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Streptozotocin-induced diabetes in rats resulted in depressed atrial function, enhanced right ventricular function with calcium supersensitivity, and a 36% decrease in beta-adrenoceptor Bmax at 4 weeks.
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In a rat model of STZ-induced diabetes, early cardiac changes at 4 weeks include depressed atrial pacemaker function and enhanced ventricular function associated with altered calcium utilization.
Responses in cardiac tissue isolated from streptozotocin (STZ)-treated and age-matched control rats to isoproterenol (ISO) and calcium were studied. 4 weeks after STZ, atrial function was found to be depressed, whereas right ventricular function was enhanced. Neither tissue exhibited an alteration in sensitivity to ISO. In contrast, while sensitivity to calcium was found to be unaltered in atrial tissue, supersensitivity to calcium was observed in ventricles after STZ treatment. beta-Adrenoceptor number determination revealed a 36% decrease in Bmax with no change in affinity after STZ treatment. These results suggest that 4 weeks after STZ treatment pacemaker function is depressed, while enhancement in ventricular function is associated with an alteration in calcium utilization.
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Ramanadham et al. (2008) studied Experimentally-Induced Diabetes. Streptozotocin (STZ) treatment vs. Age-matched control rats was evaluated on Cardiac tissue response to isoproterenol (ISO) and calcium, and beta-Adrenoceptor number (36% decrease in Bmax). Streptozotocin-induced diabetes in rats resulted in depressed atrial function, enhanced right ventricular function with calcium supersensitivity, and a 36% decrease in beta-adrenoceptor Bmax at 4 weeks.
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