ischaemic preconditioning of the human heart. - Leicester Research ...

stunning) and electrical events [33,119,199,2001 that may place in jeopardy the life of the
patient. The contribution of ischaernia and of reperfusion to tissue injury has been the
subject of exhaustive debate for more than 3 decades.
Reperfusion at an early stage causes massive cell swelling with the formation of
sarcolemmal blebs, contraction band necrosis with rupture of cell membranes [ 148,1521.
This is also linked with calcium accumulation in the mitochondrial granules and release
of cytosolic enzymes into the extracellular space[ 185]. Severe cellular changes have also
been described following reperfusion late in the reversible phase of ischaernia [ 156].
Irreversible ischaernia seems to render cells, ion and energy depleted with complete
disorgamsation of the enzymatic systems causing mechanical and osmotic fragility of the
myocytes [25 1 ]. Due to the loss of ionic homeostasis, once reperfusion occurs, the final
blow is then delivered. the myocytes rupture with loss of integrity of the cell membrane.
Needless to say that the role played by reperfusion in either accelerating the death of
severely ischaernic myocytes, or actually causing their death remains unresolved and can
only add to the complexity of the situation.
The consequences of ischaemia-reperfusion may be local, but tissue destruction may also
occur at sites distant from critical injury. The "no-reflow" phenomenon associated with
reperfusion may also be considered a form of reperfusion induced injury [371. In this
patho-physiological process progressive microcirculatory obstruction due to clumping of
blood cells may lead to failure to establish coronary blood flow to the ischaemic regions
( 185]. The phenomenon remains poorly understood, but microscopic examination of the
infarcted regions which suffered relatively short periods of ischaernia showed sludged red
and white cells and oederna of the endothelial cell lining of the microcirculation [ 1851.
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