Document Detail


The initial rate of troponin I release post-reperfusion reflects the effectiveness of myocardial protection during cardiac allograft preservation.
MedLine Citation:
PMID:  12829065     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To determine if the initial rate of troponin I release post-reperfusion reflects the effectiveness of myocardial protection during cardiac allograft preservation. METHODS: A porcine model of orthotopic heart transplantation was used. Data from two control groups (CON(4) and CON(14)) and two treatment groups (CAR(4) and CAR(14)) were analysed. Hearts in CON(4) (n=6) and CAR(4) (n=6) were subjected to 4 h of ischaemia while hearts in CON(14) (n=3) and CAR(14) (n=6) were subjected to 14 h of ischaemia. All hearts were arrested and stored in the same extracellular preservation solution. Both donor and recipient animals in the CAR(4) and CAR(14) groups received a single intravenous dose of cariporide (2 mg/kg), prior to explantation and reperfusion, respectively. RESULTS: Mean (SEM) plasma troponin I levels (microg/ml) 3 h post-reperfusion were: CON(4) 210+/-52, CAR(4) 68+/-21, CON(14) 633+/-177, CAR(14) 346+/-93. On multiple linear regression analysis, the rate of troponin I release over the first 3 h post-reperfusion was significantly lower in hearts stored for 4 h compared to hearts stored for 14 h (P<0.0001) and in hearts treated with cariporide compared to control hearts (P=0.0017). Early graft function was superior in hearts treated with cariporide, when compared to control hearts stored for the same period of time. All of the CAR(14) hearts could be weaned from cardiopulmonary bypass whereas none of the CON(14) could be weaned (6/6 vs. 0/3; P=0.012). While all hearts stored for 4 h could be weaned, contractility, as measured by the preload recruitable stroke work (PRSW) relationship, was significantly better preserved in CAR(4) hearts than in CON(4) hearts (P<0.0001). CONCLUSIONS: The initial rate of troponin I release post-reperfusion is determined by the duration of cardiac allograft ischaemia. Altering the myocardial preservation strategy can reduce the rate of release. Such reductions are associated with improvements in early graft function. These findings validate the initial rate of troponin I release post-reperfusion as an end-point when comparing cardiac allograft preservation strategies. In addition, the present study provides indirect evidence that troponin I degradation during ischaemia-reperfusion is related to the accumulation of intracellular calcium.
Authors:
Jonathon B Ryan; Mark Hicks; Jonathan R Cropper; Sarah R Garlick; Scott H Kesteven; Michael K Wilson; Michael P Feneley; Peter S Macdonald
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery     Volume:  23     ISSN:  1010-7940     ISO Abbreviation:  Eur J Cardiothorac Surg     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-06-27     Completed Date:  2003-09-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8804069     Medline TA:  Eur J Cardiothorac Surg     Country:  England    
Other Details:
Languages:  eng     Pagination:  898-906     Citation Subset:  IM    
Affiliation:
Heart and Lung Transplant Unit, St. Vincent's Hospital and the Victor Chang Cardiac Research Institute, Sydney, Australia. j.ryan@garvan.unsw.edu.au
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Inbred Strains
Guanidines / therapeutic use
Heart Transplantation*
Models, Animal
Myocardial Contraction
Myocardial Reperfusion Injury / diagnosis*
Postoperative Period
Sodium-Hydrogen Antiporter / antagonists & inhibitors
Sulfones / therapeutic use
Swine
Time Factors
Tissue Preservation / methods
Transplantation, Homologous
Troponin I / blood*
Chemical
Reg. No./Substance:
0/Guanidines; 0/Sodium-Hydrogen Antiporter; 0/Sulfones; 0/Troponin I; 0/cariporide

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


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