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

to multiple cycles [57,224] of ischaerma and reperfusion. There is no evidence to date
investigating the optimal preconditioning protocol in man, but it may be possible that the
optimal ischaernic preconditioning protocol depends on the species studied and the model
used
Ischaernic preconditioning has been shown to cause specific and favourable metabolic
changes in the myocardium during the prolonged ischaemic insult. These include
preservation of adenosine triphosphate (ATP) [226], reduced lactate production
j 11,167,226,2871 and decreased intra-myocardial acidosis [IIJ. These findings have been
confirmed in various species [88,1501, and have been used in elucidating preconditioning
in man [3]. Preconditioning has been shown to delay cell death, but does not completely
abolish it. It has been shown that extending the ischaemic insult will eventually
overwhelm preconditioning with loss of protection [2241. Ischaemic preconditioning has
now been shown to protect the heart against infarction, reperfusion-induced arrhythmias,
contractile dysfunction and ischaernic contracture [ 11,56,224,277].
There appears to be a bimodal phase to the cardioprotective nature of this phenomenon.
There is an early phase (described by many investigators as classical) although very
potent in terms of protection is short lived and decreases with time, lasting for 1-2 hours
in most species [ 189,321 J. Recently there has been evidence to suggest that there may be
the reappearance of a delayed protective effect 24 hours later (second window or delayed
protection) [177,201,291,323]. This delayed effect has also been shown to last for 72
hours [24]. There is no evidence to date that this delayed phase exists in man.
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