Document Detail


Calpain inhibitor-1 protects the rat heart from ischemia-reperfusion injury: analysis by mechanical work and energetics.
MedLine Citation:
PMID:  15528229     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Yoshiro Yoshikawa; Hiroji Hagihara; Yoshimi Ohga; Chikako Nakajima-Takenaka; Ken-ya Murata; Shigeki Taniguchi; Miyako Takaki
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Publication Detail:
Type:  Journal Article     Date:  2004-11-04
Journal Detail:
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:
Created Date:  2005-03-17     Completed Date:  2005-04-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1690-8     Citation Subset:  IM    
Affiliation:
Dept. of Physiology II, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan.
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MeSH Terms
Descriptor/Qualifier:
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:
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

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