| Na+ accumulation increases Ca2+ overload and impairs function in anoxic rat heart. | |
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MedLine Citation:
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PMID: 2157854 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Maintenance of low coronary flow (1 ml/min) during 40 or 70 min of anoxia maintained function and prevented Ca2+ overload during reoxygenation in isolated rat hearts. In comparison, recovery from 40 min of global ischemia resulted in only 20% of preischemic function and an increase in end-diastolic pressure (LVEDP) to 39 mmHg. Reperfusion Ca2+ uptake rose from 0.6 to 10.2 mumol/g dry tissue. Intracellular Na+ (Nai+) increased from 13 to 61 mumol/g dry tissue after 40 min of global ischemia, but was unchanged in hearts with low flow anoxia. When glucose and pyruvate were omitted from buffer used for anoxic perfusion, recovery was only 15% of preanoxic values, LVEDP rose to 32 mmHg, and reperfusion Ca2+ uptake was 7.2 mumol/g dry. In addition, Nai+ increased (47.4 mumol/g dry tissue) and ATP was depleted (1.0 mumol/g dry tissue) in the absence of substrate. In anoxic hearts supplied substrate, Nai+ stayed low (12 mumol/g dry tissue) and ATP was preserved (11.6 mumol/g dry tissue). Addition of ouabain (100 or 200 microM) and provision of zero-K+ buffer increased Nai+ and resulted in impaired functional recovery, increased LVEDP, and greater reperfusion Ca2+ uptake. These interventions also decreased energy availability in anoxic hearts. To distinguish between effects of Na+ accumulation and ATP depletion, monensin, a Na+ ionophore, was added during low flow anoxia. Monensin increased Nai+, decreased functional recovery and increased reperfusion Ca2+ uptake in a dose-dependent manner (1-10 microM) without changing ATP content. These results suggested that reduction of Nai+ accumulation by maintenance of Na+, K+ pump activity was the major mechanism of the beneficial effects of low coronary flow on reperfusion injury. |
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Authors:
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M Tani; J R Neely |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 22 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 1990 Jan |
Date Detail:
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Created Date: 1990-05-24 Completed Date: 1990-05-24 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 57-72 Citation Subset: IM |
Affiliation:
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Sigfried and Janet Weis Center for Research, Geisinger Clinic, Danville, PA 17822. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism Animals Anoxia / metabolism* Biological Transport, Active / drug effects Calcium / metabolism* Coronary Circulation / physiology Coronary Disease / metabolism Energy Metabolism Male Monensin / pharmacology Myocardial Reperfusion Injury / physiopathology, prevention & control Myocardium / metabolism* Perfusion Rats Rats, Inbred Strains Sodium / metabolism* Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors |
| Grant Support | |
ID/Acronym/Agency:
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HL-37936/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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17090-79-8/Monensin; 56-65-5/Adenosine Triphosphate; 7440-23-5/Sodium; 7440-70-2/Calcium; EC 3.6.3.9/Sodium-Potassium-Exchanging ATPase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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