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The understanding of dry eye disease has advanced recently through increasing recognition that the etiology of the condition involves both tear evaporation and insufficient tear production, and that tear film instability and inflammation play roles in the various stages of the disease. Of significance, it has been recognized that lipid layer thickness correlates with tear film stability. The management of dry eye involves various strategies and therapeutic approaches that address one or more etiopathological components of the disease. The purpose of this review is to outline the characteristics and clinical utility of the Systane® ocular lubricants that contain hydroxypropyl-guar and one or both of the demulcents, ie, polyethylene glycol 400 and propylene glycol. Clinically, these products are safe and are indicated for the temporary relief of burning and irritation due to dryness of the eye. In particular, this review describes the formulations, mechanisms of action, and clinical utility of the newest additions to this topical ocular lubricant family, Systane Ultra® and Systane Balance®. Both of these ocular products are formulated with an intelligent delivery system and both provide symptomatic relief to patients with dry eye. However, Systane Balance is a novel formulation that contains both polymer and lipid components designed to protect the ocular surface and replenish tear film lipids simultaneously, a factor that is of particular relevance to patients who have dry eye associated with meibomian gland dysfunction.

The aim of the present study was to test the ability of the chemotherapeutic agent suramin to inhibit angiogenesis in experimental models in vitro and in vivo. In the culture of rat aortic rings on fibronectin, suramin dose-dependently inhibited vascular cell growth, achieving the maximal effect (mean - 88% versus controls, P < 0.05) at 400 microg/ml. Image analysis showed that suramin could inhibit microvessel sprouting in fibrin from rat aortic rings as evaluated by the ratio between the cellular area and the mean gray value of the sample (sprouting index); suramin at 50 microg/ml significantly reduced the sprouting index from the control value of 0.35+/-0.04 to 0.14+/-0.02 mm2/gray level (P < 0.05). Likewise, the area occupied by cells was 19.2+/-1.8 mm2 as compared with 41.8+/-4.2 mm2 in controls (P < 0.05). In the rat model of neovascularization induced in the cornea by chemical injury, suramin at 1.6 mg/eye per day reduced the length of blood vessels (0.7+/-0.1 mm as compared with 1.5+/-0.1 mm in controls, P < 0.05). In the same model the ratio between the area of blood vessels and the total area of the cornea (area fraction score) was decreased by suramin from 0.19+/-0.02 in controls to 0.03+/-0.003 (P < 0.05). Suramin given i.p. at 30 mg/ kg per day markedly inhibited the neovascularization induced in the rat mesentery by compound 48/80 or conditioned medium from cells secreting the angiogenic protein fibroblast growth factor-3 (FGF-3). The area fraction score in control rats treated with compound 48/80 was 0.31+/-0.03, and this was reduced to 0.07+/-0.01 by suramin (P < 0.05). After i.p. administration of FGF-3 the area fraction score was reduced by suramin from 0.29+/-0.03 to 0.05+/-0.01 (P < 0.05). These results provide evidence that suramin exerts inhibitory effects on angiogenesis in both in vitro and in vivo models.

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