sorbinil and Ischemia

sorbinil has been researched along with Ischemia* in 2 studies

Reviews

1 review(s) available for sorbinil and Ischemia

Article	Year
Somatic neurophysiology in diabetes. Basic observations and the effect of treatment. Clinical physiology (Oxford, England), 1985, Volume: 5 Suppl 5 Topics: Adolescent; Adult; Aged; Animals; Calcium; Diabetic Neuropathies; Humans; Imidazoles; Imidazolidines; Inositol; Insulin; Ischemia; Middle Aged; Neural Conduction; Perception; Peripheral Nerves; Potassium; Vibration	1985

Other Studies

1 other study(ies) available for sorbinil and Ischemia

Article	Year
Resistance of the diabetic rat nerve to ischemic inactivation. Canadian journal of physiology and pharmacology, 1985, Volume: 63, Issue:7 The resistance of the action potential to ischemic inactivation observed in diabetic patients has been reproduced in vivo in rat rendered diabetic with streptozotocin and, acutely, in normal rats given p.o. a load of glucose. The resistance phenomenon was not detected in galactosemic rats. The preservation of the action potential was reversed by the administration of insulin, but not by treatment with an aldose reductase (AR) inhibitor. The ischemic resistance is attributed to the metabolic availability of excess glucose to the nerve. AR does not appear to be involved in the phenomenon. Topics: Action Potentials; Aldehyde Reductase; Animals; Blood Glucose; Body Temperature; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Galactosemias; Glucose; Imidazoles; Imidazolidines; Insulin; Ischemia; Neural Conduction; Rats; Rats, Inbred Strains	1985

Article

Year

Resistance of the diabetic rat nerve to ischemic inactivation.

Canadian journal of physiology and pharmacology, 1985, Volume: 63, Issue:7

The resistance of the action potential to ischemic inactivation observed in diabetic patients has been reproduced in vivo in rat rendered diabetic with streptozotocin and, acutely, in normal rats given p.o. a load of glucose. The resistance phenomenon was not detected in galactosemic rats. The preservation of the action potential was reversed by the administration of insulin, but not by treatment with an aldose reductase (AR) inhibitor. The ischemic resistance is attributed to the metabolic availability of excess glucose to the nerve. AR does not appear to be involved in the phenomenon.

Topics: Action Potentials; Aldehyde Reductase; Animals; Blood Glucose; Body Temperature; Diabetes Mellitus, Experimental; Diabetic Neuropathies; Galactosemias; Glucose; Imidazoles; Imidazolidines; Insulin; Ischemia; Neural Conduction; Rats; Rats, Inbred Strains

1985