Journal
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 99, Issue 2, Pages 218-223Publisher
CANADIAN SCIENCE PUBLISHING
DOI: 10.1139/cjpp-2020-0400
Keywords
ischemia/reperfusion; ischemic preconditioning; cardiac hypertrophy; myocardial infarct size; leakage of CPK; phosphorylated p38-MAPK
Categories
Funding
- Jordan University of Science and Technology, School of Medicine, Irbid, Jordan
- St. Boniface Hospital Research Foundation, Winnipeg, Canada
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The study found that ischemic preconditioning can reduce the injury induced by ischemia/reperfusion in both normal and hypertrophied hearts. In hypertrophied hearts, reduced activation of p38-MAPK may lead to a diminished cardioprotective effect of ischemic preconditioning.
This study examined the effects of ischemic preconditioning (IP) on the ischemia/reperfusion (I/R) induced injury in normal and hypertrophied hearts. Cardiac hypertrophy in rabbits was induced by L-thyroxine (0.5 mg/kg/day for 16 days). Hearts with or without IP (3 cycles of 5 min ischemia and 10 min reperfusion) were subjected to I/R (60 min ischemia followed by 60 min reperfusion). IP reduced the I/R-induced infarct size from 68% to 24% and 57% to 33% in the normal and hypertrophied hearts, respectively. Leakage of creatine phosphokinase in the perfusate from the hypertrophied hearts due to I/R was markedly less than that form the normal hearts; IP prevented these changes. Although IP augmented the increase in phosphorylated p38-mitogen-activated protein kinase (p38-MAPK) content due to I/R, this effect was less in the hypertrophied than in the normal heart. These results suggest that reduced cardioprotection by IP of the I/R-induced injury in hypertrophied hearts may be due to reduced activation of p38-MAPK in comparison with normal hearts.
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