TY - JOUR
T1 - Delayed afterdepolarizations and triggered activity in ventricular muscle from rats with streptozotocin-induced diabetes
AU - Nordin, C.
AU - Gilat, E.
AU - Aronson, R. S.
PY - 1985
Y1 - 1985
N2 - Previous studies have shown that myocardium of the diabetic rat has impaired myoplasmic calcium metabolism. Delayed afterdepolarizations and triggered activity are potentiated by conditions believed to increase intracellular calcium concentration therefore, we performed this study to investigate the possibility that myocardium of the diabetic rat is more susceptible than normal tissue to develop afterdepolarizations and triggered activity. We used standard microelectrode techniques to record the electrical activity of papillary muscles from hearts of control rats and rats made diabetic with streptozotocin. We compared the response of control and diabetic preparations to conditions presumed to create progressively more severe degrees of myoplasmic calcium loading, viz. perfusion with solutions containing ouabain (5 x 10-5 M) and increasing concentrations of calcium (2.4, 4.8, 7.2, and 9.6 mM). Our results showed the following. (1) Ventricular muscle from diabetic rats was more prone than normal myocardium to develop delayed afterdepolarizations and triggered activity under conditions believed to cause myoplasmic calcium overload. (2) The external calcium concentration correlated with the incidence but not the magnitude or coupling interval of the delayed afterdepolarizations in fibers of diabetic rats. (3) The action potentials in fibers of diabetic rats decreased markedly in duration after exposure to ouabain, whereas normal action potentials were not affected significantly; as external calcium was increased with ouabain still present, the action potential duration in diabetic fibers decreased slightly more, whereas the action potential duration in normal fibers did not change significantly. These results suggest that normal rat myocardium is resistant to developing myoplasmic calcium overload, whereas myocardium from diabetic rat is susceptible to calcium loading, at least as measured by development of afterdepolarizations.
AB - Previous studies have shown that myocardium of the diabetic rat has impaired myoplasmic calcium metabolism. Delayed afterdepolarizations and triggered activity are potentiated by conditions believed to increase intracellular calcium concentration therefore, we performed this study to investigate the possibility that myocardium of the diabetic rat is more susceptible than normal tissue to develop afterdepolarizations and triggered activity. We used standard microelectrode techniques to record the electrical activity of papillary muscles from hearts of control rats and rats made diabetic with streptozotocin. We compared the response of control and diabetic preparations to conditions presumed to create progressively more severe degrees of myoplasmic calcium loading, viz. perfusion with solutions containing ouabain (5 x 10-5 M) and increasing concentrations of calcium (2.4, 4.8, 7.2, and 9.6 mM). Our results showed the following. (1) Ventricular muscle from diabetic rats was more prone than normal myocardium to develop delayed afterdepolarizations and triggered activity under conditions believed to cause myoplasmic calcium overload. (2) The external calcium concentration correlated with the incidence but not the magnitude or coupling interval of the delayed afterdepolarizations in fibers of diabetic rats. (3) The action potentials in fibers of diabetic rats decreased markedly in duration after exposure to ouabain, whereas normal action potentials were not affected significantly; as external calcium was increased with ouabain still present, the action potential duration in diabetic fibers decreased slightly more, whereas the action potential duration in normal fibers did not change significantly. These results suggest that normal rat myocardium is resistant to developing myoplasmic calcium overload, whereas myocardium from diabetic rat is susceptible to calcium loading, at least as measured by development of afterdepolarizations.
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U2 - 10.1161/01.RES.57.1.28
DO - 10.1161/01.RES.57.1.28
M3 - Article
C2 - 4006103
AN - SCOPUS:0021972402
SN - 0009-7330
VL - 57
SP - 28
EP - 34
JO - Circulation Research
JF - Circulation Research
IS - 1
ER -
