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Background: Complaints of glare, halos, and disturbances of night vision after photorefractive keratectomy (PRK) probably result from changes in the corneal aberration structure induced by the laser ablation procedure. The purpose of this article is to characterize changes in the corneal aberration structure after PRK and to demonstrate the effect of pupil dilation on these changes. Methods: Videokeratographs obtained preoperatively (n = 112) and at 1 (n = 94), 3 (n = 103), 6 (n = 91), 12 (n = 60), 18 (n = 53), and 24 (n = 44) months postoperatively from 112 eyes of 89 patients who had undergone PRK for myopia were analyzed. The data were used to calculate the wavefront variance of the cornea for both small (3-mm) and large (7-mm) pupils.

SUMMARY1. The mechanism underlying stromal oedema subsequent to epithelial hypoxia was investigated in isolated rabbit corneas.2. Stromas swelled about 20 ,tm following a 1 hr period of tear side hypoxia in both whole corneal isolates and in preparations in which fluid movement across the endothelium was blocked with silicone oil. In the experiments using whole corneas, stromal thickness was independent of tear side oxygen tension as long as aqueous humour Po2 was greater than 40 mmHg.3. Neither epithelial thickness nor epithelial electrical resistance, a measure of total ion permeability, was significantly affected by blocking respiration. 4. A 10 'C reduction in corneal temperature markedly reduced the rate of hypoxic swelling, suggesting the involvement of a metabolism-dependent hydrating process and implicating the stromal accumulation of a catabolyte.5. When CN-was used to mimic the hypoxic effect in isolated whole corneas, the passive 36C1 unidirectional flux was unaffected, but lactate production rate and stromal [lactate] more than doubled.6. These measurements were used with a mathematical model for corneal hydration dynamics to examine the causes of hypoxic oedema. The principal conclusions were: epithelial hypoxia enhances epithelial lactate production and release to the stroma; this process causes an increase in stromal lactate concentration and a decrease in stromal NaCl concentration (primarily through dilution); stromal lactate accumulation exceeds in osmotic load the dilutional effect on [NaCl], producing stromal oedema. Whereas hypoxia produces corneal metabolic acidosis, effects on endothelial permeability of HC03-transport need not be postulated to explain the stromal oedema that results from hypoxia.

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The wavefront error correlation to acuity was moderately strong, but the corneal elevation fit error also strongly correlated with visual acuity, indicating that Zernike polynomials do not fully characterize the surface shape features that influence vision and that exist in postsurgical or pathologic eyes. In addition, the change in wavefront error when using a larger expansion series was found to increase or diminish somewhat unpredictably. The authors conclude that Zernike polynomials fail to model all the information that influences visual acuity, which may confound clinical diagnosis and treatment.

SUMMARY1. The potentials and resistances associated with the cell membranes of the rabbit corneal epithelium were studied with 3 M-KCl-filled microelectrodes.2. In the isolated cornea, the transepithelial potential was identical in polarity and magnitude to the simultaneously measured total cornea] potential. In contrast to previous findings, the stromal potential was positive to the tear side. Negative stromal potentials apparently derive from inadequate electrodes or method of penetration, and were not found to be a function of filling solution. Transepithelial potential was also identical to over-all corneal potential in the living rabbit eye.3. In the isolated preparation, the average potential profile occurred in three distinct steps across the epithelium. By means of iontophoretic dye injection it was shown that these steps occurred across the outer membrane of the squamous cell, the transition region between the wing and basal cell, and across the inner membrane of the basal cell.4. The transverse membrane resistance of the outer epithelial membrane accounted for 60 % of total corneal resistance. As a result, short-circuit current, which depolarizes the cornea, led to a hyperpolarization of the outer membrane, while affecting deeper membrane potentials little or not at all.5. The spontaneous potential of the outer membrane varied inversely with corneal potential in both normal and chloride-free Ringer, while the potential of the inner membrane of the basal cell was relatively constant, approaching the theoretical Nernst potential for potassium. The potential of the outer membrane was at chloride equilibrium and was sensitive to extracellular shunts. A Thevenin equivalent drawn for the epithelium suggested that half of the outer membrane potential could be attributed to