tissues was titrated in mouse embryonic fibroblasts. The mode of viral spread (either carried by macro­phages or free in the bloodstream) was assessed by inhibiting macrophage function with toxic silica in the peritoneal cavity and then administering poly-clonal murine anti-murine cytomegalovirus antibody in the circulation. The virus reached the eyelid, conjunctiva, and cornea before spreading into the extraocular muscles, choroid, and retina. Ocular tis­sues were involved as part of a systemic infection. Hindering macrophage function did not affect viral distribution, suggesting that free virus, and not mac-rophage-bound virus, disseminates via the blood­stream. The authors concluded that "passive transfer of antibody ameliorates the disease in immunocom-promised patients with systemic CMV infection, although the final clearance of the virus needs further cooperation of cell-mediated immunity and cyto-kines."—George B. Bartley

*Public Health Research Institute, Kobe, Japan.

• Long term effect of apraclonidine. Araujo SV, Bond JB*, Wilson RP, Moster MR, Schmidt CM Jr, Spaeth GL. Br J Ophthalmol 1995;79:1098-1101.

THE AUTHORS STUDIED THE EFFICACY AND COMPLI-

cations of apraclonidine 0.5% eyedrops twice or thrice daily for the therapy of increased intraocular pressure in 185 patients, all of whom were being treated unsuccessfully with other medications but who wished to avoid surgery. One-hundred forty-seven patients (80%) had primary open-angle glauco­ma. Twenty-eight patients left the study because of the development of intolerable side effects or a change in therapy. The average follow-up interval was ten weeks (range, one day to 35 weeks). The mean difference in intraocular pressure between treated eyes and control eyes was — 2.1 mm Hg (P < .001); a similar pressure-lowering effect was found when com­parisons were made with the baseline value in the treated eye only. By the end of the follow-up interval, 54% of the patients were no longer using apracloni­dine. The medication was discontinued because of side effects (23%), most commonly a transient blur­ring of vision or allergy, or because intraocular

pressure was not decreased satisfactorily (31%). Forty-six percent of patients were still being treated with apraclonidine. The authors concluded that the drug "should not be considered as first line treatment because of its high rate of tachyphylaxis and signifi­cant incidence of allergic reactions."—George B. Bartley

*Wills Eye Hospital, Thomas Jefferson Medical College, Ninth and Walnut Sts., Philadelphia, PA 19107.

• Trabecular meshwork and elastin. Segawa K*. J Jpn Ophthalmol Soc 1995;99:129-302.

E LASTIC FIBERS IN THE TRABECULAR MESHWORK MAY

play a role in aqueous outflow resistance. The fibers consist of abundant microfibrillar components containing glycoproteins and amorphous components containing elastin. Digestion of trabecular meshwork tissue with elastase demonstrates that the cells consti­tuting the trabecular meshwork and Schlemm's canal separate when elastin is decreased and appose when elastin is added. Intraocular pressure decreases as outflow resistance is lowered when the anterior seg­ments of eyes are perfused with elastase. Large amounts of elastin are present in fine fibrils lying beneath the trabecular wall of Schlemm's canal in eyes with primary open-angle glaucoma, in pseudoex-foliative material of eyes with pseudoexfoliative glau­coma, and in basement membranes of eyes with corticosteroid-associated glaucoma. In contrast, eyes with congenital or juvenile glaucoma contain fibro-nectin, rather than elastin, in basement membrane and fine fibril-like materials. Trabecular membrane tissue exposed to corticosteroids synthesize and se­crete microfibrils and elastin. The elastin gene is expressed in human trabecular meshwork. Because orally administered elastase appears in aqueous hu­mor and digests elastin in the trabecular meshwork, the author concluded that a similar drug possibly could decrease the outflow resistance in eyes with glaucoma.—George B. Bartley

*Department of Ophthalmology, Shinshu University School of Medicine, Asahi 3-1-1, Matsumoto-shi, Nagano-ken 390, Japan.

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