| Calpain inhibitor-1 protects the rat heart from ischemia-reperfusion injury: analysis by mechanical work and energetics. | |
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MedLine Citation:
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PMID: 15528229 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We hypothesized that calpain inhibitor-1 protected left ventricular (LV) function from ischemia-reperfusion injury by inhibiting the proteolysis of alpha-fodrin. To test this hypothesis, we investigated the effect of calpain inhibitor-1 on LV mechanical work and energetics in the cross-circulated rat hearts that underwent 15-min global ischemia and 60-min reperfusion (n = 9). After ischemia-reperfusion with calpain inhibitor-1, mean end-systolic pressure at midrange LV volume and systolic pressure-volume area (PVA) at midrange LV volume (total mechanical energy per beat) were hardly changed, although they were significantly (P < 0.01) decreased after ischemia-reperfusion without calpain inhibitor-1. Mean myocardial oxygen consumption per beat (Vo(2)) intercepts (PVA-independent Vo(2); Vo(2) for the total Ca(2+) handling in excitation-contraction coupling and basal metabolism) of Vo(2)-PVA linear relations were also unchanged after ischemia-reperfusion with calpain inhibitor-1, although they were significantly (P < 0.01) decreased after ischemia-reperfusion without calpain inhibitor-1. There were no significant differences in O(2) costs of LV PVA and contractility among the hearts in control (or normal) postischemia-reperfusion and postischemia-reperfusion with calpain inhibitor-1. Western blot analysis of alpha-fodrin and the immunostaining of 150-kDa products of alpha-fodrin confirmed that calpain inhibitor-1 almost completely protected the proteolysis of alpha-fodrin. Our results indicate that calpain inhibitor-1 prevents the heart from ischemia-reperfusion injury associated with the impairment of total Ca(2+) handling by directly inhibiting the proteolysis of alpha-fodrin. |
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Authors:
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Yoshiro Yoshikawa; Hiroji Hagihara; Yoshimi Ohga; Chikako Nakajima-Takenaka; Ken-ya Murata; Shigeki Taniguchi; Miyako Takaki |
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Publication Detail:
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Type: Journal Article Date: 2004-11-04 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 288 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2005 Apr |
Date Detail:
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Created Date: 2005-03-17 Completed Date: 2005-04-20 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1690-8 Citation Subset: IM |
Affiliation:
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Dept. of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / drug effects, physiology Blotting, Western Calcium / metabolism Calcium-Transporting ATPases / metabolism Cardiotonic Agents / pharmacology Carrier Proteins / metabolism Cysteine Proteinase Inhibitors / pharmacology* Electrophoresis, Polyacrylamide Gel Energy Metabolism / drug effects, physiology Glycoproteins / pharmacology* Lactic Acid / metabolism Male Microfilament Proteins / metabolism Myocardial Contraction / drug effects, physiology Myocardial Reperfusion Injury / drug therapy*, physiopathology* Oxygen Consumption / drug effects, physiology Rats Rats, Wistar Sarcoplasmic Reticulum Calcium-Transporting ATPases Sodium-Calcium Exchanger / metabolism Sodium-Potassium-Exchanging ATPase / metabolism Ventricular Function, Left / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Cardiotonic Agents; 0/Carrier Proteins; 0/Cysteine Proteinase Inhibitors; 0/Glycoproteins; 0/Microfilament Proteins; 0/Sodium-Calcium Exchanger; 0/calpain inhibitors; 0/fodrin; 50-21-5/Lactic Acid; 7440-70-2/Calcium; EC 3.6.1.8/Calcium-Transporting ATPases; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases; 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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