ici-105552 and Diabetic-Neuropathies

ici-105552 has been researched along with Diabetic-Neuropathies* in 2 studies

Other Studies

2 other study(ies) available for ici-105552 and Diabetic-Neuropathies

Article	Year
Prevention of defects of axonal transport and nerve conduction velocity by oral administration of myo-inositol or an aldose reductase inhibitor in streptozotocin-diabetic rats. Diabetologia, 1983, Volume: 25, Issue:5 The effects of orally-administered myo-inositol have been compared with those of an aldose reductase inhibitor on acute neurological defects in experimentally diabetic rats. Three groups of streptozotocin-treated diabetic rats (50 mg/kg, IP) together with three groups of age-matched controls (saline, IP) were compared. One pair of groups (control and diabetic) were untreated for 3 weeks, another pair of groups received daily oral myo-inositol (667 mg/kg) and the third pair received an aldose reductase inhibitor (ICI 105 552; 50 mg . kg-1, day-1, orally). The untreated diabetic group showed statistically significant deficits in accumulation, proximal to 24 h sciatic nerve constrictions, of choline acetyltransferase activity by comparison with untreated controls (2.8 +/- 0.4 versus 5.1 +/- 0.4 nmol acetylcholine . h-1 . nerve-1; p less than 0.001). The untreated diabetic rats also showed a fall in motor nerve conduction velocity of 6.2 +/- 0.7 m/s which was statistically significant (p less than 0.001). Treatment of the diabetic group with myo-inositol prevented the development of both defects of axonal transport and conduction velocity; both measurements were similar to those of the myo-inositol treated control rats. Likewise the diabetic rats which received aldose reductase inhibitor showed prevention of both defects. Nerves from untreated diabetic rats showed marked sorbitol accumulation and a statistically significant reduction in myo-inositol content by comparison with the untreated controls (sorbitol, 1.56 +/- 0.22 versus 0.8 +/- 0.01 and myo-inositol, 1.47 +/- 0.10 versus 2.3 +/- 0.10 nmol/mg; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS) Topics: Aldehyde Reductase; Animals; Axonal Transport; Blood Glucose; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Inositol; Male; Motor Neurons; Neural Conduction; Quinolines; Quinolones; Rats; Rats, Inbred Strains; Sciatic Nerve; Sorbitol; Streptozocin; Sugar Alcohol Dehydrogenases	1983
Reversal, by treatment with an aldose reductase inhibitor, of impaired axonal transport and motor nerve conduction velocity in experimental diabetes mellitus. Neuroscience letters, 1982, Aug-16, Volume: 31, Issue:2 Topics: Aldehyde Reductase; Animals; Axonal Transport; Choline O-Acetyltransferase; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Male; Motor Neurons; Neural Conduction; Quinolines; Quinolones; Rats	1982

Article

Year

Prevention of defects of axonal transport and nerve conduction velocity by oral administration of myo-inositol or an aldose reductase inhibitor in streptozotocin-diabetic rats.

Diabetologia, 1983, Volume: 25, Issue:5

The effects of orally-administered myo-inositol have been compared with those of an aldose reductase inhibitor on acute neurological defects in experimentally diabetic rats. Three groups of streptozotocin-treated diabetic rats (50 mg/kg, IP) together with three groups of age-matched controls (saline, IP) were compared. One pair of groups (control and diabetic) were untreated for 3 weeks, another pair of groups received daily oral myo-inositol (667 mg/kg) and the third pair received an aldose reductase inhibitor (ICI 105 552; 50 mg . kg-1, day-1, orally). The untreated diabetic group showed statistically significant deficits in accumulation, proximal to 24 h sciatic nerve constrictions, of choline acetyltransferase activity by comparison with untreated controls (2.8 +/- 0.4 versus 5.1 +/- 0.4 nmol acetylcholine . h-1 . nerve-1; p less than 0.001). The untreated diabetic rats also showed a fall in motor nerve conduction velocity of 6.2 +/- 0.7 m/s which was statistically significant (p less than 0.001). Treatment of the diabetic group with myo-inositol prevented the development of both defects of axonal transport and conduction velocity; both measurements were similar to those of the myo-inositol treated control rats. Likewise the diabetic rats which received aldose reductase inhibitor showed prevention of both defects. Nerves from untreated diabetic rats showed marked sorbitol accumulation and a statistically significant reduction in myo-inositol content by comparison with the untreated controls (sorbitol, 1.56 +/- 0.22 versus 0.8 +/- 0.01 and myo-inositol, 1.47 +/- 0.10 versus 2.3 +/- 0.10 nmol/mg; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aldehyde Reductase; Animals; Axonal Transport; Blood Glucose; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Inositol; Male; Motor Neurons; Neural Conduction; Quinolines; Quinolones; Rats; Rats, Inbred Strains; Sciatic Nerve; Sorbitol; Streptozocin; Sugar Alcohol Dehydrogenases

1983

Reversal, by treatment with an aldose reductase inhibitor, of impaired axonal transport and motor nerve conduction velocity in experimental diabetes mellitus.

Neuroscience letters, 1982, Aug-16, Volume: 31, Issue:2

Topics: Aldehyde Reductase; Animals; Axonal Transport; Choline O-Acetyltransferase; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Male; Motor Neurons; Neural Conduction; Quinolines; Quinolones; Rats

1982