be230cLecture3Ischemia

Reentry can even develop in part aided by reduced gap

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Unformatted text preview: tochondrial oxidaDve metabolism leads to a fall in ATP •  Further, diversion of pyruvate into lacDc acid formaDon causes intracellular acidosis that impairs troponin C binding of Ca2+ •  AlteraDons in acDon potenDal reduce contracDlity and make heart prone to arrhythmia (to be covered in subsequent lectures) •  •  •  •  •  Effects of Ischemia on the Cardiac AcDon PotenDal Reduced membrane potenDal (less negaDve) due to less Na/K ATPase impairs phase 0 of AP (fewer Na channels open) Increased KATP channel acDvaDon (less ATP) reduces phase 2 duraDon Increased intracellular [Na+] (because of reduced Na/K ATPase acDvity and intracellular acidosis sDmulates Na+/H+ exchanger) inhibits Na+/Ca2+ exchanger, hence increases intracellular [Ca2+] SR Ca2+ overload due partly to above, and to compensatory, beta adrenergic sympatheDc ­driven increase in Ca2+ influx Overloaded SR Ca2+ store may release Ca2+ during diastole, in turn sDmulaDng an influx of Na+ due to sDmulaDon of the Na+/Ca2+ exchanger, generaDng an a\er depolarizaDon that might trigger an extra beat. Re ­entry can even develop, in part aided by reduced gap juncDonal communicaDon between cardiomy...
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This document was uploaded on 04/09/2014.

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