Search Results
You are looking at 1 - 1 of 1 items for
- Author: AD Cokkinos x
- Refine by access: All content x
Search for other papers by C Pantos in
Google Scholar
PubMed
Search for other papers by V Malliopoulou in
Google Scholar
PubMed
Search for other papers by I Mourouzis in
Google Scholar
PubMed
Search for other papers by K Sfakianoudis in
Google Scholar
PubMed
Search for other papers by S Tzeis in
Google Scholar
PubMed
Search for other papers by P Doumba in
Google Scholar
PubMed
Search for other papers by C Xinaris in
Google Scholar
PubMed
Search for other papers by AD Cokkinos in
Google Scholar
PubMed
Search for other papers by H Carageorgiou in
Google Scholar
PubMed
Search for other papers by DD Varonos in
Google Scholar
PubMed
Search for other papers by DV Cokkinos in
Google Scholar
PubMed
The present study investigated the response of the hypothyroid heart to ischaemia-reperfusion. Hypothyroidism was induced in Wistar rats by oral administration of propylthiouracil (0.05%) for 3 weeks (HYPO rats), while normal animals (NORM) served as controls. Isolated hearts from NORM and HYPO animals were perfused in Langendorff mode and subjected to zero-flow global ischaemia followed by reperfusion (I/R). Post-ischaemic recovery of left ventricular developed pressure was expressed as % of the initial value (LVDP%). Basal expression of protein kinase C epsilon (PKCepsilon) and PKCdelta and phosphorylation of p46 and p54 c-jun NH(2)-terminal kinases (JNKs) in response to I/R were assessed by Western blotting. LVDP% was found to be significantly higher in HYPO hearts than in NORM. At baseline, PKCepsilon expression was 1.4-fold more in HYPO than in NORM hearts, P<0.05, while PKCdelta was not changed. Furthermore, basal phospho-p54 and -p46 JNK levels were 2.2- and 2.6-fold more in HYPO than in NORM hearts, P<0.05. In response to I/R, in NORM hearts, phospho-p54 and -p46 JNK levels were 5.5- and 6.0-fold more as compared with the baseline values, P<0.05, while they were not significantly altered in HYPO hearts. HYPO hearts seem to display a phenotype of cardioprotection against ischaemia-reperfusion and this is associated with basal PKCepsilon overexpression and attenuated JNK activation after I/R.
