Document Detail


Glucocorticoids preserve calpastatin and troponin I during cardiopulmonary bypass in immature pigs.
MedLine Citation:
PMID:  12646718     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Degradation of troponin I (TnI) by calpain occurs with myocardial stunning in ischemia-reperfusion injury. Glucocorticoids attenuate myocardial ischemia-reperfusion injury, but their effect on TnI degradation is unknown. A piglet model was used to test the hypotheses that cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) are associated with TnI degradation and that TnI alterations could be prevented by glucocorticoid treatment. Piglets were cooled to 18 degrees C, subjected to 2 h of circulatory arrest, rewarmed to 37 degrees C, and allowed to recover for 2 h. Methylprednisolone was administered 6 h before surgery (3 0 mg/kg) and at initiation of CPB (30 mg/kg). The untreated group received saline. Left ventricular tissue was collected after recovery and analyzed by Western blot for TnI, calpain, and calpastatin (the natural inhibitor of calpain). CPB/DHCA animals had 27.4 +/- 0.2% of total detected TnI present in degraded form. Glucocorticoid treatment significantly decreased the percentage of degraded TnI (12.0 +/- 0.1%, p < 0.05). Calpain I and calpain II increased after CPB/DHCA compared with non-CPB/DHCA controls (p < 0.05), with or without glucocorticoid treatment. Calpastatin significantly decreased in untreated CPB/DHCA animals compared with non-CPB/DHCA controls (p < 0.05), but levels were preserved by glucocorticoids. Glucocorticoids were associated with preservation of maximum rate of increase of left ventricular pressure at 95 +/- 10% of baseline, whereas maximum rate of increase of left ventricular pressure decreased to 62 +/- 12% of baseline without steroids. TnI degradation occurs after CPB/DHCA in neonatal pigs. Reduction in reperfusion injury by glucocorticoids may depend partly on preservation of calpastatin activity and intact TnI.
Authors:
Steven M Schwartz; JodieE Y Duffy; Jeffrey M Pearl; Semin Goins; Connie J Wagner; David P Nelson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2003-03-19
Journal Detail:
Title:  Pediatric research     Volume:  54     ISSN:  0031-3998     ISO Abbreviation:  Pediatr. Res.     Publication Date:  2003 Jul 
Date Detail:
Created Date:  2003-06-23     Completed Date:  2004-02-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0100714     Medline TA:  Pediatr Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  91-7     Citation Subset:  IM    
Affiliation:
Division of Cardiology, Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA. schws0@chmcc.org
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MeSH Terms
Descriptor/Qualifier:
Age Factors
Animals
Calcium-Binding Proteins / metabolism*
Calpain / metabolism
Cardiac Output
Cardiopulmonary Bypass*
Cells, Cultured
Glucocorticoids / pharmacology*
Myocytes, Cardiac / cytology,  enzymology*
Swine
Troponin I / metabolism*
Vascular Resistance
Grant Support
ID/Acronym/Agency:
HD22827/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Calcium-Binding Proteins; 0/Glucocorticoids; 0/Troponin I; 79079-11-1/calpastatin; EC 3.4.22.-/Calpain

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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