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Laboratory and Animal Investigations |

Heparin Added to Cardioplegic Solution Inhibits Tumor Necrosis Factor-α Production and Attenuates Myocardial Ischemic-Reperfusion Injury*

Dimitry Pevni, MD; Inna Frolkis, MD, PhD; Itzhak Shapira, MD; Doron Schwartz, MD; Yael Yuhas, PhD; Idit F. Schwartz, MD; Tamara Chernichovski, MSc; Gideon Uretzky, MD
Author and Funding Information

*From the Departments of Thoracic and Cardiac Surgery (Drs. Pevni, Frolkis, Shapira, and Uretzky) and Nephrology (Drs. D. Schwartz and I.F. Schwartz, and Ms. Chernichovski), Tel-Aviv Sourasky Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel; and the Felsenstein Medical Research Center (Dr. Yuhas), Petah-Tikva, Israel.

Correspondence to: Inna Frolkis, MD, PhD, Department of Thoracic and Cardiovascular Surgery, Tel Aviv Sourasky Medical Center, 6 Weizmann St, Tel Aviv 64239, Israel; e-mail: frolkisi@tasmc.health.gov.il



Chest. 2005;128(3):1805-1811. doi:10.1378/chest.128.3.1805
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Objectives: Tumor necrosis factor (TNF)-α is known to be a proinflammatory cytokine that has a pronounced negative inotropic effect and plays an important role in ischemic-reperfusion injury.

Methods: Twenty isolated rat hearts were randomly divided equally into two groups (heparin and nonheparin) and were perfused with a Krebs-Henseleit solution using a modified Langendorff model. The influence of heparin on the synthesis and release of TNF-α by isolated rat hearts after 1 h of global cardioplegic ischemia and on left ventricular (LV) performances during 30 min of postischemic reperfusion was investigated.

Results: Significant mean (± SEM) amounts of TNF-α in myocardial tissue (1,149 ± 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 LV function in the postischemic heart (p < 0.0001 for all measurements). TNF-α protein production in the heparin-treated hearts was below detectable levels despite a postischemic increase of TNF-α messenger RNA expression in both heparin-treated hearts and nontreated hearts (0.71 ± 0.06 and 0.8 ± 0.12 relative optical density, respectively).

Conclusion: This study shows, for the first time, that heparin causes the inhibition of TNF-α protein synthesis and release from the isolated ischemic rat heart within the posttranscriptional stage, and that it prevents the depression of LV function caused by ischemic-reperfusion injury.

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