Modification of ischemia/reperfusion induced infarct size by ischemic preconditioning in hypertrophied hearts.

Autor: Nusier M; School of Medicine, Department of Physiology and Biochemistry, Jordan University of Science and Technology, Irbid, Jordan., Alqudah M; School of Medicine, Department of Physiology and Biochemistry, Jordan University of Science and Technology, Irbid, Jordan., Elimban V; Institute of Cardiovascular Sciences, St. Boniface Hospital, Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada., Dhalla NS; Institute of Cardiovascular Sciences, St. Boniface Hospital, Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada.
Jazyk: angličtina
Zdroj: Canadian journal of physiology and pharmacology [Can J Physiol Pharmacol] 2021 Feb; Vol. 99 (2), pp. 218-223. Date of Electronic Publication: 2021 Feb 05.
DOI: 10.1139/cjpp-2020-0400
Abstrakt: 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.
Databáze: MEDLINE
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