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

Title:

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

Creator:

Mourouzis, I., Dimopoulos, A., Saranteas, T., Tsinarakis, N., Livadarou, E., Spanou, D., Kokkinos, A. D., Xinaris, C., Pantos, C., and Cokkinos, D. V.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:ad3532b6-ea79-47fc-a5ce-33a56313fdf7
uuid:ad3532b6-ea79-47fc-a5ce-33a56313fdf7

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, ischemická choroba srdeční, hormony štítné žlázy, hypotyreóza, physiology, ischemic heart disease, thyroid hormones, hypothyreosis, ischemic preconditioning, JNKs, p38 MAPK, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print

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<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts ( P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts., I. Mourouzis ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2009 Volume:58 | Number:1

Harvested from:

CDK

Metadata only:

false