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

Furthermore, Van den Hoek et al [3 16] have suggested that reactive oxygen species
released by mitochondria during a brief period of hypoxia can precondition isolated
myocytes, and Becker et al [271 have shown that PC reduces superoxide production and
prevents the impairment of state 3 mitochondrial respiration induced by ischaemia and
reperfusion. The interaction between the mito K.
N-1-p channel and free radicals is not fully
elucidated, however, several studies have demonstrated
that free radicals open sarc K %-11,
channels[20,303] and thus, it is possible that such an interaction may also occur within
mitochondria [ 173,316]. The mechanism of how this ultimately stimulates mitochondrial
respiration and consequently the cytoprotective effect is much less clear and warrants
further research.
A potential limitation of this study was the use of atnal tissue as opposed
ventricular myocardium and therefore any extrapolation must be conducted with caution,
however, Yellon and colleagues have suggested that preconditioning exerts identical
protection in both tissues [52,2821. Undoubtedly, as mentioned previously, K. %,,,
channels are present in both atrium and ventncle j 1321 , although their density in both
tissues is unknown. As mentioned previously also, another possible limitation might be
that fight atrial appendages were obtained ftom patients subjected to various medical
treatments (e. g. nitrates, O-blockers, calcium antagonists) and that in principle may have
influenced ischaernia/reperfusion
injury and the protection Induced by preconditioning.
However, it should be emphasized, that all medication was stopped the daV betbre
surgery when specimens were taken for the study and that significant effect of the
medication was unlikely since all preparations responded to ischemia/reperfusion with a
similar degree of injury and preconditioning was protective in all instances when applied.
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