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

contractile dysfunction was initially proposed as the underlying mechanism of ischaernic
preconditioning protection, since reduced contractile activity may lead to energy
conservation [34].
The lack of temporal relation between the induction and elimination of stunning, and of
ischaemic preconditioning has suggested that the two processes are not inter-dependent.
Thus, it has been shown that prolonging the reperfusion part of the ischaemic
preconditioning stimulus results in loss of protection prior to elimination of myocardial
stunning [225]. Also the time course of stunning is much more prolonged than that of
preconditioning and can persist for hours to days [341, also the degree of stunning does
not correlate with the limitation of infarct size [3261.
Since in the setting of stunning myocardial contractility is depressed but is expected to
undergo full recovery, myocardial contractility could be improved to pre-ischaemic
levels. The use of inotropes such as adrenaline and isoprenaline is a potent method of
improving contractility of the stunned myocardium. The potency of these P
adrenoreceptor agonists has been established both experimentally and clinically. In
animal experiments Ic
isoprenaline, for example, has been used to the so called inotropi
reserve of stunned myocardium, which is probably independent of the size and extent of
myocardial infarction/necrosis [271-272].
1.6.3 Heat Shock Proteins -
Increasing whole body temperature causes the heart to
become more resistant to subsequent ischaernla 1344]. This increased myocardiai
tolerance has been associated with an increase in heat shock protein synthesis (a family of
proteins synthesized upon stress, to protect from stress) [68-69,3441. Ischaernia itself can
also cause an increase in the synthesis of these stress proteins, in particular the 72
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