Brief pressure overload of the left ventricle reduces myocardial infarct size via activation of protein kinase C

2015 ◽  
Vol 78 (9) ◽  
pp. 506-512
Author(s):  
Chia-Yu Tang ◽  
Chang-Chi Lai ◽  
Shu-Chiung Chiang ◽  
Kuo-Wei Tseng ◽  
Cheng-Hsiung Huang
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Left Ventricle ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Pressure Overload ◽  
Myocardial Infarct Size ◽  
Kinase C

Does protein kinase C play a role in ischemic preconditioning in rat hearts?

1995 ◽  
Vol 268 (1) ◽  
pp. H426-H431 ◽  
Author(s):  
Y. Li ◽  
R. A. Kloner
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Coronary Occlusion ◽  
Myocardial Infarct ◽  
Specific Inhibitor ◽  
Myocardial Infarct Size ◽  
Calphostin C ◽  
Kinase C

Protein kinase C (PKC) has been implicated in the cardioprotective effects of ischemic preconditioning in rabbits, but whether it plays a role in rats is unknown. We tested this preconditioning PKC theory by assessing whether the inhibition of PKC with calphostin C, a potent and specific inhibitor of PKC, can block the preconditioning effects in this model. Four groups of rats were studied: 1) control + vehicle, 2) control + calphostin C, 3) preconditioning + vehicle, and 4) preconditioning + calphostin C. All rats underwent 90 min of coronary occlusion followed by 4 h of reperfusion; in addition, preconditioned rats underwent three 3-min episodes of ischemia and 5 min of reperfusion before the 90 min of ischemia. Two injections of vehicle or calphostin C (0.1 mg/kg) were administered in intravenous boluses 29 min and 3 min before the 90-min coronary occlusion, i.e., one dose was given 5 min before preconditioning, and another dose was given between preconditioning and the sustained 90 min of ischemia in preconditioned rats. After 4 h of reperfusion, the area at risk (AR) was delineated by dye injection and area of necrosis was assessed by triphenyltetrazolium chloride staining. The electrocardiogram was recorded for the incidence of ventricular tachycardia (VT) and ventricular fibrillation. AR was similar in all four groups. In the nonpreconditioned control rats receiving vehicle, myocardial infarct size expressed as a percentage of the AR averaged 45.7 +/- 1.7%. Pretreatment with calphostin C had no effect on infarct size (48.9 +/- 3.4%) in nonpreconditioned control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Treatment with Sheng-Mai-San Reduces Myocardial Infarct Size Through Activation of Protein Kinase C and Opening of Mitochondrial KATP Channel

2001 ◽  
Vol 29 (02) ◽  
pp. 367-375 ◽  
Author(s):  
Ningyuan Wang ◽  
Shinya Minatoguchi ◽  
Yoshihiro Uno ◽  
Masazumi Arai ◽  
Kazuaki Hashimoto ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Katp Channels ◽  
Myocardial Infarct Size ◽  
Mitochondrial Katp Channel ◽  
Kinase C ◽  
Radix Ginseng ◽  
Mitochondrial Katp Channels

Sheng-Mei-San (SMS), a traditional Chinese formulation comprising Radix Ginseng, Radix Ophiopogonis and Fructus Schisandrae, has long been used for more than 700 years for patients with coronary heart disease. We attempted to clarify 1) whether SMS reduces myocardial infarct size, and 2) whether the infarct size-reducing effect of SMS is related to activation of protein kinase C and the opening of the mitochondrial KATP channels in Japanese white rabbits without collateral circulation. The results indicate that three days treatment but not acute treatment with SMS reduces myocardial infarct size through activation of protein kinase C and opening of the mitochondrial KATP channels.

Opening of mitochondrial KATP channel occurs downstream of PKC-ε activation in the mechanism of preconditioning

2002 ◽  
Vol 283 (1) ◽  
pp. H440-H447 ◽  
Author(s):  
Yoshito Ohnuma ◽  
Tetsuji Miura ◽  
Takayuki Miki ◽  
Masaya Tanno ◽  
Atsushi Kuno ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Left Ventricle ◽  
Infarct Size ◽  
Katp Channel ◽  
The Other ◽  
Particulate Fraction ◽  
K Channel ◽  
Mitochondrial Katp Channel ◽  
Kinase C

We examined whether the mitochondrial ATP-sensitive K channel (KATP) is an effector downstream of protein kinase C-ε (PKC-ε) in the mechanism of preconditioning (PC) in isolated rabbit hearts. PC with two cycles of 5-min ischemia/5-min reperfusion before 30-min global ischemia reduced infarction from 50.3 ± 6.8% of the left ventricle to 20.3 ± 3.7%. PC significantly increased PKC-ε protein in the particulate fraction from 51 ± 4% of the total to 60 ± 4%, whereas no translocation was observed for PKC-δ and PKC-α. In mitochondria separated from the other particulate fractions, PC increased the PKC-ε level by 50%. Infusion of 5-hydroxydecanoate (5-HD), a mitochondrial KATP blocker, after PC abolished the cardioprotection of PC, whereas PKC-ε translocation by PC was not interfered with 5-HD. Diazoxide, a mitochondrial KATP opener, infused 10 min before ischemia limited infarct size to 5.2 ± 1.4%, but this agent neither translocated PKC-ε by itself nor accelerated PKC-ε translocation after ischemia. Together with the results of earlier studies showing mitochondrial KATP opening by PKC, the present results suggest that mitochondrial KATP-mediated cardioprotection occurs subsequent to PKC-ε activation by PC.

scholarly journals Mechanically Unloading the Left Ventricle Before Coronary Reperfusion Reduces Left Ventricular Wall Stress and Myocardial Infarct Size

Circulation ◽  
2013 ◽  
Vol 128 (4) ◽  
pp. 328-336 ◽  
Author(s):  
Navin K. Kapur ◽  
Vikram Paruchuri ◽  
Jose Angel Urbano-Morales ◽  
Emily E. Mackey ◽  
Gerard H. Daly ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Wall Stress ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Myocardial Infarct Size ◽  
Ventricular Wall ◽  
Coronary Reperfusion
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