Abstract
To elucidate the abnormality of cardiac vagal control in streptozotocin-induced type
1 diabetic rats, we measured left ventricular myocardial interstitial acetylcholine
(ACh) release in response to α2-adrenergic stimulation as an index of in vivo cardiac vagal nerve activity. A cardiac
microdialysis technique was applied to the rat left ventricle, and the effect of α2-adrenergic stimulation by intravenous medetomidine (100 μg/kg) on myocardial interstitial
ACh levels was examined in anesthetized diabetic rats (4–6 weeks after intraperitoneal
streptozotocin) and age-matched control rats (protocol 1). The effect of electrical
vagal nerve stimulation on ACh levels was also examined in separate rats (protocol
2). In protocol 1, medetomidine increased the ACh levels in control (from 1.76 ± 0.65
to 3.13 ± 1.41 nM, P < 0.05, n = 7) but not in diabetic rats (from 2.01 ± 0.47 to 1.62 ± 0.34 nM, not significant,
n = 7). In protocol 2, electrical vagal nerve stimulation at 20 Hz significantly increased
the ACh levels in both control (from 1.49 ± 0.26 to 6.39 ± 1.81 nM, P < 0.001, n = 6) and diabetic rats (from 1.77 ± 0.54 to 6.98 ± 1.38 nM, P < 0.001, n = 6). In
conclusion, medetomidine-induced central vagal activation was impaired in diabetic
rats, whereas peripheral cardiac vagal control of ACh release was preserved. The impairment
of central vagal activation may lead to relative sympathetic predominance and promote
cardiovascular complications in diabetes.
Keywords
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Article info
Publication history
Published online: September 07, 2018
Accepted:
September 6,
2018
Received in revised form:
August 6,
2018
Received:
June 8,
2018
Identification
Copyright
© 2018 Elsevier B.V. All rights reserved.