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J Thorac Cardiovasc Surg 1999;117:1172-1179
© 1999 Mosby, Inc.
SURGERY FOR CONGENITAL HEART DISEASE |
From the Department of Cardiac Surgery, Children's Hospital, and the Department of Surgery, Harvard Medical School,a and the Departments of Pathologyb and Neurology,c Children's Hospital and Harvard Medical School, Boston, Mass.
Supported by a Habilitandenstipendium of the Deutsche Forschungsgemeinschaft NO344/1-1 (G.N.). The S-100 enzyme kit was kindly provided by Sangtec Medical AB, Bromma, Sweden. The NIRO 500 system was provided by Hamamatsu Photonics KK, Hamamatsu City, Japan.
Received for publication Aug 28, 1998. Revisions requested Oct 30, 1998. Revisions received Feb 2, 1999. Accepted for publication Feb 19, 1999. Address for reprints: Richard A. Jonas, MD, Department of Cardiac Surgery, Children's Hospital, 300 Longwood Ave, Boston, MA 02115.
Objectives: Laboratory studies suggest that myocardial reperfusion injury is exacerbated by free radicals when pure oxygen is used during cardiopulmonary bypass. In phase I of this study we demonstrated that normoxic perfusion during cardiopulmonary bypass does not increase the risk of microembolic brain injury so long as a membrane oxygenator with an arterial filter is used. In phase II of this study we studied the hypothesis that normoxic perfusion increases the risk of hypoxic brain injury after deep hypothermia with circulatory arrest.
Methods: With membrane oxygenators with arterial filters, 10 piglets (8-10 kg) underwent 120 minutes of deep hypothermia and circulatory arrest at 15°C, were rewarmed to 37°C, and were weaned from bypass. In 5 piglets normoxia (PaO2 64-181 mm Hg) was used during cardiopulmonary bypass and in 5 hyperoxia (PaO2 400-900 mm Hg) was used. After 6 hours of reperfusion the brain was fixed for histologic evaluation. Near-infrared spectroscopy was used to monitor cerebral oxyhemoglobin and oxidized cytochrome a,a3 concentrations.
Results: Histologic examination revealed a significant increase in brain damage in the normoxia group (score 12.4 versus 8.6, P = .01), especially in the neocortex and hippocampal regions. Cytochrome a,a 3 and oxyhemoglobin concentrations tended to be lower during deep hypothermia and circulatory arrest in the normoxia group (P = .16).
Conclusions: In the setting of prolonged deep hypothermia and circulatory arrest with membrane oxygenators, normoxic cardiopulmonary bypass significantly increases histologically graded brain damage with respect to hyperoxic cardiopulmonary bypass. Near-infrared spectroscopy suggests that the mechanism is hypoxic injury, which presumably overwhelms any injury caused by increased oxygen free radicals. (J Thorac Cardiovasc Surg 1999;117:1172-9)
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