Resistance of the diabetic rat nerve to ischemic inactivation.
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.
D000200:Action Potentials / Q000187:drug effects; D000449:Aldehyde Reductase / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001831:Body Temperature; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000503:physiopathology*; D005693:Galactosemias / Q000503:physiopathology; D005947:Glucose / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D048289:Imidazolidines; D007328:Insulin / Q000494:pharmacology; D007511:Ischemia / Q000503:physiopathology; D009431:Neural Conduction / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D007093:Imidazoles; D048289:Imidazolidines; D007328:Insulin; D000449:Aldehyde Reductase; C026411:sorbinil; D005947:Glucose