Myocardial stunning: the role of oxidative substrate metabolism

1996 ◽  
pp. 88-90
Author(s):  
R. Lerch
Keyword(s):  
Myocardial Stunning ◽  
Substrate Metabolism

scholarly journals Bifunctional Role of Protein Tyrosine Kinases in Late Preconditioning Against Myocardial Stunning in Conscious Rabbits

1999 ◽  
Vol 85 (12) ◽  
pp. 1154-1163 ◽  
Author(s):  
Buddhadeb Dawn ◽  
Yu-Ting Xuan ◽  
Yumin Qiu ◽  
Hitoshi Takano ◽  
Xian-Liang Tang ◽  
...  
Keyword(s):  
Tyrosine Kinases ◽  
Myocardial Stunning ◽  
Protein Tyrosine Kinases ◽  
Protein Tyrosine ◽  
Late Preconditioning ◽  
Conscious Rabbits

Isoflurane Alters Energy Substrate Metabolism to Preserve Mechanical Function in Isolated Rat Hearts following Prolonged No-Flow Hypothermic Storage

2003 ◽  
Vol 98 (2) ◽  
pp. 379-386 ◽  
Author(s):  
Barry A. Finegan ◽  
Manoj Gandhi ◽  
Matthew R. Cohen ◽  
Donald Legatt ◽  
Alexander S. Clanachan
Keyword(s):  
Enhanced Recovery ◽  
Metabolic Effects ◽  
Mechanical Function ◽  
Cardioplegic Arrest ◽  
Channel Activation ◽  
Energy Substrate ◽  
Myocardial Glucose Metabolism ◽  
Substrate Metabolism ◽  
Rat Hearts

Background Isoflurane enhances mechanical function in hearts subject to normothermic global or regional ischemia. The authors examined the effectiveness of isoflurane in preserving mechanical function in hearts subjected to cardioplegic arrest and prolonged hypothermic no-flow storage. The role of isoflurane in altering myocardial glucose metabolism during storage and reperfusion during these conditions and the contribution of adenosine triphosphate-sensitive potassium (K(atp)) channel activation in mediating the functional and metabolic effects of isoflurane preconditioning was determined. Methods Isolated working rat hearts were subjected to cardioplegic arrest with St. Thomas' II solution, hypothermic no-flow storage for 8 h, and subsequent aerobic reperfusion. The consequences of isoflurane treatment were assessed during the following conditions: (1) isoflurane exposure before and during storage; (2) brief isoflurane exposure during early nonworking poststorage reperfusion; and (3) isoflurane preconditioning before storage. The selective mitochondrial and sarcolemmal K(atp) channel antagonists, 5-hydroxydecanoate and HMR 1098, respectively, were used to assess the role of K(atp) channel activation on glycogen consumption during storage in isoflurane-preconditioned hearts. Results Isoflurane enhanced recovery of mechanical function if present before and during storage. Isoflurane preconditioning was also protective. Isoflurane reduced glycogen consumption during storage under the aforementioned circumstances. Storage of isoflurane-preconditioned hearts in the presence of 5-hydroxydecanoate prevented the reduction in glycogen consumption during storage and abolished the beneficial effect of isoflurane preconditioning on recovery of mechanical function. Conclusions Isoflurane provides additive protection of hearts subject to cardioplegic arrest and prolonged hypothermic no-flow storage and favorably alters energy substrate metabolism by modulating glycolysis during ischemia. The effects of isoflurane preconditioning on glycolysis during hypothermic no-flow storage appears to be associated with activation of mitochondrial K(atp) channels.

scholarly journals Protective Effect of Qiliqiangxin Capsule on Energy Metabolism and Myocardial Mitochondria in Pressure Overload Heart Failure Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Junfang Zhang ◽  
Cong Wei ◽  
Hongtao Wang ◽  
Siwen Tang ◽  
Zhenhua Jia ◽  
...  
Keyword(s):  
Heart Failure ◽  
Energy Metabolism ◽  
Mitochondrial Function ◽  
Pressure Overload ◽  
Metabolic Intermediate ◽  
Substrate Metabolism ◽  
Myocardial Mitochondria ◽  
Tcm Theory

Qiliqiangxin capsule (QL) was developed under the guidance of TCM theory of collateral disease and had been shown to be effective and safe for the treatment of heart failure. The present study explored the role of and mechanism by which the herbal compounds QL act on energy metabolism,in vivo, in pressure overload heart failure. SD rats received ascending aorta constriction (TAC) to establish a model of myocardial hypertrophy. The animals were treated orally for a period of six weeks. QL significantly inhibited cardiac hypertrophy due to ascending aortic constriction and improved hemodynamics. This effect was linked to the expression levels of the signaling factors in connection with upregulated energy and the regulation of glucose and lipid substrate metabolism and with a decrease in metabolic intermediate products and the protection of mitochondrial function. It is concluded that QL may regulate the glycolipid substrate metabolism by activating AMPK/PGC-1αaxis and reduce the accumulation of free fatty acids and lactic acid, to protect cardiac myocytes and mitochondrial function.

scholarly journals Myocardial Stunning After Electrocution With Complete Reversibility Within 24 Hours: Role of Repeat Transthoracic Echocardiograms in Potential Cardiac Transplant Donors

2018 ◽  
Vol 9 (4) ◽  
pp. 268-272
Author(s):  
Hassan Tahir ◽  
Sarina Sachdev ◽  
Landai Nguyen ◽  
Nikky Bardia ◽  
Bassam Omar ◽  
...  
Keyword(s):  
Myocardial Stunning ◽  
Cardiac Transplant

scholarly journals Staged reperfusion attenuates myocardial stunning in dogs. Role of transient acidosis during early reperfusion.

Circulation ◽  
1991 ◽  
Vol 84 (5) ◽  
pp. 2135-2145 ◽  
Author(s):  
M Hori ◽  
M Kitakaze ◽  
H Sato ◽  
S Takashima ◽  
K Iwakura ◽  
...  
Keyword(s):  
Myocardial Stunning ◽  
Early Reperfusion
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