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Ischemic preconditioning fails to confer additional protection against ischemia-reperfusion injury in the hypothyroid rat heart

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There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfus ion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts ( P
Library of the Czech Academy of Sciences
Title: Ischemic preconditioning fails to confer additional protection against ischemia-reperfusion injury in the hypothyroid rat heart
Description:
There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states.
The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction.
Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.
05 %).
Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfus ion.
A preconditioning protocol (PC) was also applied prior to ischemia.
HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release.
Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.
0 and 3.
0 fold lower in HYPO as compared to normal hearts ( P.

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