Experimental retinopathy by hyperbaric oxygenation.

Retinopathy of prematurity (ROP) usually occurs after a prolonged exposure to normobaric hyperoxia in newborn mammals and infants. We hypothesized that experimental ROP also could develop after acute exposures to hyperbaric oxygenation (HBO), providing that a severe and maintained retinal vasoconstriction occurred during HBO exposure. Five- to seven-day-old, Long Evans Sprague-Dawley rats were exposed for 5 h either to 5 atm abs oxygen or to 5 atm abs O2 with 190 mmHg inspired PCO2 (hypercapnia). Control rats breathed air at atmospheric pressure. Two months after exposures, rats were anesthetized, perfused intraventricularly with India ink, and retinal images were obtained. Retinal vascular density (RVD) in each image was calculated as the number of pixels in the retinal vessel area divided by the total number of pixels in the image (retinal tissue and vessels). The RVD was significantly increased from 0.0112 +/- 0.004 in the air-exposed controls to 0.0417 +/- 0.029 in the HBO-exposed rats (mean +/- SD; n = 4 in each group). HBO with hypercapnia produced a nonsignificant increase in RVD (0.0255 +/- 0.007; n = 4), reducing the HBO-induced increase in RVD by 39%. These results are consistent with the hypothesis that a sustained HBO-induced retinal vasoconstriction in newborn rats, followed by a hypoxic-ischemic injury, might result in vascular proliferation, thereby initiating ROP development on return to air. Hypercapnia does not completely prevent HBO-induced retinal vasoproliferation, probably because possible vasodilation, induced by hypercapnia, can greatly elevate retinal tissue PO2 and promote oxidative damage.

Microwave-induced retinal destruction with sparing of sclera and choriocapillaris.

We studied the effect of short-term hyperthermia on sclera, choroid, and retina by delivering microwave radiation (2.45 GHz) for 1 minute to 12 eyes of Dutch belted pigmented rabbits. Four eyes each were treated with 43 degrees C, 45 degrees C, and 47 degrees C and followed for 4 weeks. The 43 degrees C group showed minimal disruption of retinal pigment epithelium and outer retina, with pigment migration; the 45 degrees C and 47 degrees C groups showed complete retinal and RPE damage, pigment migration, and glial proliferation. At the same time, the sclera and choroid in all of the eyes remained essentially unchanged. We conclude that microwave-induced hyperthermia can create retinal scarring without significant damage to sclera and choriocapillaris. The next experimental step will be to refine the microwave delivery system to ensure predictable and reproducible lesions.

Hyperthermia and temperature-sensitive liposomes: selective delivery of drugs into the eye.

Experiments were performed to quantitate the delivery of two drugs into the eye following hyperthermia. The drugs, cytosine arabinoside and 5-fluorouridine, were encapsulated in temperature-sensitive liposomes. After systemic injection of the liposome-encapsulated drug, microwave hyperthermia was applied to the superior limbus of rabbit eyes in an attempt to locally release the drug. Samples of aqueous humor and vitreous showed significantly higher drug levels in the heated versus the unheated eyes. Histology of the heated eyes showed no significant damage to ocular structures at the power level used to release the entrapped drug. Heating at higher power levels did damage the eye, confirming earlier studies. The potential uses and limitations of this drug delivery modality are discussed.

Contact application of Nd:YAG laser through a fiberoptic and a sapphire tip.

We evaluated the effects of Nd:YAG laser energy directly applied to ocular tissue through a fiberoptic and a sapphire tip. All ocular tissue could be easily cut with the maximum 4 watts of energy. The coagulated borders extended 20 to 200 mu into the healthy tissue depending on the speed with which the cutting was performed.