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ABSTRACT
Acute coronary occlusion, causing a heart attack, is best treated by prompt intervention and re-opening of the blocked artery. Such acute reperfusion, although saving many threatened heart cells from death, also paradoxically causes lethal reperfusion injury due to calcium overload in the mitochondria. There are protective molecular rescue paths that lessen the extent of such reperfusion injury. We discuss the evolution of these pathways during primitive times when heart attacks were rare. We believe that these paths evolved to counter acute stress situations in our ancestors when stimulated by intense physical effort, environmental conditions or hunting hazards, often accompanied by blood loss and hypotension. To test our hypothesis, we developed an underperfused model of acute heart failure with low perfusion pressure in the isolated rat heart to simulate the hypotensive response. We also increased the contents of free fatty acids (FFA) in the perfusate to supraphysiological levels to mimic the rapid fear-driven elevation of FFA in the hunter. FFA have a deleterious effect on a failing heart while glucose is proposed as protecting the acutely failing heart. We found that glucose given to the acutely failing heart improved the functional recovery by increasing the heart rate and contractility. We hypothesise that similar metabolic principles may protect against acute heart failure as against regional ischemia with lethal injury. We further suggest that the requirement for protection against acute stress in primitive persons led to the evolution of the molecular pathways now known to protect from lethal reperfusion injury.