PHYS30001 Lecture Notes - Lecture 20: Ischemia, Sodium-Calcium Exchanger, Myocyte
Document Summary
Makes ncx work in reverse mode: na out, ca in > increases ca load. Excess ca activates degradation of protein, e. g. junctophilin. 10 min: @ 50% atp, cell swelling (electrolytes building up in wrong places); rmp, arrhythmias. Reversible at this stage (stunned) - contraction stops. 2-4 days: extensive phagocytosis of myocytes, fibroblasts, connective tissue. 1 week+: thinning & dilation in infarct zone, myocyte slippage. Heartbeat stopped 10 sec = unconsciousness; stopped 5-10 min = brain death. Reinstate blood flow to heart, restore oxygen availability. But can further increase heart dysfunction and death ! Contractile dysfunction: contractions so strong, it rips myocytes apart from each other. Activated by increases in ca2+: ca binds to camkii, phosphorylates and upregulates ca2. + & na+ handling proteins (indirect action on ncx) Turbo boost to upregulation in ca e. g. for fight/flight - self regenerating system. Normal: compressing at 70mmhg, 4 times per second. Turn off solution, heart becomes ischemic, rapid cessation of contraction.
