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Biomedical subjects

Jay W McLaren

Publications and source records attributed to Jay W McLaren.

At least 19 recordsLinked to original sources

Objective measurement of backscattered light from the anterior and posterior cornea in vivo.

PURPOSE: To develop an objective and repeatable method of measuring corneal backscattered light from different depths of the cornea in vivo. METHODS: A modified slit lamp ("scatterometer"), with a video camera and synchronous white strobe light, was used to capture images of a 0.1-mm-wide slit beam through the cornea. Image analysis software was developed to measure backscatter from digitized high-magnification images of 82 normal corneas of 41 subjects. Forty eyes of 20 of the same subjects were examined again after 1 month. Mean backscatter from the anterior, middle, and posterior thirds of the cornea was compared between repeated measurements, and expressed in arbitrary scatter units (SU). RESULTS: Backscatter in the anterior third of the cornea was 451 +/- 42 SU (mean +/- SD, n = 82), from the middle third was 274 +/- 29 SU (n = 82), and from the posterior third was 242 +/- 28 SU (n = 82). The difference in backscatter measured a month apart was 5 +/- 27 SU (P = 0.34), 2 +/- 17 SU (P = 0.42), and 0 +/- 15 SU (P = 0.95) in the anterior, middle, and posterior thirds of the cornea, respectively. Minimum detectable differences between measurements were 12, 8, and 7 SU in the anterior, middle and posterior thirds, respectively (alpha = 0.05, beta = 0.20, n = 40). CONCLUSIONS: Backscatter can be measured at different depths of the cornea from high-magnification digitized images of a narrow slit beam through the cornea. The method is objective and repeatable and can be applied in prospective studies of deep and posterior lamellar keratoplasty.

Adult↗

Prevalence of floppy eyelid syndrome in obstructive sleep apnea-hypopnea syndrome.

OBJECTIVES: To determine the prevalence of floppy eyelid syndrome (FES) in obstructive sleep apnea-hypopnea syndrome (OSAHS) and to develop a method to measure eyelid laxity. DESIGN: Masked cross-sectional (prevalence) study examining patients referred to the Mayo Sleep Disorders Center. PARTICIPANTS AND/OR CONTROLS: Fifty-nine subjects were examined before undergoing polysomnography. Forty-four subjects had OSAHS, and 15 did not have it. TESTING: Subjects underwent slit-lamp examination and eyelid laxity measurements, followed by polysomnography. MAIN OUTCOME MEASURES: Presence of FES as defined by subjectively easy eyelid eversion, tarsal papillary conjunctivitis, and lash ptosis; force required to displace the upper lid 5 mm, as measured by a strain gauge device; number of apnea or hypopnea episodes per hour (apnea-hypopnea index [AHI]); presence of OSAHS, as defined by an AHI of > or =5; and abnormalities on electrocardiography. RESULTS: One patient with OSAHS was found to have FES, yielding a prevalence of 2.3% (95% confidence interval [CI]: 0.1%-12.0%). One patient was referred to the Sleep Disorders Center due to a diagnosis of FES; if this patient were included, the prevalence would be 4.5% (95% CI: 0.5%-15.1%). Subjectively easy lid eversion was more common in OSAHS patients than in non-OSAHS patients. When adjusted for age and body mass index, there was a trend for association between subjectively easy lid eversion and OSAHS, but this did not reach statistical significance. Subjectively easy lid eversion was associated with AHI. Force required to displace the upper lid 5 mm was lower in lids with subjectively easy eversion, but was not associated with OSAHS or AHI. Intraclass correlation among 3 strain gauge measurements was good for both right (82%) and left (83%) lids. There were no statistically significant differences in frequency of electrocardiographic abnormalities among the various groups. CONCLUSIONS: The prevalence of FES among OSAHS patients is low. Patients with subjectively easy upper lid eversion are at risk for OSAHS. By recognizing the potential for OSAHS in these patients, the ophthalmologist may play an important role in initiating their evaluation and treatment.

Adolescent↗

Corneal keratocyte deficits after photorefractive keratectomy and laser in situ keratomileusis.

PURPOSE: To measure changes in keratocyte density up to five years after photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK). DESIGN: Prospective, nonrandomized clinical trial. METHODS: Eighteen eyes of 12 patients received PRK to correct a mean refractive error of -3.73 +/- 1.30 diopters, and 17 eyes of 11 patients received LASIK to correct a mean refractive error of -6.56 +/- 2.44 diopters. Corneas were examined by using confocal microscopy before and six months, one year, two years, three years, and five years after the procedures. Keratocyte densities were determined in five stromal layers in PRK patients and in six stromal layers in LASIK patients. Differences between preoperative and postoperative cell densities were compared by using paired t tests with Bonferroni correction for five comparisons. RESULTS: After PRK, keratocyte density in the anterior stroma decreased by 40%, 42%, 45%, and 47% at six months, two years, three years, and five years, respectively (P < .001). At five years, keratocyte density decreased by 20% to 24% in the posterior stroma (P < .05). After LASIK, keratocyte density in the stromal flap decreased by 22% at six months (P < .02) and 37% at five years (P < .001). Keratocyte density in the anterior retroablation zone decreased by 18% (P < .001) at one year and 42% (P < .001) at five years. At five years, keratocyte density decreased by 19% to 22% (P < .05) in the posterior stroma. CONCLUSIONS: Keratocyte density decreases for at least five years in the anterior stroma after PRK and in the stromal flap and the retroablation zone after LASIK.

Adult↗

Effects of glaucoma medications on corneal endothelium, keratocytes, and subbasal nerves among participants in the ocular hypertension treatment study.

PURPOSE: To compare subbasal corneal nerve and keratocyte density and endothelial characteristics of ocular hypertensive patients treated with medications or observation. METHODS: Participants in the Ocular Hypertensive Treatment Study (OHTS) randomized at Mayo Clinic to medication or observation were evaluated with specular microscopy annually for 6 years. Confocal microscopy was performed 78 to 108 months after enrollment. Subbasal nerve density was calculated by manual tracing and digital image analysis. Keratocyte density was determined by manual counting methods. Data were compared using a t test and a rank sum test. RESULTS: After 6 years, corneal endothelial cell density, percent hexagonal cells, and coefficient of variation of cell area for the observation (n = 21) and medication groups (n = 26) were similar (2415 +/- 300 vs. 2331 +/- 239 cells/mm; 63% +/- 11% vs. 65% +/- 10%; and 0.32 +/- 0.07 vs. 0.30 +/- 0.06, respectively). Of 38 participants undergoing confocal examination, the medication group (n = 19) had fewer nerves (3.8 +/- 2.1 vs. 5.9 +/- 2.0 nerves/frame; P = 0.02) and a lower nerve density (5643 +/- 2861 vs. 9314 +/- 3743 mum/mm; P = 0.007) than the observation patients (n = 10). An additional 9 patients in the observation group, who began medication before confocal scanning, had intermediate nerve densities. Full-thickness keratocyte density was similar, with 22,257 +/- 2419 and 23,430 +/- 3285 cell/mm in the observation and medication groups, respectively. CONCLUSIONS: Chronic administration of glaucoma medications causes a decrease in the number and density of corneal subbasal nerve fiber bundles but does not affect keratocyte density or corneal endothelial characteristics.

Antihypertensive Agents↗

Retinopathy from a green laser pointer: a clinicopathologic study.

OBJECTIVE: To report retinopathy following exposure to light from a commercially available class 3A green laser pointer. METHODS: A 55-year-old woman with a ring melanoma was scheduled for enucleation. The eye (visual acuity 20/20) had a healthy-appearing macular retina. The retina was exposed to light from a commercially available class 3A green laser: 60 seconds to the fovea, 5 minutes to a site 5 degrees below the fovea, and 15 minutes to a site 5 degrees superior to the fovea. Color photographs were obtained before and after exposure. The eye was enucleated 20 days after exposure. RESULTS: Laser power measurements averaged less than 5 mW. Retinopathy was observed 24 hours after laser exposure. This was characterized by a yellowish discoloration at the level of the retinal pigment epithelium (RPE) in the subfoveal region and at the site superior to the macula where the retina received 15 minutes of laser exposure. Each site developed granular changes at the level of the RPE within 5 days of exposure. Histologic study showed RPE damage in the exposed subfoveal and parafoveal regions. CONCLUSION: A class 3A green laser pointer caused visible retinopathy in the human eye with exposures as short as 60 seconds.

Ciliary Body↗

Recovery of corneal subbasal nerve density after PRK and LASIK.

PURPOSE: To measure and compare the return of corneal innervation up to 5 years after photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK). DESIGN: Prospective, nonrandomized clinical trial. METHODS: Eighteen eyes of 12 patients received PRK to correct a mean refractive error of -3.73 +/- 1.30 diopters, and 16 eyes of 11 patients received LASIK to correct a mean refractive error of -6.56 +/- 2.44 diopters. Corneas were examined by confocal microscopy before and at 1, 2, 3, and 5 years after the procedures. Subbasal nerve fiber bundles were measured to determine density (visible length of nerve/frame area) and expressed as micrometers per square millimeters. Differences were compared by Friedman's test and adjusted for multiple comparisons by the Student-Newman-Keuls procedure. RESULTS: After PRK, mean subbasal nerve density was reduced by 59% at 1 year (2764 +/- 1321 microm/mm(2) [+/-SD]) when compared with preoperative (6786 +/- 1948 microm/mm(2); P < .001). By 2 years, subbasal nerve density (6242 +/- 1763 microm/mm(2)) was not significantly different from density before PRK and remained unchanged to 5 years (5903 +/- 3086 microm/mm(2)). After LASIK, subbasal nerve density was reduced by 51%, 35%, and 34% at 1, 2, and 3 years, respectively (P < .001). By 5 years, subbasal nerves had returned to densities (4441 +/- 2819 microm/mm(2)) that were not significantly different from densities before LASIK (5589 +/- 2436 microm/mm(2)). CONCLUSION: Corneal subbasal nerve density does not recover to near preoperative densities until 5 years after LASIK, as compared with 2 years after PRK.

Adult↗

Keratocyte density: comparison of two confocal microscopes.

PURPOSE: The ConfoScan 3 clinical confocal microscope provides sharper images of cells in the stroma than the Tandem Scanning confocal microscope does. In this study, we compared volumetric densities of stromal cells determined from images recorded by these two instruments. METHODS: Fifty corneas of 25 normal subjects were examined by confocal microscopy, first by using a Tandem Scanning confocal microscope and then by using a ConfoScan 3 confocal microscope. Bright objects, assumed to represent keratocytes, were counted in a known area of two frames selected from the mid-stroma. The effective depth of the sample volume represented by each frame was estimated from the number of consecutive frames and the corresponding distance that selected cells were visible and countable during a scan. Density was the number of visible cells in the sample area divided by the effective sample volume. RESULTS: The effective focal depth of the Tandem Scanning microscope was 11.9 +/- 2.6 microm (mean +/- SD), and was 25.9 +/- 7.1 microm for the ConfoScan 3. Mean cell density at mid stroma was 23,013 +/- 4,420 cells/mm(3) with the Tandem Scanning microscope and 23,996 +/- 2,898 cells/mm(3) with the ConfoScan 3. This difference was not significant (P = 0.15). CONCLUSIONS: In normal corneas, the ConfoScan 3 and the Tandem Scanning confocal microscopes indicate stromal cell densities that are not significantly different from each other. Estimates of cell density from both instruments require an accurate estimate of the effective depth of the sample volume; this depth is approximately 2.2 times greater with the ConfoScan 3. This difference must be considered when comparing results from studies that use one instrument with results from studies that use the other.

Adult↗

The effect of age on the corneal subbasal nerve plexus.

PURPOSE: To measure subbasal nerve density and orientation in normal human corneas across a broad age range. METHODS: Sixty-five normal corneas of 65 subjects were examined by using tandem scanning confocal microscopy. Ages of subjects ranged from 15 to 79 years (mean 46 +/- 19 years), with 5 subjects from each hemidecade. Subbasal nerve fiber bundles appeared as bright, well-defined linear structures in confocal images of the central cornea. Images from 3 to 8 scans per eye (mean 4.6 +/- 1.8 scans) were randomly presented to a masked observer for analysis. The mean subbasal nerve density (total nerve length [microm] within a confocal image [area = 0.166 mm]), the mean nerve number per confocal scan, and the mean nerve orientation were determined by using a custom software program. Correlations between age and nerve density and age and nerve orientation were assessed by using Pearson correlation coefficients. RESULTS: The subbasal nerve plexus was visible in the central cornea of all subjects. The mean subbasal nerve density was 8404 +/- 2012 microm/mm (range 4735 to 14,018 microm/mm). The mean subbasal nerve number was 4.6 +/- 1.6 nerves (range 1 to 8 nerves). The mean subbasal nerve orientation was 94 +/- 16 degrees (range 58 to 146 degrees). There was no correlation between age and subbasal nerve density (r = 0.21, P = 0.09) or between age and subbasal nerve orientation (r = -0.19, P = 0.12). CONCLUSION: The density and orientation of the subbasal nerve plexus in the central human cornea does not change with age.

Adolescent↗

Comparison of corneal endothelial cell images from a noncontact specular microscope and a scanning confocal microscope.

PURPOSE: We compared endothelial cell density (ECD) from images recorded by the ConfoScan 3 confocal microscope and a noncontact specular microscope. METHODS: Endothelial micrographs of 50 normal corneas of 25 subjects were acquired by a Konan Noncon Robo noncontact specular microscope (Konan Medical, Inc., Hyogo, Japan) and a ConfoScan 3 confocal microscope (Nidek Technologies, Inc, Greensboro, NC). ECD was determined in images from both instruments by using the HAI CAS System Corners Method (HAI Labs, Inc., Lexington, MA). Distances in the images from both machines were calibrated from images of an external scale. Images from the ConfoScan 3 were also assessed using the automated endothelial analysis software provided by the manufacturer, with and without manual correction. RESULTS: The ECD was 2634 +/- 186 cells/mm(2) (mean +/- SD) and 2664 +/- 173 cells/mm(2) by the Robo and ConfoScan 3 Corners methods, respectively. Differences between these 2 methods were not significant. When the automated analysis software was used, however, significant differences were found (P = 0.001). The uncorrected analysis program provided with the ConfoScan 3 indicated a higher ECD (2742 +/- 284 cells/mm(3)) than the Corners method did with images from the Robo and ConfoScan 3. The ECD from the manually corrected ConfoScan 3 method was 2716 +/- 229 cells/mm(3), not significantly different from the ConfoScan 3 Corners method but significantly different from the Robo Corners method. CONCLUSIONS: The ConfoScan 3 can be used interchangeably with the Robo when the Corners method is used to assess ECD and the magnification of both microscopes is calibrated with an external scale. If the proprietary software provided with the ConfoScan 3 is used, it should be manually corrected.

Adult↗

Long-term corneal keratoctye deficits after photorefractive keratectomy and laser in situ keratomileusis.

PURPOSE: To measure changes in keratocyte density up to 5 years after photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK). METHODS: This was a prospective, nonrandomized clinical trial. Eighteen eyes of 12 patients received PRK to correct a mean refractive error of -3.73 +/- 1.30 D, and 17 eyes of 11 patients received LASIK to correct a mean refractive error of -6.56 +/- 2.44 D. Corneas were examined by using confocal microscopy before and 6 months, 1 year, 2 years, 3 years, and 5 years after the procedures. Keratocyte densities were determined in five stromal layers in PRK patients and in six stromal layers in LASIK patients. Differences between preoperative and postoperative cell densities were compared by using Bonferroni-adjusted paired t tests. RESULTS: After PRK, keratocyte density in the anterior stroma was decreased by 39%, 42%, 45%, and 47% at 6 months, 2 years, 3 years, and 5 years, respectively (P < .001). At 5 years, keratocyte density was decreased by 20% to 24% in the posterior stroma (P < .05). After LASIK, keratocyte density in the stromal flap was decreased by 22% at 6 months (P < .02) and 37% at 5 years (P < .005). Keratocyte density in the anterior retroablation zone was decreased 18% (P < .005) at 1 year and 43% (P < .005) at 5 years. At 5 years, keratocyte density was decreased by 19% to 22% (P < .05) in the posterior stroma. CONCLUSIONS: Keratocyte density is decreased in the anterior stroma after PRK and in the stromal flap and the retroablation zone after LASIK for up to 5 years. Posterior stromal keratocyte deficits are first noted at 5 years.

Adult↗

Corneal thickness measurement by confocal microscopy, ultrasound, and scanning slit methods.

PURPOSE: To measure corneal thickness by using a calibrated confocal microscope and to compare this measurement to thickness determined by ultrasonic and noncontact scanning slit pachymetry. DESIGN: Comparison of corneal thickness measured by using four instruments in normal subjects. METHODS: Thickness measured by a clinical confocal microscope (Tandem Scanning) was calibrated from measurements of polymethylmethacrylate contact lenses with known thickness. Corneal thickness was measured in one eye of 24 normal subjects by using this instrument, two ultrasonic pachymeters (DHG-1000 and Sonogage), and a noncontact optical scanning slit pachymeter (Orbscan II). RESULTS: Mean corneal thickness measured by confocal microscopy was 516 +/- 30 microm (+/-SD). This was less than the mean thickness measured by both ultrasonic pachymeters, 554 +/- 28 microm by the DGH, and 555 +/- 28 microm by the Sonogage (P <.001). Thickness measured by the Orbscan II pachymeter was 540 +/- 35 microm (P <.001, compared with either confocal or ultrasound) after applying an "acoustic factor" of 0.92, a default correction of the software. CONCLUSION: Corneal thickness measured by calibrated confocal microscopy is approximately 39 microm (7.0%) less than thickness measured by two commonly used ultrasonic pachymeters and approximately 24 microm (4.4%) less than thickness measured by the corrected Orbscan II pachymeter. These differences are important for planning and measuring the effects of refractive and other surgical procedures. The precision of confocal microscopy is limited by corneal motion in an anterior-posterior direction. The difference between instruments suggests that verification of clinical ultrasonic pachymeters should be revisited.

Adult↗

Clinical responses of the corneal endothelium.

The corneal endothelium maintains corneal deturgescence and clarity by a pump-leak mechanism first described by David Maurice. This cell layer can be investigated clinically with specular microscopy, fluorophotometry, and pachymetry. We describe the clinical responses of the corneal endothelium to aging, drugs, glaucoma, contact lens wear, trauma, disease, and surgery.

Aging↗

Long-term keratocyte deficits in the corneal stroma after LASIK.

PURPOSE: To determine changes in keratocyte density up to 3 years after LASIK. DESIGN: Prospective, nonrandomized, comparative trial. PARTICIPANTS: Seventeen eyes of 11 patients received LASIK with a planned 180-microm flap to correct refractive errors between -2.0 diopters (D) and -11.0 D (mean, -6.56+/-2.44). METHODS: Corneas were examined by using confocal microscopy before LASIK and 1, 3, 6, 12, 24, and 36 months after LASIK. Bright objects that resembled keratocyte nuclei were manually counted by a masked observer. Cell densities were determined in anterior and posterior halves of the stromal flap, anterior and posterior halves of the 100-microm-thick layer immediately behind the ablation (retroablation layer), and the posterior third of the stroma. The region of stroma that was ablated (as measured 1 month after LASIK) was omitted from preoperative analysis. Cell densities after LASIK were compared (using1-factor repeated-measures analysis of variance) with densities in the corresponding layer of the normal preoperative stroma (which served as its own control). MAIN OUTCOME MEASURE: Corneal keratocyte density. RESULTS: Before LASIK, keratocyte densities in the anterior and posterior stromal flap and the anterior retroablation layer were 34 818+/-5108 cells/mm(3) (mean +/- SD), 25 390+/-4045 cells/mm(3), and 21 328+/-2980 cells/mm(3), respectively, and densities in these layers decreased 14% to 20% at 1 month after LASIK (P<0.001). Keratocyte densities in these layers remained stable at 3 and 6 months, and then gradually decreased further (P<0.001) to 26% to 36% below pre-LASIK densities by 3 years. Keratocyte densities in the remaining stromal layers did not change after LASIK. CONCLUSION: Keratocyte densities in the stromal flap and in the anterior retroablation layer decrease during the first 6 months after LASIK and then decrease further during the next 2.5 years. Further studies on these patients and others are warranted to confirm these findings and learn their significance.

Adult↗

Mechanism of ocular hypotensive action of bimatoprost (Lumigan) in patients with ocular hypertension or glaucoma.

PURPOSE: To determine the mechanism of ocular hypotensive action of bimatoprost in patients with ocular hypertension or glaucoma. DESIGN: Double-masked, placebo-controlled, randomized, paired comparison crossover study of the effect of bimatoprost on aqueous humor dynamics. PARTICIPANTS AND CONTROLS: Twenty-nine patients with ocular hypertension or glaucoma. METHODS: Bimatoprost and a placebo were administered once a day, in the evening, for 7 days before assessment of aqueous dynamics using tonometry, Schiötz tonography, and fluorophotometry. Intraocular pressure (IOP) response to water drinking was measured. MAIN OUTCOME MEASURES: Aqueous humor flow rate, outflow facility, and IOP. RESULTS: Intraocular pressure was lowered 29% in the morning and 33% at noon by bimatoprost. Aqueous humor flow was unchanged. Tonographic facility of outflow was increased 47% by bimatoprost relative to the placebo. Assuming an extraocular pressure of 8 mmHg and that extraocular pressure is not altered by bimatoprost, the calculated rate of pressure-insensitive outflow was increased 95% by bimatoprost. During the first hour after water drinking, bimatoprost dampened the IOP rise. CONCLUSION: As was seen in healthy normal eyes, bimatoprost increased both the pressure-sensitive and the pressure-insensitive outflows of aqueous humor in patients with ocular hypertension or glaucoma. Bimatoprost had no significant effect on aqueous humor formation.

Adult↗

Corneal reinnervation after LASIK: prospective 3-year longitudinal study.

PURPOSE: To measure the return of innervation to the cornea during 3 years after LASIK. METHODS: Seventeen corneas of 11 patients who had undergone LASIK to correct myopia from -2.0 D to -11.0 D were examined by confocal microscopy before surgery, and at 1, 3, 6, 12, 24, and 36 months after surgery. In all available scans, the number of nerve fiber bundles and their density (visible length of nerve per frame area), orientation (mean angle), and depth in the cornea were measured. RESULTS: The number and density of subbasal nerves decreased >90% in the first month after LASIK. By 6 months these nerves began to recover, and by 2 years they reached densities not significantly different from those before LASIK. Between 2 and 3 years they decreased again, so that at 3 years the numbers remained <60% of the pre-LASIK numbers (P <0.001). In the stromal flap most nerve fiber bundles were also lost after LASIK, and these began recovering by the third month, but by the third year they did not reach their original numbers (P <0.001). In the stromal bed (posterior to the LASIK flap interface), there were no significant changes in nerve number or density. As the subbasal nerves returned, their mean orientation did not change from the predominantly vertical orientation before LASIK. Nerve orientation in the stromal flap and the stromal bed also did not change. CONCLUSIONS: Both subbasal and stromal corneal nerves in LASIK flaps recover slowly and do not return to preoperative densities by 3 years after LASIK. The numbers of subbasal nerves appear to decrease between 2 and 3 years after LASIK. The orientation of the regenerated subbasal nerves remains predominantly vertical.

Adult↗

Keratocyte density in the human cornea after photorefractive keratectomy.

OBJECTIVE: To perform a quantitative analysis of keratocyte density in human corneas after photorefractive keratectomy (PRK). METHODS: In a prospective comparative trial, 24 eyes of 14 patients received PRK to correct refractive errors of between -1.25 diopters (D) and -5.75 D. Corneas were examined by using confocal microscopy before and 1 day, 5 days, and 1, 3, 6, 12, 24, and 36 months after PRK. Keratocyte nuclei were counted in 5 stromal layers in 3 to 6 scans per eye per visit. Keratocyte density in each layer post-PRK was compared with the density in the corresponding layer of the pre-PRK full stroma (included stroma that would later be photoablated) and the pre-PRK future unablated stroma (thickness adjusted by omitting the future ablation depth) (Bonferroni-adjusted paired t test). RESULTS: Keratocyte density in the anterior 10% of the post-PRK stroma decreased by 25% (P =.002), 41% (P<.001), 40% (P<.001), 43% (P<.001), and 45% (P<.001) at 3, 6, 12, 24, and 36 months compared with the anterior 10% of the pre-PRK full stroma and was reduced by 15% at 36 months (P =.02) compared with the anterior 10% of the pre-PRK future unablated stroma. CONCLUSION: After PRK, keratocyte density in the anterior stroma is not restored to the high-density levels found in the preoperative stroma.

Adult↗

Effect of ibopamine on aqueous humor production in normotensive humans.

PURPOSE: Ibopamine is a prodrug of epinine (deoxyepinephrine) that exhibits activity at dopaminergic and adrenergic receptors. Topical ocular application has been shown to cause mydriasis without cycloplegia and to increase the rate of aqueous humor flow in normotensive human eyes. Mydriasis can interfere with the measurement of aqueous flow. In this study ibopamine's effect on aqueous humor production was measured while making allowance for the potential artifact caused by its mydriatic effect. METHODS: The effects of topical ibopamine on pupillary diameter, aqueous humor flow measured by fluorophotometry, and intraocular pressure were studied in 24 healthy, blue-eyed humans. Ibopamine was administered with and without the alpha-adrenergic antagonist dapiprazole, and its effects were compared with those of tropicamide, with and without dapiprazole in a double-masked, randomized, crossover design. RESULTS: Ibopamine dilated the pupil from a diameter of 3.7 +/- 0.64 (mean +/- SD, n=24) to 7.7 +/- 0.70 mm. Ibopamine, during its peak mydriasis, was associated with a very large increase in the rate of clearance of topically applied fluorescein from the cornea and anterior chamber, an effect that was not associated with tropicamide during its peak mydriasis. The mydriatic effect of ibopamine was completely blocked by dapiprazole, and the increase in fluorescein clearance was partially blocked. When mydriasis was blocked, ibopamine increased fluorescein clearance by 13% (P<0.0001), which was interpreted as an increased rate of aqueous humor production. Compared with placebo and with the tropicamide control, ibopamine decreased intraocular pressure, despite its stimulation of aqueous humor flow. CONCLUSIONS: Ibopamine is in a specific class of drug, along with pilocarpine, epinephrine, and bimatoprost that in humans increases the rate of aqueous humor flow as measured by fluorophotometry. This effect is partly responsible for its ability to increase intraocular pressure in persons suspected to have abnormally low aqueous humor outflow facility. The transient apparent doubling of aqueous humor flow, measured by fluorescein clearance after administration of ibopamine is an artifact of increased fluorescein clearance through the dilated pupil while accommodation is active.

Adrenergic alpha-Antagonists↗

Keratocyte density of central human cornea after laser in situ keratomileusis.

PURPOSE: To determine changes in keratocyte density in the first year after laser in situ keratomileusis (LASIK). DESIGN: Prospective interventional cohort study. METHODS: Seventeen eyes of 11 patients received LASIK with a planned 180-microm flap to correct refractive errors between -2.0 diopters and -11.0 diopters. Images of the full-thickness cornea were obtained by using confocal microscopy in vivo before LASIK and at 1 week, 1, 3, 6, and 12 months after LASIK. Bright objects (that resembled keratocytes) in images without motion blur were manually counted by one observer. Cell densities were determined in anterior and posterior halves of the stromal flap, anterior and posterior halves of the layer 100 microm-thick immediately deep to the ablation (retroablation layer), and in the posterior third of the stroma. The region of stroma that was ablated (as measured 1 month after LASIK) was omitted from the preoperative analysis. RESULTS: Keratocyte density in the anterior flap was 28,978 +/- 5849 cells/mm(3) (mean +/- SD) pre-LASIK, and was decreased at all postoperative examinations, but the difference was not significant until 12 months after LASIK (22% decrease). Keratocyte densities in the posterior flap were 20,397 +/- 4215 cells/mm(3) pre-LASIK and were decreased by 20%-40% at all postoperative examinations 1 week to 1 year after LASIK. Keratocyte densities in the anterior half of the retroablation layer were 16,605 +/- 3595 cells/mm(3) pre-LASIK and decreased by 16%-30% between 3 and 12 months after LASIK. Keratocyte densities in the posterior half of the retroablation layer and posterior stroma did not change. CONCLUSIONS: Keratocyte densities in the posterior flap and anterior retroablation layer (regions adjacent to the lamellar cut) decrease at 1 week and 3 months, respectively, after LASIK and remain decreased in these regions at 12 months after LASIK. In the anterior flap, keratocyte density decreases 1 year after LASIK. The long-term effects of these cellular deficits, if any, require further study.

Adult↗