Substrate Metabolism as a Determinant for Postischemic Functional Recovery of the Heart

Taegtmeyer, Heinrich; Goodwin, Gary W.; Doenst, Torsten; Frazier, O. H.

doi:10.1016/s0002-9149(97)00452-9

Cited by 108 publications

(86 citation statements)

References 48 publications

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“…Secondly, it is important for physiological concentrations of the metabolic substrates normally consumed by the heart, namely, glucose, lactate, and free fatty acids, to be present in coronary perfusate because the myocardial response to ischemia is highly dependent on the concentrations of the metabolic substrates present during ischemia (14). Hence, significant differences in cardiac performance might exist in the current experiment due to the absence of erythrocyte, lactate, and free fatty.…”

Section: Discussionmentioning

confidence: 95%

Analysis of Cardioprotective Effects Using Purified Salvia miltiorrhiza Extract on Isolated Rat Hearts

et al. 2006

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Abstract. The purpose of the current study is to evaluate the cardioprotective effects of purified Salvia miltiorrhiza extract (PSME) on myocardial ischemia / reperfusion injury in isolated rat hearts. Hearts were excised and perfused at constant flow (7 -9 ml ⋅ min −1 ) via the aorta. Non-recirculating perfusion with Krebs-Henseleit (KH) solution was maintained at 37°C and continuously gassed with 95% O 2 and 5% CO 2 . KH solution with or without PSME (100 mg per liter solution) was used after 30-min zero-flow ischemia for the PSME and control group, respectively. Left ventricular (LV) developed pressure; its derivatives, diastolic pressure, and so on were continuously recorded via a pressure transducer attached to a polyvinylchloride balloon that was placed in the left ventricle through an incision in the left atrium. PSME treated hearts showed significant postischemic contractile function recovery (developed pressure recovered to 44.2 ± 4.9% versus 17.1 ± 5.7%, P<0.05; maximum contraction recovered to 57.2 ± 5.9% versus 15.1 ± 6.3%, P<0.001; maximum relaxation restored to 69.3 ± 7.3% versus 15.4 ± 6.3%, P<0.001 in the PSME and control group, respectively). Significant elevation in end-diastolic pressure, which indicated LV stiffening in PSME hearts might have resulted from the excess high dose of PSME used. Further study will be conducted on the potential therapeutic value with lower dose of PSME on prevention of ischemic heart disease.

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Section: Discussionmentioning

confidence: 95%

Analysis of Cardioprotective Effects Using Purified Salvia miltiorrhiza Extract on Isolated Rat Hearts

et al. 2006

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“…In the disease hereditary hemochromomatosis there is a systemic deficiency of triosephosphate isomerase, causing wide ranging cardiac pathologies (41). Inhibition of this enzyme is likely to contribute to the metabolic deficit that is known to occur during reperfusion (42). We also detected the oxidation of another isomerase during reperfusion, the enzyme aconitase.…”

Section: S-thiolation During Cardiac Oxidant Stress and Functionalmentioning

confidence: 89%

Detection, Quantitation, Purification, and Identification of Cardiac Proteins S-Thiolated during Ischemia and Reperfusion

Eaton¹,

Byers²,

Leeds³

et al. 2002

Journal of Biological Chemistry

167

133

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We have developed methods that allow detection, quantitation, purification, and identification of cardiac proteins S-thiolated during ischemia and reperfusion. Cysteine was biotinylated and loaded into isolated rat hearts. During oxidative stress, biotin-cysteine forms a disulfide bond with reactive protein cysteines, and these can be detected by probing Western blots with streptavidin-horseradish peroxidase. S-Thiolated proteins were purified using streptavidin-agarose. Thus, we demonstrated that reperfusion and diamide treatment increased S-thiolation of a number of cardiac proteins by 3-and 10-fold, respectively. Dithiothreitol treatment of homogenates fully abolished the signals detected. Fractionation studies indicated that the modified proteins are located within the cytosol, membrane, and myofilament/cytoskeletal compartments of the cardiac cells. This shows that biotin-cysteine gains rapid and efficient intracellular access and acts as a probe for reactive protein cysteines in all cellular locations. Using Western blotting of affinity-purified proteins we identified actin, glyceraldehyde-3-phosphate dehydrogenase, HSP27, protein-tyrosine phosphatase 1B, protein kinase C␣, and the small G-protein ras as substrates for S-thiolation during reperfusion of the ischemic rat heart. MALDI-TOF mass fingerprint analysis of tryptic peptides independently confirmed actin and glyceraldehyde-3-phosphate dehydrogenase S-thiolation during reperfusion. This approach has also shown that triosephosphate isomerase, aconitate hydratase, M-protein, nucleoside diphosphate kinase B, and myoglobin are S-thiolated during post-ischemic reperfusion.

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“…22,28,29 During myocardial ischemia, acute elevations in systemic fatty acids have been shown to waste oxygen and reduce contractility, 30 to induce insulin resistance, 31 to lead to dangerous arrhythmias, 32 and to impair postischemic functional recovery. [33][34][35][36] …”

Section: Ffas and Ischemic Injurymentioning

confidence: 99%

Glucose-Insulin-Potassium Revived

et al. 2013

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Substrate Metabolism as a Determinant for Postischemic Functional Recovery of the Heart

Cited by 108 publications

References 48 publications

Analysis of Cardioprotective Effects Using Purified Salvia miltiorrhiza Extract on Isolated Rat Hearts

Analysis of Cardioprotective Effects Using Purified Salvia miltiorrhiza Extract on Isolated Rat Hearts

Detection, Quantitation, Purification, and Identification of Cardiac Proteins S-Thiolated during Ischemia and Reperfusion

Glucose-Insulin-Potassium Revived

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