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J Thorac Cardiovasc Surg 2002;123:1199-1205
© 2002 The American Association for Thoracic Surgery

General Thoracic Surgery (GTS)

Cardiopulmonary bypass reduction of bronchial blood flow: A potential mechanism for lung injury in a neonatal pig model

From the Departments of Cardiovascular Surgery^a and Pathology,^b Albert-Ludwigs-University, Freiburg, Germany.

C.S. was supported by the Zentrum für Klinische Forschung of the University of Freiburg. T.D. was supported by the Emmy Noether-Program of the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG, Do602/2-1).

Received for publication Aug 16, 2001. Revisions requested Oct 24, 2001; revisions received Nov 14, 2001. Accepted for publication Nov 20, 2001. Address for reprints: Christian Schlensak, MD, Department of Cardiovascular Surgery, University of Freiburg, Hugstetter Strasse 55, D-79106 Freiburg, Germany (E-mail: schlensa{at}ch11.ukl.uni-freiburg.de).

Background: During total cardiopulmonary bypass, blood flow to the lungs is limited to flow through the bronchial arteries. We tested the hypothesis that bronchial blood flow during cardiopulmonary bypass is insufficient to prevent ischemia of the lung and that perfusion of the pulmonary arteries with oxygenated blood during bypass would reduce lung injury.
Methods: Eighteen piglets (5.0 ± 0.5 kg) were subjected to 120 minutes of normothermic total cardiopulmonary bypass, followed by 60 minutes of postbypass perfusion. Nine of them received continuous pulmonary perfusion with oxygenated blood during bypass. Six additional piglets served as a control group and were mechanically ventilated after sternotomy for 180 minutes only. We quantitated bronchial arterial blood flow, tissue lactate content, and alveolar septal thickness and surface area. We also obtained bronchioalveolar lavage fluid samples.
Results: With the beginning of cardiopulmonary bypass, bronchial arterial blood flow decreased to 13% of baseline (42.1 ± 10.4 to 5.6 ± 1.0 mL/min). It remained decreased until the end of bypass and returned to starting levels 60 minutes after bypass. The decrease in bronchial blood flow was associated with a 3-fold increase in tissue lactate content. At the end of reperfusion there was a 2-fold increase in alveolar septal thickness and significant accumulations relative to control in the bronchoalveolar lavage fluid of albumin, lactate dehydrogenase, neutrophils, and elastase. Controlled pulmonary perfusion significantly ameliorated all the observed changes.
Conclusion: Cardiopulmonary bypass caused a reduction in bronchial arterial blood flow, which was associated with injury of the lung. Controlled pulmonary perfusion reduced injury to the lung during bypass. The inflammatory response, as evidenced by bronchoalveolar lavage fluid, may be caused by ischemia.

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