Effects of cold-induced vasospasm in glaucoma: the role of endothelin-1.

Purpose: Vasospasm has been associated with glaucoma, but its mechanisms have not been elucidated. The present study was designed to evaluate the role of endothelin (ET)-1, a potent endogenous vasoconstrictor, in the genesis of vasospasm in glaucoma.

Methods: Our sample contained patients with open-angle glaucoma (n = 43) and subjects with normal nonglaucomatous eyes and without acral vasospasm (n = 27). After the eligibility visit, all subjects underwent a provocative cooling test, consisting of wearing for 30 minutes a head-vest cooling garment containing coolant fluid. Blood was collected before and after cooling, and plasma ET-1 was determined by immunoassay. In addition, visual fields and retinal blood flow, measured with a confocal scanning laser and Doppler flowmeter, were measured before and after cooling. Peripheral finger flow, skin temperature, and blood pressure were monitored during the experiment. A recovery visit was performed within 1 month, when visual field and retinal blood flow measurements were repeated.

Results: Baseline plasma ET-1 levels were similar between patients with glaucoma and control subjects (mean +/- SD: 2.81 +/- 1.29 and 2.56 +/- 1.36 pg/mL, respectively, P = 0.465). Patients with glaucoma, however, had a significant increase in plasma ET-1 after cooling (mean +/- SD increase of 34% +/- 52%, P = 0.001), not observed in control subjects (mean +/- SD increase of 7% +/- 43%, P = 0.750). No significant change in visual fields or retinal blood flow was observed after cooling in either group. Patients with glaucoma who had evidence of acral vasospasm, however, were more likely to show deterioration in visual fields after cooling than patients without acral vasospasm (P = 0.007).

Conclusions: Patients with glaucoma have an abnormal increase in plasma ET-1 after the body cools. It is possible that at least in some patients, increased levels of ET-1 in response to vasospastic stimuli may be involved in the pathogenesis of glaucomatous damage.