scholarly journals Intrinsic remote conditioning of the myocardium as a comprehensive cardiac response to ischemia and reperfusion

Oncotarget ◽  
2017 ◽  
Vol 8 (40) ◽  
pp. 67227-67240 ◽  
Author(s):  
Noemi Pavo ◽  
Dominika Lukovic ◽  
Katrin Zlabinger ◽  
David Lorant ◽  
Georg Goliasch ◽  
...  
2019 ◽  
Vol 125 (Suppl_1) ◽  
Author(s):  
Marco Piccoli ◽  
Maria Elena Canali ◽  
Andrea Ghiroldi ◽  
Federica Cirillo ◽  
Luigi Anastasia

1987 ◽  
Vol 65 (2) ◽  
pp. 201-209 ◽  
Author(s):  
Morris Karmazyn ◽  
Magda Horackova ◽  
Mary G. Murphy

Three-week-old male and female rats were placed either on standard rat chow or chow supplemented with 10% cod liver oil for 12 weeks. Animals fed cod liver oil demonstrated reduced body weights. Cod liver oil feeding produced a significant reduction in the ratio of (n−6)/(n−3) fatty acids in phospholipids of the isolated myocytes. The primary changes included a significant decrease in archidonic acid (20:4, n−6) and elevations in eicosapentaenoic acid (20:5, n−3) and docosahexaenoic acid (22:6, n−3). Furthermore, isolated myocytes from cod liver oil fed rats exhibited an enhanced 45Ca2+ uptake, although 45Ca2+ release was unaffected. Dietary cod liver oil had little effect on cardiac response to ischemia and reperfusion. Thus, neither developed force or resting tension was significantly affected by diet, although the latter tended to be elevated in hearts from cod liver oil fed animals. Release of creatine kinase was unaltered by diet. The release of 6-ketoprostaglandin F1α from isolated hearts was significantly reduced by dietary cod liver oil, likely due to the reduced levels of arachidonic acid. Our study indicates that dietary cod liver oil and subsequent changes in phospholipid fatty-acid content are accompanied by changes in Ca2+ transport in isolated cardiac myocytes. However, this diet produces little effect on the cardiac response to acute ischemia and reperfusion.


2003 ◽  
Vol 17 (2) ◽  
pp. 61-68 ◽  
Author(s):  
Michal Kuniecki ◽  
Robert Barry ◽  
Jan Kaiser

Abstract The effect of stimulus valence was examined in the evoked cardiac response (ECR) elicited by the exposition of neutral and negative slides as well as by an innocuous auditory stimulus presented on the affective foregrounds generated by the slides. The exposition of the aversive slide produced prolonged cardiac deceleration in comparison with the neutral slide. Similar prolonged deceleration accompanied exposition of the neutral auditory stimulus on the negative visual foreground in comparison with the neutral foreground. We interpret these results as an autonomic correlate of extended stimulus processing associated with the affective stimulus. The initial deceleration response, covering two or three slower heart beats, may be prolonged for several seconds before HR reaches the baseline level again. In such a case the evoked cardiac deceleration can be functionally divided into two parts: the reflexive bradycardia (ECR1) elicited by neutral stimuli and a late decelerative component (LDC). We can speculate that the latter is associated with an additional voluntary continuation of processing of the stimulus. This must involve some cognitive aspect different from the mental task performance which leads to the accelerative ECR2, and we suggest that processing of a stimulus with negative valence is involved in generating the LDC.


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