scholarly journals Difference in the Cardioprotective Mechanisms Between Ischemic Preconditioning and Pharmacological Preconditioning by Diazoxide in Rat Hearts

2004 ◽  
Vol 68 (2) ◽  
pp. 156-162 ◽  
Author(s):  
Nobuyuki Wakahara ◽  
Hideki Katoh ◽  
Yasuhiro Yaguchi ◽  
Akihiko Uehara ◽  
Hiroshi Satoh ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Rat Hearts ◽  
Pharmacological Preconditioning

scholarly journals Exercise Training Preserves Ischemic Preconditioning in Aged Rat Hearts by Restoring the Myocardial Polyamine Pool

2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Weiwei Wang ◽  
Hao Zhang ◽  
Guo Xue ◽  
Li Zhang ◽  
Weihua Zhang ◽  
...  
Keyword(s):  
Exercise Training ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Polyamine Metabolism ◽  
Aged Rat ◽  
Isolated Hearts ◽  
Age Related ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion

Background. Ischemic preconditioning (IPC) strongly protects against myocardial ischemia reperfusion (IR) injury. However, IPC protection is ineffective in aged hearts. Exercise training reduces the incidence of age-related cardiovascular disease and upregulates the ornithine decarboxylase (ODC)/polyamine pathway. The aim of this study was to investigate whether exercise can reestablish IPC protection in aged hearts and whether IPC protection is linked to restoration of the cardiac polyamine pool.Methods. Rats aging 3 or 18 months perform treadmill exercises with or without gradient respectively for 6 weeks. Isolated hearts and isolated cardiomyocytes were exposed to an IR and IPC protocol.Results. IPC induced an increase in myocardial polyamines by regulating ODC and spermidine/spermine acetyltransferase (SSAT) in young rat hearts, but IPC did not affect polyamine metabolism in aged hearts. Exercise training inhibited the loss of preconditioning protection and restored the polyamine pool by activating ODC and inhibiting SSAT in aged hearts. An ODC inhibitor,α-difluoromethylornithine, abolished the recovery of preconditioning protection mediated by exercise. Moreover, polyamines improved age-associated mitochondrial dysfunctionin vitro.Conclusion. Exercise appears to restore preconditioning protection in aged rat hearts, possibly due to an increase in intracellular polyamines and an improvement in mitochondrial function in response to a preconditioning stimulus.

Ischemic preconditioning-mediated restoration of membrane dystrophin during reperfusion correlates with protection against contraction-induced myocardial injury

2004 ◽  
Vol 287 (1) ◽  
pp. H81-H90 ◽  
Author(s):  
Masakuni Kido ◽  
Hajime Otani ◽  
Shiori Kyoi ◽  
Tomohiko Sumida ◽  
Hiroyoshi Fujiwara ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Myocardial Injury ◽  
Contractile Activity ◽  
Integral Membrane Protein ◽  
Contractile Force ◽  
Global Ischemia ◽  
Blue Dye ◽  
Perfused Heart ◽  
Complete Restoration ◽  
Rat Hearts

Dystrophin is an integral membrane protein involved in the stabilization of the sarcolemmal membrane in cardiac muscle. We hypothesized that the loss of membrane dystrophin during ischemia and reperfusion is responsible for contractile force-induced myocardial injury and that cardioprotection afforded by ischemic preconditioning (IPC) is related to the preservation of membrane dystrophin. Isolated and perfused rat hearts were subjected to 30 min of global ischemia, followed by reperfusion with or without the contractile blocker 2,3-butanedione monoxime (BDM). IPC was introduced by three cycles of 5-min ischemia and 5-min reperfusion before the global ischemia. Dystrophin was distributed exclusively in the membrane of myocytes in the normally perfused heart but was redistributed to the myofibril fraction after 30 min of ischemia and was lost from both of these compartments during reperfusion in the presence or absence of BDM. The loss of dystrophin preceded uptake of the membrane-impermeable Evans blue dye by myocytes that occurred after the withdrawal of BDM and was associated with creatine kinase release and the development of contracture. Although IPC did not alter the redistribution of membrane dystrophin induced by 30 min of ischemia, it facilitated the restoration of membrane dystrophin during reperfusion. Also, myocyte necrosis was not observed when BDM was withdrawn after complete restoration of membrane dystrophin. These results demonstrate that IPC-mediated restoration of membrane dystrophin during reperfusion correlates with protection against contractile force-induced myocardial injury and suggest that the cardioprotection conferred by IPC can be enhanced by the temporary blockade of contractile activity until restoration of membrane dystrophin during reperfusion.

scholarly journals Down-regulation of Connexin43 in Early Myocardial Ischemia and Protective Effect by Ischemic Preconditioning in Rat Hearts In Vivo

2004 ◽  
Vol 45 (6) ◽  
pp. 1007-1019 ◽  
Author(s):  
Kazuhito Hatanaka ◽  
Hiroyuki Kawata ◽  
Toshihiko Toyofuku ◽  
Ken-ichi Yoshida
Keyword(s):  
Myocardial Ischemia ◽  
Protective Effect ◽  
Ischemic Preconditioning ◽  
Down Regulation ◽  
Rat Hearts

scholarly journals 770-6 Effect of Ischemic Preconditioning and Udocaine Pretreatment on [Ca 2+ ] i in Rat Hearts

1995 ◽  
Vol 25 (2) ◽  
pp. 283A-284A ◽  
Author(s):  
Thomas Stefenelli ◽  
Shao T. Wu ◽  
Christian P. Zaugg ◽  
Geoff Smith ◽  
Joan Wikman-Coffelt ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Rat Hearts

scholarly journals Energy Metabolism After Ischemic Preconditioning in Streptozotocin-Induced Diabetic Rat Hearts

1998 ◽  
Vol 31 (3) ◽  
pp. 707-715 ◽  
Author(s):  
Tetsuya Tatsumi ◽  
Satoaki Matoba ◽  
Miyuki Kobara ◽  
Natsuya Keira ◽  
Akira Kawahara ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Ischemic Preconditioning ◽  
Diabetic Rat ◽  
Rat Hearts

Menadione mimics the infarct-limiting effect of preconditioning in isolated rat hearts

2001 ◽  
Vol 281 (2) ◽  
pp. H590-H595 ◽  
Author(s):  
Yuankun Yue ◽  
Maike Krenz ◽  
Michael V. Cohen ◽  
James M. Downey ◽  
Stuart D. Critz
Keyword(s):  
Free Radicals ◽  
Infarct Size ◽  
P38 Mapk ◽  
Ischemic Preconditioning ◽  
Free Radical Scavenger ◽  
Mitogen Activated Protein Kinase ◽  
Radical Scavenger ◽  
Risk Zone ◽  
Regional Ischemia ◽  
Rat Hearts

The role of mitochondrial free radicals in the cardioprotective effect of ischemic preconditioning was examined in isolated buffer-perfused rat hearts. Infarct size in control rat hearts subjected to 30 min of regional ischemia and 120 min of reperfusion was 32.6 ± 3.4% of the risk zone. Ischemic preconditioning (3 cycles of 5-min global ischemia/5-min reperfusion) before the same regional ischemia and reperfusion protocol significantly reduced infarct size to 2.6 ± 0.8% of the risk zone. Perfusion with menadione (3.0 μM), a generator of mitochondrial free radicals, in lieu of preconditioning ischemia significantly reduced infarction to 10.9 ± 2.7%. N-2-mercaptopropionylglycine (1.0 mM), a free radical scavenger, blocked the protection of menadione, significantly increasing infarction to 23.5 ± 1.1%. Myxothiazol (0.6 μM), a site III mitochondrial inhibitor, blocked the protection of menadione and significantly increased infarction to 25.2 ± 3.8%. The infarct-limiting effect of menadione was attenuated to 19.7 ± 1.5% of the risk zone by 10 μM SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor. Furthermore, menadione significantly increased p38 MAPK phosphorylation to a level 5.6-fold over basal. These results indicate that free radicals that originate within mitochondria can activate p38 MAPK and protect hearts against infarction.

Sign in / Sign up

Export Citation Format

Share Document