SUMMARY One hundred and fifty-five premature infants weighing 600-2000 g were followed up during for the presence of retinopathy of prematurity (ROP) and for the existence of myopia. 50% of the premature infants who had ROP were myopic, while only 16% myopic premature infants were found among those who did not have ROP. There was a positive correlation between the degree of myopia and the severity of cicatricial ROP. No difference existed in the frequency and degree of myopia between premature infants in which ROP cicatrised spontaneously and in those where it cicatrised after cryopexy.Myopia is a frequent finding in premature babies." Comparative studies2 showed that premature infants tend to develop myopia and that there is a close relationship between myopia and retrolental fibroplasia. However, the relationship has not been clearly established.In the present study we investigated the prevalence of myopia in premature infants and its relation to the cicatricial stages of ROP in untreated eyes and in eyes treated by cryopexy. Material and methodsOne hundred and fifty-five premature babies weighing from 600 to 2000 g, born in 1974-80, were examined for the presence of ROP and for the existence of myopia at the age of 2 weeks; they were followed-up for 2-8 years, the mean follow-up time being 3 years. The family history was taken, and the premature babies with one or both parents myopic above -6-0 dioptres were excluded from the study. The examination included indirect ophthalmoscopy and retinoscopy, and in 10 out of 26 eyes in which the myopia exceeded -3-0 dioptres a measurement of the axial length of the globe was performed by Amode ultrasound. Cycloplegia for retinoscopy was achieved by instilling cyclopentolate 0-5%

Using theoretical models for the flow of fluourescein dye in retinal arteries and veins, we have determined the effects of optical absorption in blood of the incident excitation light and the emitted fluorescent light on the time course of measured fluorescence intensity, I(t). Our results indicate that I(t) curves recorded from arteries adequately represent the mean time course of the fluorescein concentration (C(t)), when either a circular or rectangular light-collecting aperture is used. I(t) curves recorded from veins adequately represent C(t), but only when a circular aperture of approximately the same diameter as that of the vessel is used. A two-point fluorophotometer, which provides simultaneous, on-line measurements of arterial and venous I(t) curves is described. Typical recordings obtained with the instrument are shown and the method employed to analyze the curves quantitatively is described in detail. This method, which consists of fitting the first passage of the fluorescence intensity curve with a log-normal function, provides results that are more accurate than those obtained using the standard exponential extrapolation method.

Laser Doppler velocimetry was used to measure the velocity of blood in human retinal vessels. The mean flow velocities obtained were 1.9 centimeters per second in a retinal vein and 2.2 centimeters per second in a retinal artery. Scattered light from a weak helium-neon laser beam focused on the vessel was detected by a photomultiplier, and the temporal correlation of the intensity fluctuations was measured with a photon counting autocorrelator. Autocorrelation functions for blood flowing through glass capillaries were used for calibration.

SUMMARY Intraocular pressure was artificially raised to 60-70 mmHg in 7 albino rabbits for periods of 15 minutes to 4 hours. The corneal endothelium of these eyes was studied by transmission and scanning electron microscopy. A correletion between exposure time to elevated IOP, clinical signs observed by slit-lamp examination, and extent of morphological damage is clearly shown. In eyes exposed to high pressure for 15 and 30 minutes corneas remained transparent and only minimal changes could be detected by SEM, which consisted of small areas of cells with unevenness of their surface, occasional cellular ruptures, and diminution of cilia and microvilli. After 1-2 hours of exposure small, solitary corneal opacifications appeared. In these eyes more severe morphological changes affecting larger areas were observed, with additional cellular blebbing, excariocytosis, cellular rupture, disintegration, and disappearance seen in SEM. Thin sections revealed swelling of mitochondria, disorganisation of endoplasmic reticulum, and the existence of myelin bodies. In eyes exposed for 3 and 4 hours to high IOP diffuse corneal haziness, implying stromal oedema, appeared. In these eyes the areas affected were larger, the extent of damage being more severe. Many areas were bare of endothelium, surrounded by scattered cellular debris, and showed cells with ballooning surfaces and multiple ruptures. Even in severe cellular damage cellular junctions appeared intact. It is assumed that endothelial cells are more sensitive to IOP elevation than the cellular junctions and that injury to the active pump system due to morphological damage is responsible for the resultant corneal oedema.It is widely accepted that endothelial integrity and metabolic activity are essential for continuous maintenance of corneal dehydration and transparency. On the one hand the endothelium is the site of a metabolically dependent fluid pump that counteracts fluid leakage, while on the other it acts as a barrier to solutes from the anterior chamber.--5 Corneal oedema accompanying acute glaucoma was shown to result from noncompensated corneal endothelium.1 2 4-6 This noncompensation, which allows excessive flow of fluid to the corneal stroma, might be explained by two mechanisms: (1) High intraocular pressure (IOP) affects the metabolic active-pumping mechanism without any morphological changes, thus reducing resistance to aqueous flow to the stroma with resultant stromal oedema.5 (2) Elevated IOP causes morphological cellular Correspondence to Dr S. Melamed. damage, thus reducing anatomically and functionally the barrier to flow of fluid into the stroma. In 47 eyes with chronic glaucoma decreased concentration of endothelial cells along with progressive atrophy and degeneration were described.6More recently other investigators using scanning electron microscopy (SEM) and transmission electron microscopy (TEM)7-10 have shown various morphological changes which could be attributed to the nonfunctioning endothelium. Among these changes were flattening of cells, bl...

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