Contribution of both the sarcolemmal K ATP and mitochondrial K ATP channels to infarct size limitation by K ATP channel openers: differences from preconditioning in the role of sarcolemmal K ATP channels

2001 ◽  
Vol 364 (3) ◽  
pp. 226-232 ◽  
Author(s):  
Masaya Tanno ◽  
Tetsuji Miura ◽  
Akihito Tsuchida ◽  
Takayuki Miki ◽  
Yasuhiro Nishino ◽  
...  
Keyword(s):  
Infarct Size ◽  
Size Limitation ◽  
Infarct Size Limitation

Differential role of PI3K/Akt pathway in the infarct size limitation and antiarrhythmic protection in the rat heart

2006 ◽  
Vol 297 (1-2) ◽  
pp. 111-120 ◽  
Author(s):  
Táňa Ravingerová ◽  
Jana Matejíková ◽  
Jan Neckář ◽  
Eva Andelová ◽  
František Kolář
Keyword(s):  
Infarct Size ◽  
Rat Heart ◽  
Akt Pathway ◽  
Size Limitation ◽  
Infarct Size Limitation

Protective role of gap junctions in preconditioning against myocardial infarction

2004 ◽  
Vol 286 (1) ◽  
pp. H214-H221 ◽  
Author(s):  
Tetsuji Miura ◽  
Yoshito Ohnuma ◽  
Atsushi Kuno ◽  
Masaya Tanno ◽  
Yoshihiko Ichikawa ◽  
...  
Keyword(s):  
Infarct Size ◽  
Lucifer Yellow ◽  
Protective Role ◽  
Ischemic Region ◽  
Kinase C ◽  
Size Limitation ◽  
Butanedione Monoxime ◽  
Series Of Experiments ◽  
Infarct Size Limitation

The aim of the present study was to examine the hypothesis that acceleration of gap junction (GJ) closure during ischemia contributes to anti-infarct tolerance afforded by preconditioning (PC). First, the effects of PC on GJ communication during ischemia were assessed. Isolated buffer-perfused rabbit hearts were subjected to 5-min global ischemia with or without PC with two cycles of 5-min ischemia/5-min reperfusion or a GJ blocker (2 mM heptanol), and then the tissue excised from the ischemic region was incubated in anoxic buffer containing lucifer yellow (LY; 2.5 mg/ml), a tracer of GJ permeability, for 20 min at 37°C. PC and heptanol significantly reduced the area to which LY was transported in the ischemic myocardium by 39% and by 54%, respectively. In the second series of experiments, three GJ blockers (heptanol, 18β-glycyrrhetinic acid, and 2,3-butanedione monoxime) infused after the onset of ischemia reduced infarct size after 30-min ischemia/2-h reperfusion to an extent equivalent to that in the case of PC. In the third series of experiments, Western blotting for connexin43 (Cx43) showed that PC shortened the time to the onset of ischemia-induced Cx43 dephosphorylation but reduced the extent of Cx43 dephosphorylation during a 30-min period of ischemia. Calphostin C, a protein kinase C (PKC) inhibitor, abolished preservation of phosphorylated Cx43 but not the early onset of Cx43 dephosphorylation after ischemia in the preconditioned myocardium. These results suggest that PC-induced reduction of GJ permeability during ischemia, presumably by PKC-mediated Cx43 phosphorylation, contributes to infarct size limitation.

Pharmacological approaches to infarct size limitation

1986 ◽  
Vol 18 ◽  
pp. 141-141
Author(s):  
D YELLON ◽  
D HEARSE ◽  
J DOWNEY
Keyword(s):  
Infarct Size ◽  
Size Limitation ◽  
Infarct Size Limitation
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