Literature DB >> 10672450

Effects of diabetic cardiomyopathy on regional electrophysiologic characteristics of rat ventricle.

O Casis1, M Gallego, M Iriarte, J A Sánchez-Chapula.   

Abstract

AIMS/HYPOTHESIS: To identify the possible causes of the lengthening of the action potential duration described in patients affected by diabetes mellitus.
METHODS: We studied the effects of streptozotocin-induced diabetes on the current density of the repolarising potassium currents It(o), IK, Iss and IK1 in enzymatically isolated myocytes from three different regions of rat heart: total right ventricle, subepicardium at the apex of the left ventricle and subendocardium at the base of the left ventricle.
RESULTS: No changes in IK1 were found due to diabetes, but there was a uniform decrease in It(o) (50%) and Iss (40%) current densities in the three regions. In contrast, IK diminished unevenly, with the greatest decrease in the subendocardium at the base of the left ventricle (48%), followed by the subepicardium at the apex of the left ventricle (32%) and right ventricle (10%). CONCLUSION/
INTERPRETATION: These findings suggest the existence of regional differences in ion channel expression associated with diabetes. The decrease of these repolarising currents could account for the lengthening of action potential and the consequent change in the Q-T interval of the ECG observed in diabetic rats.

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Year:  2000        PMID: 10672450     DOI: 10.1007/s001250050013

Source DB:  PubMed          Journal:  Diabetologia        ISSN: 0012-186X            Impact factor:   10.122


  19 in total

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5.  Endothelin-1 receptor blockade prevented the electrophysiological dysfunction in cardiac myocytes of streptozotocin-induced diabetic rats.

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9.  Altered gene expression may underlie prolonged duration of the QT interval and ventricular action potential in streptozotocin-induced diabetic rat heart.

Authors:  F C Howarth; M Jacobson; M A Qureshi; M Shafiullah; R S Hameed; E Zilahi; A Al Haj; N Nowotny; E Adeghate
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10.  A mathematical model of the electrophysiological alterations in rat ventricular myocytes in type-I diabetes.

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