HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:
Guest Access | Sign In via User Name/Password

This Article Full Text Free Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Pevni, D. Articles by Uretzky, G. Search for Related Content PubMed PubMed Citation Articles by Pevni, D. Articles by Uretzky, G.

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

^* 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{at}tasmc.health.gov.il

Objectives: Tumor necrosis factor (TNF)- 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- 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- 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- protein production in the heparin-treated hearts was below detectable levels despite a postischemic increase of TNF- 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- 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.

Key Words: cardioplegia • isolated perfused heart • messenger RNA • tumor necrosis factor-

This article has been cited by other articles:

				M. Paciaroni, G. Agnelli, S. Micheli, and V. Caso Efficacy and Safety of Anticoagulant Treatment in Acute Cardioembolic Stroke: A Meta-Analysis of Randomized Controlled Trials Stroke, February 1, 2007; 38(2): 423 - 430. [Abstract] [Full Text] [PDF]