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Ventricular vulnerability in diabetes and myocardial norepinephrine release
1Department of Medicine, University of Medicine and Dentistry, New Jersey Medical School, Newark 07103-2757.
The American Journal of the Medical Sciences
|October 1, 1989
Summary
Severe hyperglycemia significantly lowers the ventricular fibrillation threshold in dogs, increasing susceptibility to arrhythmias. Beta-blockers normalize this threshold, suggesting sympathetic nervous system involvement in diabetic cardiac instability.
Area of Science:
- Cardiology
- Endocrinology
- Physiology
Background:
- Previous studies indicated reduced ventricular fibrillation threshold (VFT) in mild diabetic models.
- Severe hyperglycemia's impact on VFT and sympathetic nervous system modulation remains less understood.
Purpose of the Study:
- To investigate the effect of severe hyperglycemia on VFT.
- To determine the role of the sympathetic nervous system in modulating VFT in diabetes.
Main Methods:
- Alloxan-induced diabetes in mongrel dogs (n=8) compared to controls.
- VFT measurement via electrode catheter, epinephrine infusion, and beta-blocker (esmolol) administration.
- Cardiac sympathetic activity assessed via ventricular pacing and catecholamine (norepinephrine) assay.
Main Results:
- Diabetic dogs (Group 2) showed a significantly lower VFT (27.8 ma) compared to controls (Group 1, 41.7 ma).
- Epinephrine infusion caused a greater VFT decline in diabetics; esmolol normalized the threshold.
- Diabetic dogs exhibited increased norepinephrine release from the heart during sympathetic stimulation.
Conclusions:
- Severe hyperglycemia significantly reduces VFT, increasing cardiac arrhythmia risk.
- The sympathetic nervous system plays a crucial role in the altered VFT observed in diabetes.
- Beta-blockade can mitigate the proarrhythmic effects of hyperglycemia.