Document Detail


Cardiovascular autonomic regulation in Non-Obese Diabetic (NOD) mice.
MedLine Citation:
PMID:  18166503     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Non-Obese Diabetic (NOD) mice show profound pathomorphological changes in sympathetic ganglia during the development of type 1 diabetes mellitus. We tested the hypothesis that NOD mice represent an experimental model to investigate cardiovascular changes seen in humans with diabetic autonomic neuropathy. Blood glucose (BG) levels were measured once a week. Diabetes mellitus was diagnosed as BG levels exceeded 250 mg/dl twice. NOD mice that did not become diabetic served as control group. Blood pressure (BP) and heart rate (HR) were monitored by telemetry and baroreflex sensitivity (BRS) was calculated with the sequence method or with cross spectral analysis. The measurements were obtained before onset of diabetes and during the 4th week of diabetes. The onset of diabetes was accompanied by a continuous decline in HR (615+/-14 vs. 498+/-23 bpm), whereas BP values remained stable (108+/-2 vs. 111+/-2 mm Hg). The circadian HR rhythm increased in diabetic NOD mice. BRS was higher in diabetic NOD mice than in controls. Atropine reduced BRS more profoundly in diabetic mice compared to non-diabetic mice. Despite pathomorphological similarities of the diabetic autonomic neuropathy between patients with diabetes and diabetic NOD mice, the changes in blood pressure regulation are different. In conclusion the use of diabetic NOD mice as a functional model for human diabetes may be questioned.
Authors:
Volkmar Gross; Jens Tank; Hans-Joachim Partke; Ralph Plehm; André Diedrich; Andrey C da Costa Goncalves; Friedrich C Luft; Jens Jordan
Related Documents :
17478003 - Immunological aspects of 'fulminant type 1 diabetes'.
18431243 - Cd4+ t cells are sufficient to elicit allograft rejection and major histocompatibility ...
21593293 - Retinal vascular geometry predicts incident retinopathy in young people with type 1 dia...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-12-31
Journal Detail:
Title:  Autonomic neuroscience : basic & clinical     Volume:  138     ISSN:  1566-0702     ISO Abbreviation:  Auton Neurosci     Publication Date:  2008 Feb 
Date Detail:
Created Date:  2008-01-21     Completed Date:  2008-04-11     Revised Date:  2009-08-12    
Medline Journal Info:
Nlm Unique ID:  100909359     Medline TA:  Auton Neurosci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  108-13     Citation Subset:  IM    
Affiliation:
Max Delbrück Center for Molecular Medicine, Berlin, Germany. vgross@mdc-berlin.de
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adrenergic beta-Antagonists / pharmacology
Animals
Arrhythmias, Cardiac / etiology,  physiopathology*
Autonomic Nervous System / physiopathology*
Autonomic Nervous System Diseases / etiology,  physiopathology*
Baroreflex / drug effects,  physiology
Blood Glucose / physiology
Blood Pressure / drug effects,  physiology
Bradycardia / etiology,  physiopathology
Chronobiology Disorders / etiology,  physiopathology
Diabetic Neuropathies / physiopathology*
Disease Models, Animal
Female
Ganglia, Sympathetic / physiopathology
Heart / drug effects,  innervation*,  physiopathology*
Heart Rate / drug effects,  physiology
Mice
Mice, Inbred NOD
Muscarinic Antagonists / pharmacology
Reproducibility of Results
Telemetry
Chemical
Reg. No./Substance:
0/Adrenergic beta-Antagonists; 0/Blood Glucose; 0/Muscarinic Antagonists

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Evaluation of preprocessing techniques for chief complaint classification.
Next Document:  Independence of exercise-induced diaphragmatic fatigue from ventilatory demands.