of corneal chemical injury. Methods: The right eyes of 100 male Sprague-Dawley rats were randomly divided into 10 experimental groups (n = 10 per group). Chemical cauterization of the cornea was performed by using silver nitrate/potassium nitrate sticks. Immediately following corneal cauterization, the animals in groups 1–5 received subconjunctival injections of 0.02 ml of normal saline (control A), betamethasone LA (6 mg/ml) and different doses of bevacizumab (1, 5 and 25 mg/ml), respectively. In another experiment, the animals in groups 6–10 received subconjunctival injections of 0.02 ml of normal saline (control B), betamethasone LA (6 mg/ml) and different doses of bevacizumab (1, 5 and 25 mg/ml), respectively, 7 days following corneal cauterization. The numbers of major thick-walled vessels originating from the limbus reaching the corneal scar were counted 7 days after corneal cauterization in groups 1–5 and 14 days after corneal cauterization in groups 6–10. Results: The number of major vessels in groups 1–5 was 19.63 ± 3.77, 17.25 ± 5.33, 16.10 ± 5.02, 12.89 ± 2.70 and 12.36 ± 4.45 when assessed 7 days after corneal cauterization, respectively. Administration of betamethasone in group 2 had no significant effect on the corneal major vessel count compared to control A. The number of major vessels in groups 4 and 5 (bevacizumab 5 and 25 mg/ml) was significantly lower than that of group 1 (p < 0.01, Student’s t test). The number of vessels in groups 6–10 was 12.55 ± 5.64, 11.30 ± 9.33, 5.50 ± 6.34, 2.73 ± 4.73 and 2.67 ± 3.77 when assessed 14 days after corneal cauterization, respectively. Subconjunctival administration of betamethasone 7 days after corneal cauterization did not reduce the amount of corneal major vessels compared to control B. Administration of 0.02 ml of bevacizumab in doses of 1, 5 and 25 mg/ml 7 days after corneal cauterization significantly reduced the amount of major vessels compared to group 6 (p = 0.01, p < 0.01 and p < 0.01, respectively). There was no significant difference in percent area of corneal scar between different groups. Conclusion: Single subconjunctival injection of bevacizumab is efficacious in the prevention of formation as well as regression of major vessels compared to betamethasone in this rat model of corneal neovascularization. Even lower doses of bevacizumab might be efficacious.

Purpose: To investigate the effects of morphine administered after reperfusion in a rabbit model of ischemic retinopathy.Methods: The right eyes of 54 albino New Zealand rabbits were randomly allocated into nine treatment groups (n = 6 in each group). The eyes in saline-control group received 0.1 mL of phosphate-buffered saline solution intravitreally. In the ischemia-saline group, ischemia was induced by raising the intraocular pressure to 150 mmHg for 60 minutes. Then 0.1 mL of phosphate-buffered saline solution was administered intravitreally 5 minutes after reperfusion. The eyes in three ischemia-morphine groups (ischemia-morphine 0 hour, 1 hour, and 18 hours) received 0.1 mL of morphine (10 mu mol/L) intravitreally 5 minutes, 1 hour, or 18 hours after termination of 60 minutes of ischemia, respectively. The eyes in ischemia-naloxone-morphine group received 0.05 mL of naloxone (10 mu mol/L) intravitreally followed by injection of 0.05 mL morphine (10 mu mol/L) 5 minutes after termination of ischemia. Toxicity controls were performed with morphine (10 mu mol/L) and naloxone (10 mu mol/L) without ischemia. Histologic evaluation was performed for all groups on the seventh postoperative day.Results: Sixty minutes of ischemia led to severe cell loss in ganglion cell layer and thinning of the inner nuclear layer in ischemia-saline group compared with that of the saline-control group (P < 0.001). Thickness of the inner plexiform layer to the inner limiting membrane (a measure of inner retinal thickness) was significantly increased due to edema (P < 0.001). Administration of morphine 5 minutes after reperfusion significantly improved all of the above mentioned indices compared with ischemia-saline group (P < 0.001). Administration of morphine 1 hour after reperfusion had also a significant effect on the improvement of above mentioned indices compared with saline-control group (P < 0.05). However, the number of ganglion cells was significantly higher in ischemia-morphine 0 hour group compared with ischemia-morphine 1 hour group (P < 0.001). Morphine treatment 18 hours after reperfusion did not change the amount of injury. Administration of naloxone 5 minutes before morphine abolished most of the morphine protective effects.Conclusion: Intravitreal administration of morphine immediately after reperfusion maximally protects retina against ischemia-reperfusion injury. Pharmacologic evidence suggests that this protective phenomenon may be mediated in part by opioid receptors.

Results: The ultrasound AL measurements were taken in every case but measurement with the LI method was not possible in 4 eyes with asteroid hyalosis (17.3%). There was a high correlation between LI and ultrasound A-scan measurements in both asteroid hyalosis and noninvolved eyes (r 2 =0.97, P<0.001 and r 2 =0.95, P<0.001 respectively). There was no significant difference between AL taken by either method in asteroid hyalosis and noninvolved eyes. Conclusion: The failure rate of AL measurement using LI was relatively high in eyes with asteroid hyalosis. There was a high correlation between AL measured by ultrasound A-scan and LI method in both asteroid hyalosis and noninvolved eyes.

Purpose Testicular torsion/detorsion (T/D) RESULTS in enhanced formation of free radical species, which contribute to the pathophysiology of tissue damage. Numerous studies in recent years have shown protective effects of N-acetylcysteine (NAC) on cardiac and renal tissue damage following ischemia/reperfusion. We assessed the effectiveness of systemic administration of NAC – at therapeutic doses – in a rat model one-hour 720° testicular T/D. We chose the dose of NAC that reduced general ischemia/reperfusion syndrome in patients who had undergone abdominal aortic aneurysmectomy. Materials and Methods Sprague-Dawley rats were divided into 5 groups, 14 animals in each. Group 1 underwent sham operation as the control group. In group 2, rats underwent T/D and received vehicle injections. Animals in groups 3, 4 and 5 received intraperitoneal injections of 150 mg/kg NAC, 30 minutes before torsion, after torsion and after detorsion, respectively. Markers of oxidative stress as well as germ cell apoptosis indices were determined 4 and 24 hours after detorsion, respectively. Results Apoptosis indices were significantly higher in group 2 compared to control group. Four hours after detorsion, testicular level of lipid peroxidation was significantly increased and antioxidant enzymes activities were significantly decreased in group 2 in comparison with controls. Administration of NAC either 30 minutes before or after torsion (group 3 and 4), significantly improved the germ cell apoptosis indices and oxidant/antioxidant balance. Administration of NAC after detorsion had no significant effects on oxidant/antioxidant balance or germ cell apoptosis. Conclusions Administration of NAC prior to torsion or detorsion, but not after detorsion, is protective against ischemia/reperfusion tissue damage in the rat model of testicular torsion. Since NAC has an established safety after almost 40 years of clinical use as mucolytic agent and antidote of acetaminophen toxicity, one can suggest this agent as an adjunct therapy for "testicular torsion rescue". Supplying intracellular glutathione as well as anti-oxidant and anti-inflammatory properties of NAC could be the possible mechanisms of this protective effect.

Purpose: Testicular torsion/detorsion (T/D) results in enhanced formation of free radical metabolites,which contributes to the pathophysiology of tissue damage. We investigated the protective effects of ethyl pyruvate (EP) against testis tissue damage in an experimental model of testicular torsion.Methods: Sprague-Dawley rats were divided into 5 groups. In those animals that underwent T/D, right testes were rotated 720 degrees for 1 hour. Group 1 control rats underwent sham operation. In group 2, the rats underwent T/D. The EP was prepared and injected in the form of Ringer's ethyl pyruvate solution. The rats in group 3, 4, and 5 received 2 doses of 20, 50, and 100 mg/kg EP (30 minutes before and after detorsion), respectively. The right testes of 6 animals from each group were excised 4 hours after detorsion for the measurement of lipid peroxidation, myeloperoxidase (MPO), and antioxidant enzymes activities. Germ cell apoptosis was determined in right testes of 8 animals per group 24 hours after detorsion. The epididymal sperm concentration and motility were evaluated I month after treatments.Results: Germ cell apoptosis indices were significantly higher in group 2 compared with control group. The level of lipid peroxidation and MPO activity increased, whereas antioxidant enzymes activities decreased after T/D. Sperm count and motility were also reduced I month after T/D in group 2 rats. However, EP treatment at doses of 50 and 100 mg/kg significantly decreased the early apoptotic damage and improved long-term sperm count and motility. In the same dosing groups, we observed normalization of oxidant/antioxidant balance and decrement of MPO activity. However, administration of 20 mg/kg of EP conferred no protective effect.Conlusions: Administration of Ringer's ethyl pyruvate solution (in appropriate doses) is protective against apoptotic tissue damage following testicular torsion and improves long-term testicular function. The antioxidant and anti-inflammatory properties of EP seem responsible for the protective effects. Our findings suggest this resuscitation solution as a possible substitute for fluid and electrolyte maintenance during surgical detorsion. (c) 2008 Elsevier Inc. All rights reserved.

We assessed the effectiveness of sildenafil administration during ischemic period in a rat model of testicular torsion/detorsion (T/D).

Ischemic preconditioning (IPC) and pharmacologic preconditioning by morphine and adenosine may significantly decrease the amount of necrosis in rat random pattern skin flaps. We examined the role of ATP-sensitive potassium channels (K(ATP) channels) in mediating these protective phenomenon by using glibenclamide a nonspecific blocker of these channels. We also investigated whether administration of diazoxide an opener of the K(ATP) channels could mimic the same protective effect. Ninety male Sprague-Dawley rats were randomly divided into either control or treatment groups (n = 6 each). Bipedicled dorsal skin flaps (2 x 8 cm) were elevated at the midline. In pharmacologic preconditioning groups, 1 mL of morphine (5 mg/flap), adenosine (0.5 mg/flap), or different doses of diazoxide (0.5, 1, 5, and 15 mg/flap) were administered locally in the cranial half of the flap, respectively. One milliliter of saline was locally injected in the control group. In the IPC group, 1 hour after local saline injection the cranial pedicle was clamped for 20 minutes, and then 40 minutes' reperfusion was performed. In another experiment, 0.3 mg/kg of glibenclamide was injected intraperitoneally 30 minutes before local administration of saline or drug in ischemic or pharmacologic preconditioning groups. Regardless of the group, all flaps were cut at the cranial side 2 hours after elevation and were sutured back. Flap survival area was evaluated on the seventh postoperative day. IPC and pharmacologic preconditioning with morphine, adenosine, and diazoxide (in higher doses; 1, 5, and 15 mg/flap) improved survival area compared with the control group. Glibenclamide abolished their protective effect. K(ATP) channels may have a key role in anti-ischemic properties of IPC and pharmacologic preconditioning.

PURPOSE:Pharmacologic preconditioning with morphine has been shown to protect several kinds of tissues against ischemia-reperfusion injury. The aim of the present study was to investigate whether intravitreal administration of morphine induces structural protection against ischemic damage in a rabbit model of ischemic retinopathy. METHODS:Twenty-eight male white New Zealand rabbits were used. Animals in saline control group received 0.1 mL of phosphate-buffered saline (PBS) intravitreally with no postinjection ischemia. In the saline-control ischemia group, 15 minutes after injection of PBS, retinal ischemia was induced by raising intraocular pressure to 150 mmHg for 60 minutes. In three treatment-ischemia groups, morphine (1, 5, and 10 micromol/L) was administered intravitreally 15 minutes before induction of ischemia. In another experiment, naloxone (40 micromol/L) was administered 5 minutes before intravitreal administration of morphine (10 micromol/L) followed by 60 minutes of ischemia to investigate the role of opioid receptors in mediating the possible protective effect of morphine. Toxicity controls were performed with morphine (10 micromol/L) and naloxone (40 micromol/L) without ischemia. Histologic evaluation was performed for all groups on the seventh postoperative day. RESULTS:Sixty minutes of ischemia led to severe cell loss in ganglion cell layer and thinning of the inner nuclear layer in saline-control ischemia compared to that of the nonischemia control group (P < 0.001). Thickness of the inner plexiform layer to the inner limiting membrane was significantly increased due to edema (P < 0.001). Administration of morphine in higher doses (5 and 10 micromol/L) significantly improved all of the above mentioned indices (P < 0.05). Administration of naloxone 15 minutes before morphine reversed most of the morphine protective effects. CONCLUSIONS:Morphine pretreatment provides significant histologic protection against ischemic injury in rabbit retina. Pharmacologic evidence suggests that this protective phenomenon may be mediated in part by opiate receptors.

OBJECTIVES:The role of endogenous cannabinoids in ischemia/reperfusion induced germ cell apoptosis in rats was investigated.METHODS:Baseline group was for basal normal values. The Sham operated group served as a control group. The torsion/detorsion (T/D) group underwent torsion (1 h) and detorsion; AN1, AN2, and AN3 groups received anandamide (10 mg/kg) 30 min before torsion, 30 min after torsion, and just after detorsion, respectively. In the AM251 group, AM251 (0.5 mg/kg) was injected 45 min before torsion and in the AN/AM group, AM251 and anandamide were injected 45 and 30 min before torsion, respectively. Lipid peroxidation, antioxidant enzymes, and germ cell apoptosis was determined.RESULTS:Malondialdehyde (MDA) levels in the T/D group were significantly higher than the control group. Moreover, MDA values in the AN1, AN2, and AN3 groups were significantly lower than T/D. There were significant decreases in catalase and superoxide dismutase activities in the T/D group versus the control group. These values in the AN1, AN2, and AN3 groups were significantly higher than T/D. It was also shown that MDA levels in the AN/AM group were significantly higher than the AN1 group. In the AN/AM group, catalase and superoxide dismutase activities were significantly lower versus the AN1 group. The mean germ cell apoptosis scores in all animals with testicular T/D were significantly higher than the control group. There was no difference between the apoptotic indices in the AN1, AN2, AN3, and T/D groups. Apoptosis scores in AM251 and AN/AM were significantly higher compared with the T/D and AN1 groups.CONCLUSIONS:Although anandamide increased antioxidant markers, it failed to reduce germ cell apoptosis. AM251 worsened the antioxidant defense system, which is reflected as higher germ cell apoptosis.

Introduction: Numerous studies performed in recent years have shown protective effects of N-acetylcysteine (NAC) on cardiac and renal tissue damage following ischemia/reperfusion injury. We assessed the effectiveness of systemic administration of NAC, at a therapeutic dose, in a rat model of a 1-hour 720-degree testicular torsion/detorsion. Materials and Methods: Sprague-Dawley rats were divided into five groups, 14 animals in each: group 1 animals underwent sham operation as the control group; group 2 rats underwent torsion/detorsion and received saline injection, and the animals in groups 3, 4, and 5 received intraperitoneal injections of 150 mg/kg NAC 30 min before torsion, after torsion, and after detorsion, respectively. Markers of oxidative stress as well as germ cell apoptosis indices were assessed 4 and 24 h after detorsion, respectively. Results: The apoptosis indices were significantly higher in group 2 as compared with the control group. Four hours after detorsion, the testicular level of lipid peroxidation was significantly increased, and antioxidant enzyme activities were significantly decreased in group 2 as compared with the controls. Administration of NAC either 30 min before or after torsion (groups 3 and 4) significantly improved the germ cell apoptosis indices and oxidant/antioxidant balance. Administration of NAC after detorsion had no significant effect on biochemical markers or germ cell apoptosis. Conclusion: Administration of NAC prior to torsion or detorsion, but not after detorsion, induces protective effects against ischemia/reperfusion injury in a rat model of testicular torsion.