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 at
-120 days of age and twenty rats were made diabetic by intraperitoneal
injections of alloxan 150 my / kg . Diabetic rats were received daily iryec-
Lions of protamine zinc insulin arid were maintained in mildly hyperglycaemic
state (200- 250 mg / dl). The remaining 10 rats were used as
matched controls and were injected with the solvent. Sbc diabetic rats
were excluded from this study (2 rats were died after alloxan injection
and other 4 diabetic rats due to uncontrolled their blood glucose levels).
Epinephrine and norepinephrine were estimated in right adrenal gland
and also in 5 minute perfus ate fractions from left adrenal gland by using
the retrograde perfusion technique of Wakade (1981), after 4 months of
appearance of IDDM in diabetic rats
There was non signcant difference between diabetic rats and
matched controls with respect to epinephrine and norepinephrine contents
of right adrenal gland. There was a significant redaction in secretions
of epinephrine and norepinephrine in 5-minute perfus ate fractions of
left adrenal gland in diabetic rats compared with matched controls. In
conclusion, decreased secretion of catecholamines from adrenal medulla
in a chronic diabetes is not due to decreased synthesis or storage abnormalities
but may be due to chromatin cell defect and or degeneration
within the presynaptic endings of the greater splanchnic nerves. |
