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J Thorac Cardiovasc Surg 2010;139:174-180
© 2010 The American Association for Thoracic Surgery
Perioperative Management |
Department of Cardiac Surgery, The Jikei University School of Medicine, Tokyo, Japan
Received for publication April 16, 2009; revisions received July 14, 2009; accepted for publication August 9, 2009. * Address for reprints: Hiroshi Kagawa, MD, Department of Cardiac Surgery, The Jikei University School of Medicine, 3-25-8 Nishi-shinbashi, Minato-ku, Tokyo, 105-8461, Japan. (Email: hkagawa{at}jikei.ac.jp).
Objective: Pulmonary ischemia and reperfusion during routine open heart surgery with cardiopulmonary bypass can lead to pulmonary dysfunction and vasoconstriction, resulting in a high morbidity and mortality. We investigated whether ischemia/reperfusion-induced pulmonary dysfunction after full-flow cardiopulmonary bypass could be prevented by the infusion of leukocyte-depleted hypoxemic blood during the early phase of reperfusion (terminal leukocyte-depleted lung reperfusion) and whether the benefits of this method were nullified by using hyperoxemic blood for reperfusion.
Methods: Twenty-one neonatal piglets underwent 180 minutes of full-flow cardiopulmonary bypass with pulmonary artery occlusion, followed by reperfusion. The piglets were divided into 3 groups of 7 animals. In group I, uncontrolled reperfusion was achieved by unclamping the pulmonary artery. In contrast, pulmonary reperfusion was done with leukocyte-depleted hyperoxemic blood in group II or with leukocyte-depleted hypoxemic blood in group III for 15 minutes at a flow rate of 10 mL/min/kg before pulmonary artery unclamping. Then the animals were monitored for 120 minutes to evaluate post-cardiopulmonary bypass pulmonary function.
Results: Group I developed pulmonary dysfunction that was characterized by an increased alveolar-arterial oxygen difference (204 ± 57.7 mm Hg), pulmonary vasoconstriction, and decreased static lung compliance. Terminal leukocyte-depleted lung reperfusion attenuated post-cardiopulmonary bypass pulmonary dysfunction and vasoconstriction when hypoxemic blood was used for reperfusion (alveolar-arterial oxygen difference, 162 ± 61.0 mm Hg). In contrast, no benefit of terminal leukocyte-depleted lung reperfusion was detected after reperfusion with hyperoxemic blood (alveolar-arterial oxygen difference, 207 ± 60.8 mm Hg).
Conclusion: Reperfusion with leukocyte-depleted hypoxemic blood has a protective effect against ischemia/reperfusion-induced pulmonary dysfunction by reducing endothelial damage, cytokine release, and leukocyte activation.
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