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H Nagano, Y Nakayama, T Jomori, Y Saito, Y Tano; Effect of Kallidinogenase on a Model of Ocular Circulation Disturbance Induced By Endothelin-1 . Invest. Ophthalmol. Vis. Sci. 2002;43(13):305.
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Purpose:Our previous studies have demonstrated that kallidinogenase improves ocular circulation by increasing choroidal blood flow, and decreasing the number of leukocytes trapped in the retinal microcirculation induced by streptozotocin. The purpose of the present study was to investigate the effects of kallidinogenase on optic nerve head circulation in rabbit eyes with circulatory disorder induced by endothelin (ET-1). Methods:In an ocular circulatory disorder model induced by ET-1 (intravitreal injection of 10 microL of ET-1 at 10-6 M), optic nerve head blood flow was continuously measured via noncontact laser Doppler flowmetry. We evaluated the effects of kallidinogenase, which produces NO through kinin release, and a calcium antagonist (nicardipine). Fundus photographs were taken before and 60 minutes after drug administration in ET-1-treated rabbit eyes. Results:Intravitreal injection of ET-1 caused about 20% decrease in optic nerve head blood flow. However, this effect was significantly reduced in the kallidinogenase (1.0 International Unit/Kg of BW) group (n = 7 rabbits, p: < 0.01). The ET-1 group was more sensitive to kallidinogenase than the normal group, whereas., the normal group was more sensitive to nicardipine (20 microg/Kg of BW) than the ET-1 group. Fundus examination demonstrated optic nerve head arteriole contraction following ET-1 intravitreal injection, and arteriole expansion following administration of kallidinogenase. Conclusion:Kallidinogenase was shown to increase optic nerve head blood flow in rabbit eyes with ET-1-induced circulatory disorder.
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