Veterinary ophthalmology has its roots in Europe, and early publications starting in the 1880s focused mainly on the horse eye. However, major political conflicts in this region of the world delayed further development in veterinary ophthalmology until well after World War II. In America, based on the success of the American Society of Veterinary Ophthalmology, and the growth and sophistication of private small animal practices in the 1950s, the American College of Veterinary Ophthalmologists (ACVO) was established in 1970. Final approval of the College by the American Veterinary Medical Association occurred in 1974. Similar veterinary ophthalmology specialization has occurred in the United Kingdom (certificate and diploma programs), Japan, France, Norway, Sweden, and other countries. The common market countries of Europe, and most recently, the Latin America countries have formed multiple country veterinary ophthalmology certification programs.

Practice of veterinary ophthalmology in the private sector has become both profitable and a stimulating professional career. Development of the specialty colleges, such as the American College of Veterinary Ophthalmologists in America, have been critical in the establishment of higher standards for the practice of veterinary ophthalmology, training of veterinary ophthalmologists, and the genesis and distribution of the majority of new information and scientific studies. Continued vitality of the ACVO-based academic programs depends on increasing the number of successful cooperative programs with the private specialty practices for clinical training of veterinary students and residents, and for clinical research. The future for veterinary ophthalmology is indeed bright!

Significant medical and surgical advances have occurred in veterinary ophthalmology in the last fifty years. While the administration of topical ophthalmic preparations in small animals is usually simple, the use of the subpalpebral system for medication of the horse eye is of considerable benefit. New antibiotics have been introduced to combat bacterial resistance, which continues to be a problem. Topical antifungal agents remain for the most part, fungostatic, and additional drugs are needed. Drugs to control or eliminate endogenous proteinases and collaganase in corneal ulceration are urgently needed.

Medical therapy of the glaucomas has experienced continuous change with the introduction of topical beta antagonists, carbonic anhydrase inhibitors, alpha agonists, and most recently, prostaglandins. Of these agents, the prostaglandins (PGs) produce the greatest declines in intraocular pressure (IOP) in the normal and glaucomatous dogs. Preliminary reports of prostaglandins in normal cats indicate no or limited changes in IOP. New drugs that provide glaucomatous eye neuroprotection and/or neuroregeneration by the reduction of the damage associated with the release of the neurotransmittor, glutamate, and the influx of intraneuronal calcium, are forthcoming.

Cyclosporine A has markedly improved the therapy of keratoconjunctivitis sicca in dogs, causing the majority of these patients to secrete sufficient levels of tears to resolve the signs of this disease. Other immune-me-diated external eyes diseases, such as chronic superficial keratitis, and plasma cell infiltration of the nictitans, may also be controlled with topical cyclosporine A. Intracameral plasminogen tissue activator (tPA) has proven highly successful in producing fibrinolysis of blood clot and clotted fibrin of less than two weeks duration in all animal species. Medical and surgical attempts to control angiogenesis, inflammation, postoperative fibrosis, and lens capsular fibrosis are still early, but advances are forthcoming.

Opportunities for improved surgical procedures are considerable and will advance patient care with eyelid, corneal, lens and vitreoretinal disorders. Corneal grafts, improved glaucoma anterior chamber by-pass devices, improved IOLs, and higher success rates for vitreoretinal surgeries are predicted. Based on the past one-half century, significant and profound improvements in both pharmacological and surgical treatments of animal eye patients will be possible.

Retinal ganglion cells (RGCs) and their axons (optic nerve; ON) provide a good experimental model for research on damaged CNS neurons and their functional recovery. After the ON transection most RGCs degenerate retrogradely but they can be rescued and regenerated in some extent by transplantation of a piece of peripheral nerve (PN). When the nerve graft was bridged to the visual center, the central visual projection of regenerating RGC axons can be formed and the behaviors based on relatively simple visual function can be restored in rodents. Axotomized RGCs in adult cats are also shown to survive and regenerate their axons through the PN graft. Among the cat RGC types, Y cells (α-cells) tend to survive and regenerate axons better than others. X cells (β-cells), which are essential for central vision, suffer from rapid death after ON transection. To improve survival and axonal regeneration of axotomized RGCs, intravitreal injections of various neurotrophic factors and electrical stimulation to the ON are effective. To restore visual function in adult mammals with damaged optic pathway, the comprehensive and integrative strategies of multiple approaches will be needed.

安全性試験に汎用されているアルビノラットにおけるパターン刺激を用いた視覚誘発電位の測定条件を検討した。

測定は、視覚野に相当する頭蓋骨に外科的に埋め込んだ電極を用いて、キシラジン及びケタミン投与下で実施した。視覚刺激は白黒が反転するチェッカーボードを用いた。その結果、陽性波P1に陰性波N1が続く波形が認められ、チェッカーサイズが100mm以上において、P1潜時に個体間及び測定間の再現性が認められた。また、steady-state型の波形が8Hz以上の刺激頻度で認められた。刺激輝度の変化による波形への影響は認められなかった。

以上のことから、アルビノラットにおいてパターン刺激を用いたVECPは、視覚機能検出法として応用可能と考えられた。

GLC756 is an octahydrobenzo-quinoline which has combined dopamine D-1 antagonistic and dopamine D-2 agonistic properties. It may induce both a decrease in aqueous humor formation and an increase in uveoscleral outflow. The purpose of this study was to observe the effects on intraocular pressure (IOP) of topically administered 0.4% GLC756 solution, the duration of action, and any side effects in Rhesus monkeys with laser-induced ocular hypertension.

Ten male monkeys with argon laser-induced ocular hypertension in one eye were sedated with ketamine hydrochloride, and the IOP measured in both eyes at 7:00 am, 7:30 am, and then hourly until 1:00 pm with a Tonopen^TM XL applanation tonometer (Mentor^®, Norwell, MA, U.S.A). During the first week, IOP baselines were obtained. The following week, 0.4% GLC756 solution was administered at 7:00 am in the hypertensive eye and the IOP measurements repeated hourly until 1:00 pm. Baseline and drug response curves, and intraocular pressure time profiles for both eyes in each animal were developed.

The baseline IOP was significantly higher in the experimental hypertensive eye than in the normal eye (29.9±2.7 versus 14.5±0.7 mmHg, p<0.0001). The mean IOP in the lasered eye treated with 0.4% GLC756 at 7:00 am decreased from 7:00 to 9:00 am, and then slightly increased until 1:00 pm. The maximal mean IOP decrease (8.5 mmHg) occurred one hour after application of the drug solution. A significant IOP lowering effect was observed 30 minutes after administration of the solution and remained low for two hours. No ocular (such as itching or pain) or systemic side effects to the medication were observed. The IOP in the control eye varied slightly from 7:00 am to 1:00 pm. GLC756 at a concentration of 0.4% significantly lowers the IOP in Rhesus monkeys with laser-induced ocular hypertension. This differs from previous studies performed in humans and rabbits. The IOP lowering effects are more pronounced, but only for a short period of time, in monkeys when compared to the effects observed in humans and rabbits.

GLC756 could be a useful and well-tolerated ocular hypotensive agent and should be investigated further.

我々が既に報告したCrj: Hartleyモルモットの自然発生性の空胞性白内障について、さらに経日的な検索を行った。その結果、眼科学的検査において両側性の空胞性白内障が高い発症率(52%)で認められた。これら空胞性白内障は28週齢以前に発症し、その発症形態は水晶体の赤道部に空胞が認められた後、空胞が消失するものと、空胞が前極側に伸張し、白内障が重度化するものとに大別された。重度化した例の病理組織学的検査では、水晶体前極皮質の空胞化、皮質線維の変性及び配列異常が認められた。空胞性白内障が観察されたモルモットは、いずれも高い血糖値を示し、高血糖値と空胞性白内障の関連が示唆された。そこで、制限給餌により血糖値を低下させたところ、空胞は明らかに軽減した。さらに、これらの動物を制限給餌から不断給餌に戻したところ、血糖値の上昇に伴い空胞性白内障の進行が認められた。このことから、空胞性白内障の発症には、高血糖値の関与が明らかになった。

以上、高血糖値を示すモルモットに認められた空胞性白内障は、自然発生性の糖尿病性白内障と考えられた。モルモットは、ヒトと同様に糖誘導体であるアスコルビン酸（ビタミンC）を体内で合成できないことから、ヒト糖尿病性白内障の有用な疾患モデル動物となる可能性が考えられた。

視神経起始部における異所性網膜が、病理組織学的にCrj: CD (SD) IGSラットの雄80例中19例(23.8%)及び雌80例中21例(26.3%)に観察された。これらの罹患した眼球には眼科学的に視神経乳頭の異常は認められなかった。病理組織学的に異所性網膜組織は視細胞の不規則な集簇巣あるいは杆錐体層、外顆粒層、外網状層及び内顆粒層を含む組織断片から成っていた。本病変の発生に週齢あるいは性別による相違はみられなかった。加えて病変部に変性性あるいは炎症性変化はなかった。これらの結果から、Crj: CD (SD) IGSラットにおける視神経起始部における異所性網膜形成は眼杯の内板の過剰増殖といった先天的発生機序により生じたものと考えられた。

病理組織学的検査により全身の諸臓器に細動脈硬化を認め細動脈硬化症と診断されたマルチーズ犬の眼所見を経過観察した。初診時の眼所見では両眼ともに結膜、上強膜の充血がみられ、右眼では前房水の混濁、左眼では前房出血が観察された。眼内圧は右眼35mmHg、左眼31mmHgと両眼ともに中等度に上昇しており、緑内障を続発していると考えられた。眼圧降下剤、止血剤、消炎剤の投与により両眼ともに前眼部の症状は急速に改善されたが、老齢性と思われる白内障の水晶体赤道部から僅かに透見できる網膜からは正常なタペタム反射は見られず、硝子体出血ならびに網膜出血が認められた。動脈硬化症をはじめ眼所見の異常をともなう加齢性疾患が増加すると考えられ、眼科学的検査の重要性は増するものと思われる。

5～6歳の雄のカニクイザルを用いたマレイン酸チモロールの眼圧降下に塩酸ケタミンによる麻酔の及ぼす影響について調べた。

眼圧測定の都度、塩酸ケタミン麻酔を行い、麻酔の数分後に眼圧測定を行った。

塩酸ケタミン麻酔により無麻酔下に比較して有意な上昇あるいはわずかな上昇がみられた。また、マレイン酸チモロール点眼後に塩酸ケタミン麻酔下で眼圧を測定した場合、5mg/kg麻酔は無麻酔とほぼ同程度で、10mg/kgは5mg/kg麻酔および無麻酔に比べて眼圧降下が大きかった。

ケタミン麻酔量の増加がマレイン酸チモロールの眼圧降下作用をより大きくし、さらに麻酔深度の個体差が反映しバラツキもより大きくなった。サルでの眼圧測定は充分な馴化を行なったうえで、無麻酔下で実施することが望ましいと考える。