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

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esponsible for <strong>the</strong> failure to precondition <strong>the</strong> myocardium <strong>of</strong> diabetics. Several<br />

investigators [99,1961 including my work described in <strong>the</strong> chapter previously have<br />

demonstrated that mito KATp channels are involved in <strong>the</strong> protection <strong>of</strong> <strong>ischaemic</strong><br />

<strong>preconditioning</strong>. The findings by Smith et al [2791 that KATP channels are altered<br />

possessing a greater outward single-channel current in <strong>the</strong> ventficular myocardium <strong>of</strong><br />

diabetic rats fur<strong>the</strong>r support <strong>the</strong> above <strong>the</strong>sis. Clearly, fur<strong>the</strong>r research is needed to fully<br />

elucidate <strong>the</strong> contribution <strong>of</strong> <strong>the</strong> alteration <strong>of</strong> this channel to <strong>the</strong> failure to precondition<br />

<strong>the</strong> myocardium from diabetics.<br />

Preconditioning and <strong>the</strong> failing <strong>heart</strong><br />

LV hypertrophy and LV chamber dilation are among o<strong>the</strong>rs compensatory<br />

mechanisms <strong>of</strong> <strong>the</strong> failing <strong>heart</strong>. There is experimental evidence that <strong>the</strong> hypertrophied<br />

myocardium is at greater risk from ischaemia/reperfusion injury and it is generally<br />

believed that <strong>the</strong> failing <strong>heart</strong> is less tolerant to ischaemia/reperfusion injury. My results,<br />

however, have shown for <strong>the</strong> first time that <strong>the</strong> effects <strong>of</strong> i schaemi a/reoxygenat ion are<br />

similar in <strong>the</strong> failing and non-failing myocardium. In addition, I have demonstrated also<br />

for <strong>the</strong> first time, that <strong>the</strong> myocardium from <strong>heart</strong>s exhibiting a LVEF

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