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Hikaru Matsuda
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Right arrow Myocardial protection

J Thorac Cardiovasc Surg 2003;126:1813-1821
© 2003 The American Association for Thoracic Surgery

Cardiopulmonary support and physiology

Leukocyte-depleted terminal blood cardioplegia provides superior myocardial protective effects in association with myocardium-derived nitric oxide and peroxynitrite production for patients undergoing prolonged aortic crossclamping for more than 120 minutes

Yoshitaka Hayashi, MD, PhDa,*, Yoshiki Sawa, MD, PhDa, Naoto Fukuyama, MD, PhDb, Yuji Miyamoto, MD, PhDa, Toshiki Takahashi, MD, PhDa, Hiroe Nakazawa, MD, PhDb, Hikaru Matsuda, MD, PhDa

a Department of Surgery, Course of Interventional Medicine (E1), Osaka University Graduate School of Medicine, Suita, Osaka, Japan
b Second Department of Physiology, Tokai University School of Medicine, Isehara, Kanagawa, Japan

Presented in part at the First Asia Pacific Scientific Forum (supported by American Heart Association), Honolulu, Hawaii, April 23-26, 2002.

Received for publication December 25, 2002; revisions received March 21, 2003; accepted for publication April 21, 2003.

* Address for reprints: Yoshitaka Hayashi, MD, PhD, Department of Surgery, Course of Interventional Medicine (E1), Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita City, Osaka 565-0871, Japan
hayashi{at}surg1.med.osaka-u.ac.jp

OBJECTIVES: This study was designed to examine the myocardial protective effect of leukocyte-depleted terminal blood cardioplegia in association with nitric oxide and peroxynitrite production, especially for patients undergoing prolonged aortic crossclamping.

METHODS: Fifty-four patients (34 men, 20 women, mean age 56.7 ± 12.7 years) undergoing aortic valve replacement were randomly allocated to one of two groups; group LDTC (n = 27) received 10 minutes of leukocyte-depleted terminal blood cardioplegic solution, and group CONT (n = 27) served as controls. Each group was subdivided into 2 groups: aortic crossclamping for less than 120 minutes in groups LDTC-S (n = 13) and CONT-S (n = 14); aortic crossclamping for 120 minutes or more in groups LDTC-L (n = 14) and CONT-L (n = 13).

RESULTS: After aortic unclamping, group LDTC-L showed higher incidence of spontaneous defibrillation (78.6% vs 30.8%, P = .0213), higher plasma nitrate + nitrite in the coronary sinus effluent (32.5 ± 4.1 vs 28.7 ± 3.0 µmol/L, P = .0013), lower differences between coronary sinus effluent and arterial blood in the percentage ratio of nitrotyrosine to tyrosine (myocardium-derived peroxynitrite; 2.987% ± 0.576% vs 3.951% ± 0.952%, P = .0036), and plasma polymorphonuclear-elastase (113.9 ± 21.3 vs 155.5 ± 41.6 µg/L, P = .0029) and malondialdehyde (2.75 ± 0.67 vs 4.02 ± 0.96 µmol/L, P = .0005) than group CONT did. Postoperatively, group LDTC-L showed lower human-heart fatty acid–binding protein (111.4 ± 25.2 vs 156.4 ± 38.6 IU/L, P = .0013), lower creatine kinase–muscle and brain (19.2 ± 4.7 vs 24.8 ± 6.5 IU/L, P = .0120), and smaller requirement of catecholamine (5.44 ± 2.29 vs 8.45 ± 3.42 µg · kg-1 · min-1, P = .0122). There were no significant differences in these parameters between groups LDTC-S and CONT-S.

CONCLUSIONS: This study demonstrated that leukocyte-depleted terminal blood cardioplegia provided superior myocardial protective effects and regulated myocardial-derived nitric oxide and peroxynitrite production only for patients undergoing aortic crossclamping for more than 120 minutes. The results suggest that prolonged aortic crossclamping deteriorates the tolerance to leukocyte-mediated myocardial injury accompanied by endothelial dysfunction associated with nitric oxide and peroxynitrite production.






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