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Effect of an aldose reductase inhibitor, SNK‐860, on deficits in the electroretinogram of diabetic rats
Author(s) -
Hotta N,
Koh N,
Sakakibara F,
Nakamura J,
Hamada Y,
Naruse K,
Sasaki H,
Mizuno K,
Matsubara A,
Kakuta H,
et al.
Publication year - 1995
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1995.sp003909
Subject(s) - aldose reductase , sorbitol , endocrinology , electroretinography , medicine , retinal , polyol pathway , diabetes mellitus , aldose reductase inhibitor , erg , fructose , chemistry , retinopathy , streptozotocin , glycation , ophthalmology , biochemistry
To determine the effect of an aldose reductase inhibitor, SNK‐860, on the worsening of the electroretinogram (ERG) during a diabetic state, rats with streptozotocin‐induced diabetes were administered SNK‐860 (1 or 4 mg kg‐1 orally) daily for 4 weeks. The effectiveness of SNK‐860 in prolonging the peak latencies of oscillatory potentials in the b‐wave of the electroretinogram of diabetic rats varied between these different waveform components (designated O1, O2 and O3). SNK‐860 (4 mg kg‐1 day‐1) either completely or partially prevented the prolonged peak latencies at O1 and sigma(O1 + O2 + O3). The drug failed to shorten the latency of the O2 and O3 components, and produced only a modest reduction in retinal levels of sorbitol and fructose, with no increase in myo‐inositol. There was a significant correlation between the state of the ERG (components O1 and sigma(O1 + O2 + O3)) and the retinal levels of sorbitol and fructose (P < 0.01), but not of myo‐inositol. It is concluded that a better understanding of the mechanism by which SNK‐860 acts may provide new insight into the pathogenesis of hyperglycaemic retinal dysfunction and help to establish effective therapy for diabetic retinopathy.