Mechanisms of Acute Cardioprotection with Ischemic Preconditioning: Protein Kinase C and Beyond

Heart Failure ◽  
2000 ◽  
pp. 71-79
Author(s):  
Karin Przyklenk
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Kinase C

Does Ischemic Preconditioning in the Human Involve Protein Kinase C and the ATP-Dependent K + Channel?

1995 ◽  
Vol 77 (5) ◽  
pp. 1030-1035 ◽  
Author(s):  
M. E. Speechly-Dick ◽  
G. J. Grover ◽  
D. M. Yellon
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
K Channel ◽  
Kinase C

No Prevention of Ischemic Preconditioning by the Protein Kinase C Inhibitor Staurosporine in Swine

1996 ◽  
Vol 79 (3) ◽  
pp. 407-414 ◽  
Author(s):  
Christian Vahlhaus ◽  
Rainer Schulz ◽  
Heiner Post ◽  
Raouf Onallah ◽  
Gerd Heusch
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Kinase C ◽  
Protein Kinase C Inhibitor

scholarly journals Protein kinase C subtypes and retinal ischemic preconditioning

2008 ◽  
Vol 87 (4) ◽  
pp. 300-311 ◽  
Author(s):  
John C. Dreixler ◽  
Afzhal R. Shaikh ◽  
Shanti K. Shenoy ◽  
Yang Shen ◽  
Steven Roth
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Kinase C

Roles of Tyrosine Kinase and Protein Kinase C in Infarct Size Limitation by Repetitive Ischemic Preconditioning in the Rat

2000 ◽  
Vol 35 (3) ◽  
pp. 345-352 ◽  
Author(s):  
Masaya Tanno ◽  
Akihito Tsuchida ◽  
Yukinaga Nozawa ◽  
Tomoaki Matsumoto ◽  
Tohru Hasegawa ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Kinase C ◽  
Size Limitation ◽  
Infarct Size Limitation

Participation of protein kinase C in the activation of Nrf2 signaling by ischemic preconditioning in the isolated rabbit heart

2012 ◽  
Vol 372 (1-2) ◽  
pp. 169-179 ◽  
Author(s):  
Xin Zhang ◽  
Zhibin Xiao ◽  
Jianmin Yao ◽  
Genshang Zhao ◽  
Xianen Fa ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Rabbit Heart ◽  
Isolated Rabbit Heart ◽  
Kinase C

Remifentanil Preconditioning Confers Cardioprotection via  Cardiac κ- and δ-Opioid Receptors

2005 ◽  
Vol 102 (2) ◽  
pp. 371-378 ◽  
Author(s):  
Ye Zhang ◽  
Michael G. Irwin ◽  
Tak Ming Wong ◽  
Mai Chen ◽  
Chun-Mei Cao
Keyword(s):  
At Risk ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Katp Channel ◽  
Area At Risk ◽  
Mitochondrial Katp Channel ◽  
Ringer’S Solution ◽  
Kinase C

Background Remifentanil preconditioning (RPC) reduces the infarct size in anesthetized rat hearts, and this effect seems to be mediated by all three types of opioid receptors (ORs). Because there is evidence of only kappa- and delta- but not mu-ORs in the rat heart, the authors investigated whether RPC confers cardioprotection via cardiac kappa- and delta-OR as well as via extracardiac mu-OR agonist activity. The authors also investigated the involvement of signaling mechanisms, namely protein kinase C and mitochondrial adenosine triphosphate-sensitive potassium (KATP) channels. Methods The hearts of male Sprague-Dawley rats weighing 190-210 g were removed, mounted on a Langendorff apparatus, and perfused retrogradely at 100 cm H2O with Krebs-Ringer's solution. All hearts were subjected to 30 min of ischemia and 2 h of reperfusion. The study consisted of three series of experiments on the effect of ischemic preconditioning or RPC (10, 50, and 100 ng/ml remifentanil) after blockade of OR subtypes (delta-OR antagonist naltrindol, kappa-OR antagonist nor-binaltorphimine, and mu-OR antagonist CTOP). The involvement of protein kinase C or the KATP channel in the cardioprotection of RPC was also investigated using specific blockers in each group. RPC was produced by three cycles of 5-min perfusion of remifentanil in Krebs-Ringer's solution interspersed with a 5-min reperfusion with Krebs solution only. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Results Infarct size as a percentage of the area at risk was significantly reduced after RPC from 51.9 +/- 5.0% (control, n = 8) to 36.2 +/- 10.0% (100 ng/ml RPC, n = 8, P < 0.01). This effect was stopped by pretreatment with naltrindol (52.3 +/- 5.2%) and nor-binaltorphimine (43.5 +/- 6.0%) but not CTOP (37.1 +/- 6.0%). Chelerythrine and GF109203X, both protein kinase C inhibitors, abolished the effects of RPC or ischemic preconditioning on infarct size as a percentage of area at risk. 5-Hydroxydecanoate (a selective mitochondrial KATP channel blocker) also abolished the cardioprotection of RPC and IPC, but HMR-1098 (a selective inhibitor of the sarcolemmal KATP channel) did not. Conclusion Cardiac delta- and kappa- but not mu-ORs mediate the cardioprotection produced by RPC. Both protein kinase C and the mitochondrial KATP channel were involved in this effect.

Sign in / Sign up

Export Citation Format

Share Document