Linked Life Data

9352121

Source:http://linkedlifedata.com/resource/pubmed/id/9352121

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1997-12-4
pubmed:abstractText
Myocardial protection is usually studied in vitro on perfused heart preparations, but never directly on cultured cardiomyocytes. We evaluated a model of cultured newborn rat cardiomyocytes to study both the cytotoxicity and the protective effect against chemical hypoxia of three cardioplegic solutions (St Thomas' I, Bretschneider, St Thomas' II) under normothermic (37 degrees C) and hypothermic (4 degrees C) conditions. Cytotoxicity was evaluated in 50% and 100% concentrations of the cardioplegic solutions with incubation times from 90 to 360 min. Myocardial protection was studied in 50% cardioplegic solution with metabolic inhibitors. Immediate and late viabilities, after 24 h of recovery in the medium, were evaluated by simultaneous staining with fluorescein diacetate and propidium iodide. At 37 degrees C, the 50% concentration of the three cardioplegic solutions did not modify cell viability. At 37 degrees C, with 360 min of incubation, the 100% concentration of the St Thomas' I and Bretschneider solutions diminished immediate viability (mean +/- SD; medium 87% +/- 2%; St Thomas' I 58% +/- 5%; Bretschneider 37% +/- 8%; St Thomas' II 89% +/- 3%) as well as late viability (medium 69% +/- 2%; St Thomas' I 32% +/- 3%; Bretschneider 24% +/- 7%; St Thomas' II 65% +/- 4%). At 4 degrees C, immediate and late viabilities were unaffected by cardioplegic solutions. At 37 degrees C, after 360 min incubation time, metabolic inhibitors diminished immediate viability to 29% +/- 1% and late viability to zero. None of the three cardioplegic solutions used at 50% concentration prevented this effect. At 4 degrees C, immediate viability was not significantly affected by metabolic inhibitors (73% +/- 10%), but the use of Bretschneider cardioplegic solution seemed to be detrimental (53% +/- 9%). On the other hand, recovery phase after pretreatment with metabolic inhibitors with or without cardioplegic solutions for 360 min significantly diminished late viability (medium 63% +/- 7%; metabolic inhibitors 17% +/- 8%; St Thomas' I 17% +/- 6%; Bretschneider 8% +/- 6%; St Thomas' II 15% +/- 3%) and again cardioplegia was inefficient. In conclusion, in this in vitro model for the study of cardioplegic solutions, only pure concentrations of the St Thomas' I and Bretschneider solutions under normothermic conditions were cytotoxic. The well-known protective effects of hypothermia against ischemia and reperfusion injury were both reproduced. Therefore, and even though cardioplegia failed to have any protective effect, probably owing to a severe metabolic inhibition, this model may be useful for studying myocardial protection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0742-2091
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
435-44
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Validity of a model of cultured myocardial cells for assessment of cardioplegia.
pubmed:affiliation
Department of Cardiovascular Surgery, Gabriel Montpied Hospital, Clermont-Ferrand, France.
pubmed:publicationType
Journal Article