Effect of maturation on the resistance of rat hearts against ischemia. Study of potential molecular mechanisms

Title:

Effect of maturation on the resistance of rat hearts against ischemia. Study of potential molecular mechanisms

Creator:

Grecsová, L., Farkašová, V., Gáblovský, I., Khandelwal, V. K. M., Iveta Bernátová, Tatarková, Z., Peter Kaplán, and Ravingerová, T.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:f5c69e94-5ba7-4906-bc52-941bbe1c382a
uuid:f5c69e94-5ba7-4906-bc52-941bbe1c382a
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, stárnutí, aging, myocardial ischemia, preconditioning, survival cascades, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

a1_Reduced tolerance to ischemia/reperfusion (IR) injury has been shown in elder human and animal hearts, however, the onset of this unfavorable phenotype and cellular mechanisms behind remain unknown. Moreover, aging may interfere with the mechanisms of innate cardioprotection (preconditioning, PC) and cause defects in protective cell signaling. We studied the changes in myocardial function and response to ischemia, as well as selected proteins involved in “pro-survival” pathways in the hearts from juvenile (1.5 months), younger adult (3 months) and mature adult (6 months) male Wistar rats. In Langendorffperfused hearts exposed to 30-min ischemia/2-h reperfusion with or without prior PC (one cycle of 5-min ischemia/5-min reperfusion), we measured occurrence of reperfusion-induced arrhythmias, recovery of contractile function (left ventricular developed pressure, LVDP, in % of pre-ischemic values), and size of infarction (IS, in % of area at risk size, TTC staining and computerized planimetry). In parallel groups, LV tissue was sampled for the detection of protein levels (WB) of Akt kinase (an effector of PI3-kinase), phosphorylated (activated) Akt (p-Akt), its target endothelial NO synthase (eNOS) and protein kinase Cε (PKCε) as components of “pro-survival” cascades. Maturation did not affect heart function, however, it impaired cardiac response to lethal IR injury (increased IS) and promoted arrhythmogenesis. PC reduced the occurrence of malignant arrhythmias, IS and improved LVDP recovery in the younger animals, while its efficacy was attenuated in the mature adults. Loss of PC protection was associated with age-dependent reduced Akt phosphorylation and levels of eNOS and PKCε in the hearts of mature animals compared with the younger ones, as well as with a failure of PC to upregulate these proteins., a2_Agingrelated alterations in myocardial response to ischemia may be caused by dysfunction of proteins involved in protective cell signaling that may occur already during the process of maturation., L. Griecsová, V. Farkašová, I. Gáblovský, V. K. M. Khandelwal, I. Bernátová, Z. Tatarková, P. Kaplan, T. Ravingerová., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:Suppl 5

Harvested from:

CDK

Metadata only:

false