| NADH measurements in adult rat myocytes during simulated ischemia. | |
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MedLine Citation:
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PMID: 2058713 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In isolated adult rat myocytes, we tested the hypothesis that metabolic inhibition and simulated ischemia regulate the NADH/NAD+ redox couple with concomitant impairment of energy-dependent process, including contraction and maintenance of high-energy phosphate stores. We developed a method to examine the relationship among the redox couple, ATP content, and contractile performance in single cells under several conditions analogous to myocardial ischemia, with and without reperfusion. Myocytes were paced at 1 Hz while cell contraction and NADH fluorescence were determined simultaneously for single cells at 37 degrees C. Cells were exposed to cyanide and 2-deoxy-D-glucose (metabolic inhibition) or to metabolic inhibition plus 12 mM KCl and 20 mM lactate at pH 6.5 (simulated ischemia). Pyridine nucleotide fluorescence signals from single cells studied in this fashion could be modulated by metabolic inhibitors in a manner similar to that classically described for isolated mitochondria. Metabolic inhibition or simulated ischemia quickly produced maximal reduction of NAD+ to NADH. When cells were exposed to simulated ischemia for 10 min, then superfused with glucose-containing control buffer, 28% of cells exposed to conditions of simulated ischemia developed hypercontracture on reperfusion. Hypercontracture developed despite mitochondrial electron transport being reestablished. When myocyte suspensions in a cuvette were studied spectrofluorimetrically, the pyridine nucleotide fluorescence response to metabolic inhibitors was similar to that for a single cell. This permitted correlation of ATP determinations on cells in suspension with contractile and fluorescence measurements from single myocytes. In the absence of glycolysis there is correspondence among loss of electron transport, decline in high-energy phosphate concentration, and decline in contraction. Irreversible disruption of the electron transport process does not appear to be an early event in ischemic injury. |
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Authors:
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K Esumi; M Nishida; D Shaw; T W Smith; J D Marsh |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The American journal of physiology Volume: 260 ISSN: 0002-9513 ISO Abbreviation: Am. J. Physiol. Publication Date: 1991 Jun |
Date Detail:
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Created Date: 1991-08-01 Completed Date: 1991-08-01 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0370511 Medline TA: Am J Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: H1743-52 Citation Subset: IM |
Affiliation:
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Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenine Nucleotides
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analysis Adenosine Triphosphate / analysis Animals Cell Movement / drug effects Coronary Disease / metabolism*, pathology, physiopathology Cyanides / pharmacology Deoxyglucose / pharmacology Electron Transport / drug effects Energy Metabolism / drug effects Female Lactates / pharmacology Mitochondria, Heart / metabolism Myocardium / cytology*, metabolism NAD / analysis*, metabolism Oxidation-Reduction Potassium Chloride / pharmacology Rats Rats, Inbred Strains Spectrometry, Fluorescence |
| Grant Support | |
ID/Acronym/Agency:
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HL-26215/HL/NHLBI NIH HHS; HL-35781/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adenine Nucleotides; 0/Cyanides; 0/Lactates; 154-17-6/Deoxyglucose; 53-84-9/NAD; 56-65-5/Adenosine Triphosphate; 7447-40-7/Potassium Chloride |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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