| Depressed myofilament co-operativity associated with post-cardioplegic myocardial depression. | |
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MedLine Citation:
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PMID: 9769234 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The mechanism underlying myocardial depression after procedures involving cardioplegia are unknown. We tested the hypothesis that such depression was associated with altered myofilament interactions, using isolated hearts perfused with warm (37 degreesC), oxygenated (95% O2/5% CO2) Krebs-Ringer's bicarbonate (KRB) buffer. A latex balloon was inserted into the left ventricle (LV) to monitor LV function. All hearts underwent a 30-min equilibration period. One group of hearts (CPL+RPR) were arrested with St Thomas #2 cardioplegic solution (4 degreesC; 3 ml followed by 1 ml every 15 min) for 120 min, followed by reperfusion with warm, oxygenated KRB. A second group underwent cardioplegic arrest with no reperfusion (CPL). A third group underwent 60 min of warm, oxygenated perfusion with KRB beyond the equilibration period (60 MIN). The last group only underwent the equilibration period (EQUIL). LV function was assessed at the end of equilibration, and at 30 and 60 min of reperfusion (or 30 and 60 min additional perfusion in the 60 MIN group). All hearts were frozen at the end of the temporal protocol for each group, and stored at -70 degreesC for later measurement of Ca2+-stimulated Mg2+ ATPase activity after isolation of myofibrils. CPL+RPR hearts demonstrated significant depression of systolic pressure and elevation diastolic pressure at fixed volumes, compared to baseline and 60 MIN group values. There were no significant changes in the amount of constituent myofilament proteins, as assessed by densinometric analyses of Western blots. There were also no changes in the minimal or maximal ATPase activities, nor in the pCa50, indicating no effect of cardioplegic arrest on myofilament sensitivity to calcium. However, all hearts that underwent cardioplegic arrest were found to have significantly lower Hill coefficients (1.85+/-0.09 and 1.85+/-0.13 v 2.31+/-0.13 and 2.34+/-0. 14 in CPL+RPR and CPL v 60 MIN and EQUIL hearts, respectively), suggesting decreased co-operativity of the actomyosin interaction. Such a decrease in co-operativity would contribute to both the systolic and diastolic alterations associated with myocardial depression after cardioplegic arrest. These changes were associated with the cardioplegic event, and appeared to be independent of reperfusion. |
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Authors:
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F M Powers; B Fogelson; C Sturgeon; R J Solaro; W R Law |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 30 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 1998 Sep |
Date Detail:
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Created Date: 1998-11-19 Completed Date: 1998-11-19 Revised Date: 2007-11-14 |
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: 1779-87 Citation Subset: IM |
Copyright Information:
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Copyright 1998 Academic Press. |
Affiliation:
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Research Services, West Side VA Hospital, Chicago, IL, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphatases
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metabolism Animals Heart / physiopathology* Heart Arrest, Induced / adverse effects* Male Microfilaments / metabolism, physiology* Muscle Proteins / metabolism Myocardial Reperfusion / adverse effects* Myocardial Stunning / physiopathology* Myocardium / metabolism Rats Rats, Sprague-Dawley Ventricular Function |
| Grant Support | |
ID/Acronym/Agency:
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GM R01-48219/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Muscle Proteins; EC 3.6.1.-/Adenosine Triphosphatases |
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