Document Detail


Progression and resolution of myocardial reflow injury.
MedLine Citation:
PMID:  6379296     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The development of and recovery from a severe yet nonlethal myocardial injury following hyperkalemic cardioplegia and prolonged hypothermic global ischemia was examined over 14 days in a rat model of heterotopic intraabdominal cardiac isograft transplantation. Mitochondrial enzymatic markers of myocardial ischemic injury and light microscopic signs of damage were examined. Eighteen hearts were arrested in situ using hyperkalemic cardioplegia and subjected to a mean of 38 min of ischemia at 20 degrees C as transplantation was achieved. No changes in mitochondrial creatine kinase (CKm) activity, mitochondrial malate dehydrogenase (MDHm) activity, their ratio, or morphologic evidence of injury were found during 8 days of reperfusion. In a second group of 66 hearts, the duration of hypothermic cardioplegic ischemia was extended by 120 min before transplantation. Neither unreperfused hearts nor hearts reperfused for only 1 hr demonstrated significant depression of enzyme activities or microscopic evidence of injury. However, after 1 day of reperfusion, CKm and MDHm activities were depressed to 36 and 44% of control levels (P less than 0.05). These activities had returned to control levels by 2 days of reperfusion and remained stable for 12 days thereafter. Light microscopic analysis revealed cellular injury to be maximal at 1 to 2 days of reperfusion with gradual improvement noted over the following 12 days. These observations suggest the existence of a mitochondrial injury following prolonged cardioplegic arrest and hypothermic global ischemia that is maximal after 24 hr of reperfusion but shows evidence of improvement thereafter. These findings justify aggressive support of the poorly functioning heart for the first few days after prolonged global ischemia.
Authors:
A S Casale; S F Bolling; J A Rui; J T Flaherty; B H Bulkley; W E Jacobus; T J Gardner
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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.    
Journal Detail:
Title:  The Journal of surgical research     Volume:  37     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  1984 Aug 
Date Detail:
Created Date:  1984-08-29     Completed Date:  1984-08-29     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  94-9     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Coronary Disease / etiology,  pathology*
Creatine Kinase / analysis
Heart Arrest, Induced / adverse effects*
Heart Transplantation*
Malate Dehydrogenase / analysis
Male
Mitochondria, Heart / enzymology*
Potassium
Rats
Rats, Inbred Lew
Time Factors
Grant Support
ID/Acronym/Agency:
2 RO HL19414/HL/NHLBI NIH HHS; 5 M01RR35-20/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
7440-09-7/Potassium; EC 1.1.1.37/Malate Dehydrogenase; EC 2.7.3.2/Creatine Kinase

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


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