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J Thorac Cardiovasc Surg 2004;127:1723-1727
© 2004 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Pharmacologic preconditioning of JTE-607, a novel cytokine inhibitor, attenuates ischemia-reperfusion injury in the myocardium

Masahiro Ryugo, MDa, Yoshiki Sawa, MDa,*, Masamichi Ono, MDa, Yuji Miyamoto, MDa, Alexei N. Aleshin, MDa, Hikaru Matsuda, MDa

a Division of Cardiovascular Surgery, Department of Surgery, Osaka University Graduate School of Medicine, Osaka, Japan

Received for publication April 28, 2003; revisions received July 30, 2003; accepted for publication August 11, 2003.

* Address for reprints: Yoshiki Sawa, MD, Division of Cardiovascular Surgery, Department of Surgery, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
sawa{at}surg1.med.osaka-u.ac.jp

BACKGROUND: Myocardial ischemia-reperfusion injury is a main cause of postoperative cardiac dysfunction, and a burst of proinflammatory cytokines, such as tumor necrosis factor {alpha}, interleukin 1ß, interleukin 6, and interleukin 8, plays a pivotal role. Recently, JTE-607 has been reported as a potent inhibitor of the multiple inflammatory cytokines in the endotoxin shock mouse model. In this study we proved the hypothesis that JTE-607 might attenuate myocardial ischemia-reperfusion injury in a rat model.

METHODS: The isolated rat hearts in the JTE-607 preconditioning group (J group, n = 8) or control group (C group, n = 8) were subjected to warm ischemia (37°C) for 30 minutes, followed by 60 minutes of reperfusion with the Langendorff perfusion system.

RESULTS: Left ventricular developed pressure and maximum dp/dt after reperfusion were significantly improved in the J group than in the C group (P < .01). Creatine phosphokinase leakage is significantly lower in the J group (P < .05). Moreover, the tissue cytokine levels, such as tumor necrosis factor {alpha}, interleukin 6, and interleukin 8, in the myocardium were significantly lower in the J group than in the C group (P < .05).

CONCLUSION: These results suggested that the pharmacologic preconditioning of JTE-607 inhibits a burst of endogenous cytokines in the myocardium, resulting in the improvement of cardiac function after ischemia-reperfusion injury. Thus JTE-607 might be a novel therapeutic strategy for the protection of postoperative cardiac dysfunction in cardiac surgery.






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