The present study was designed to demonstrate a possibl explanation for decreased catecholamines secretion in chronic diabetic rats. Thirty male albino rats were included in this study. The rats were received cd —120 days Of age and twenty rats were made diabetic by intraperitoneål üüections of alloxan 150 rag //kg . Diabetic rats were received daily ilVec-lions of protamine zinc insulin and were maintained in mildly hypergly-
caemic state (200 - 250 mg // HI)). The remaining 10 rats Il-cere used as matched controls and were injected LL'ffh the solvent. .SLZ diabetic 7T1ts were excludedf,rom this study (2 rats uyere died after alloxan irüection and other 4 diabetic :r-æs due to uncontrolled their blood glucose levels). Epinephrine and norepinephrine Were estimated in right adrenal gland and also in 5 minute perfusatefractionsfrom left adrenal gland by using
the retrograde perfusion technique of Walcade (1981), After 4 monlhs appearance ofIDDM in diabetic rats
There Was non significant difference between diabetic rats and matched controls with respect to epinephrine and norepinephrine con-tents of fight adrenal gland. There was a significant reduction in secre-tions of epinephrine and norepinephrine in 5-minute perfusate fractions of left adrenal gland in diabetic rats compared with matched controls. In conclusion, decreased secretion off catecholamines from adrenål medulla in a chronic diabetes is not due to decreased synthesis or storage abnor-malties but rnay be due to chrornqffin cell defect and or degeneration Within the presynaptic endings the greater splanchnic nerves. |
