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Transcript
1332, Either, cat: 1
HEPARIN ADDED TO CARDIOPLEGIC SOLUTION INHIBITS TNF-ALPHA
PRODUCTION AND ATTENUATES MYOCARDIAL ISCHEMICREPERFUSION INJURY
I Frolkis , D Pevni, I Shapira, Y Paz, N Nesher, R Mohr, G Uretzky
Tel Aviv Sourasky Medical Center, Sacler Faculty of Medicine, Tel Aviv University,
Israel
Objectives: Tumor necrosis factor-alpha is known to be a proinflammatory cytokine that
has a pronounced negative inotropic effect and plays an important role in ischemicreperfusion injury. Methods: Twenty isolated rat hearts were randomly divided equally
into two heparin and non heparin groups and perfused by Krebs-Henseleit solution using
a modified Langendorff model. The influence of heparin on synthesis and release of
tumor necrosis factor-alpha by isolated rat hearts after one hour of global cardioplegic
ischemia and on left ventricular performances during 30 minutes of postischemic
reperfusion was investigated. Results: Significant amounts of tumor necrosis factor-alpha
in myocardial tissue (1149±33.7 pg/g) and effluent (951.8±27.3 pg/ml) from the coronary
sinus were detected after global cardioplegic ischemia. The addition of heparin to the
cardioplegic solution significantly improved the recovery of the postischemic heart left
ventricular function (p<0.0001 for all measurements). Tumor necrosis factor-alpha
protein production in the heparin-treated hearts was below detectable levels despite a
postischemic increase of tumor necrosis factor-alpha mRNA expression in both heparintreated (0.71±0.06) and non-treated hearts (0.81 ± 0.12). Conclusion: This study shows,
for the first time, that heparin causes inhibition of tumor necrosis factor-alpha protein
synthesis and release from the isolated ischemic rat heart within the post-transcriptional
stage, and that it prevents depression of left ventricular function caused by ischemicreperfusion injury.