Glaucoma in Fuchs' heterochromic cyclitis associated with congenital Horner's syndrome.

We report a retrospective study of five patients with monocular Fuchs' heterochromic cyclitis associated with an ipsilateral Horner's syndrome. The minimum follow-up was 10 years. The presenting findings were cyclitis in three of the patients and heterochromia iridis associated with blepharoptosis in the other two. The major factors affecting all five patients were cataract and glaucoma. The intraocular pressure was uncontrolled even with maximal therapy, and antiglaucomatous surgery was performed in all cases. A short period of good postoperative control was followed by an intractable ocular hypertension, causing loss of useful vision in all patients. The remarkable combination of Horner's syndrome with glaucoma and their interaction is discussed.

Prostaglandin metabolism and intraocular pressure.

The plasma lipid alterations characteristic of essential fatty acid deficiency (EFAD) generally appear one to two weeks after the initiation of fat free parenteral nutritional (PN), and may be associated with a reduction in prostaglandin (PG) formation. In the present study the relationship between exclusion of fat from the diet and changes in intraocular pressure (IOP) and PGE2 plasma levels were studied in 28 patients. The results indicated that three weeks after the omission of dietary fat a significant reduction in IOP levels occurred which persisted throughout the follow-up period of 7 (SD 1.2) weeks. Plasma PGE2 levels were also significantly reduced in patients on fat free PN for three weeks as compared with levels measured while patients were on a fat containing diet. This clinical observation is not yet understood and might be related to changes exerted by fatty acid deficiency.

Effect of pilocarpine on intraocular pressure in ocular hypertensive subjects.

In normal subjects, ocular administration of pilocarpine results in initial elevation of IOP succeeded by a fall. We have now examined the effect of pilocarpine on IOP in nontreated ocular hypertension. Our results demonstrate that the initial hypertensive phase is absent in these patients and that the subsequent hypotensive phase is more marked than in normotensive eyes. It is suggested that in normal eyes IOP is regulated by two opposing cholinergic effects, and imbalance the two may lead to ocular hypertension (or hypotension).

Correlation between trypsin binding to a specific receptor and prostacyclin production in cultured vascular endothelial cells.

The correlation between the binding and processing of trypsin and its effect on prostacyclin (PGI2) production in cultured adult bovine aortic endothelial (ABAE) cells was studied. ABAE cells demonstrated an ability to produce PGI2 in a dose-response manner to trypsin at the range of 0.1-2.0 micrograms/ml with a saturation at a concentration of 1 microgram/ml. Likewise, 125I-trypsin binding to the cultured cells increased in a dose-response way and reached saturation at a concentration of about 1 microgram/ml; 125I-trypsin was bound to a specific high-affinity cell-surface receptor with a dissociation constant (Kd) of 1.5 X 10(-8) M and each of the confluent ABAE cells has about 1.2 X 10(5) such receptors sites. The cell-surface receptor for trypsin displayed specific characteristics and an excess amount of unlabeled trypsin successfully abolished 125I-trypsin binding while thrombin in excess failed to compete for 125I-trypsin binding. Only a small fraction of the cell-surface-bound 125I-trypsin was internalized and subsequently degraded by ABAE cells as compared to the process of 125I-trypsin internalization by human skin fibroblasts (HSF). This study demonstrated that the stimulatory effect of trypsin on prostacyclin production and release by ABAE cells might be mediated by a specific cell-surface receptor for trypsin on these cells distinct from the thrombin receptor.

Arachidonic acid metabolism by retinas of rats with streptozotocin-induced diabetes.

Arachidonic acid metabolism via the cyclooxygenase pathway and the effects of aspirin and indomethacin were studied in whole retinas of rats with streptozotocin-induced diabetes. Diabetes was induced by intravenous injection of streptozotocin (60 mg/kg) and the animals were examined 5-6 weeks later. Whole retinas of nondiabetic and diabetic animals were incubated for 1 1/2 hours, and the amounts of prostacyclin and prostaglandin E2 (PGE2) accumulated in the media were measured. The amounts of PGE2 in the media of diabetic retinas was significantly lower than levels in media of nondiabetic group. However, the amounts of prostacyclin accumulated in the media of nondiabetic and diabetic retinas did not differ significantly. Addition of arachidonic acid (A.A.) to the incubation media caused an enhancement in the amounts of PGE2 and prostacyclin in the incubation media of both diabetic and nondiabetic retinas. Addition of indomethacin or aspirin to the incubation media caused a reduction of prostacyclin and PGE2 levels in the media of both groups.

Protein glaucoma as a possible mechanism in a case of glaucomatocyclitic crisis and periphlebitis.

A case of glaucomatocyclitis crisis with recurrent episodes of increased I0P, abnormal appearance of the angle structure and periphlebitis was presented. Some of these episodes involving first one eye and later occurring bilaterally were characterized by absence of flare in the anterior chamber. It is suggested that protein leakage following retinal periphlebitis or an inflammatory reaction involving the ciliary body might be the underlying mechanism for the elevated ocular pressure. The abnormal angle structure in our patient favored this protein glaucoma. A permanent increase in I0P observed at the latter stages of the disease indicate that the trabecular meshwork might be damaged irreversibly by protein glaucoma.

Prostanoids and thromboxane A2 involvement in diabetic retinopathy.

Alteration in prostanoid and TXA2 production are involved in the development of diabetic microangiopathy underlying DR. Diabetic microangiopathy is characterized by abnormalities in platelet function and increased susceptibility to thrombus formation. The synthesis of excessive amounts of PGs and TXA2 by platelets obtained from diabetic patients is underlying alteration in platelet responsiveness seen in diabetes mellitus. An associated reduction in PGI2 by endothelial blood vessels results in further disruption of the homeostatic mechanism regulating the aggregatory process. However, PGI2 behaviour in different tissues, and in blood vessels of varied calibre is yet unclear. PGI2 synthesis is restored to normal on reduction of blood glucose levels. Restoration of the synthesis of both prostanoids and PGI2 to normal, might be achieved by using drugs that inhibit prostanoid and TXA2 formation as well as by controlling glucose blood levels. Affecting the imbalance of prostanoid and TXA2 seen in diabetes might be of clinical implication in prevention and treatment of DR.