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

phosphates
and its influence on hydrogen ion and lactate accumulation, and subsequently
calcium accumulation, has been vigorously tested[ 22 7,229,2861 using models of
i schaemia/reperfusion.
Myocardial infarction is the clinical expression of irreversible myocardial ischaernic
injury. When ischaemia persists for increasing lengths of time cell death will inevitably
occur, becoming clinically manifest as a myocardial infarction (necrosis). In this new
setting of ischaernic injury the myocytes fail to contract, or to generate an action
potential, and energy production ceases completely [153]. This may be associated with
the clinical consequences
of myocardial infarction which include chest pain, hypotension,
arrhythmias, and pulmonary oedema. Myocardial infarction also leads to specific
electrocardiographic and serum biochemical changes that can be detected within minutes-
hours of its onset. The return of blood to the ischaemic heart may have an important role
in the development of irreversible injury and this is discussed in more detail below.
1.3 Reperfusion
In experiments performed on animals, early restoration of coronary blood flow has
been shown to limit the size of the infarct [129,149,1561. In man this may be
accomplished by the use of thrombolytic therapy, percutaneous transluminal coronary
angioplasty (PTCA) or by emergency CABG surgery.
Although garly reperfusion of the ischaemic myocardium is probably the most
important intervention in limiting the size of the evolving myocardial infarction, it may
have serious consequences and the damage associated with this period is known as
"reperfusion injury" [129]. Reperfusion injury can be manifested by contractile (eg.
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