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J Thorac Cardiovasc Surg 2001;121:923-931
© 2001 The American Association for Thoracic Surgery


Surgery for Acquired Cardiovascular Disease

Cerebral effects of cold reperfusion after hypothermic circulatory arrest

Marek P. Ehrlich, MD, Jock McCullough, MD, David Wolfe, MDa, Ning Zhang, MD, Howard Shiang, DVM, Donald Weisz, PhDb, Carol Bodian, DrPHc, Randall B. Griepp, MD

From the Departments of Cardiothoracic Surgery, Pathology,a Neurosurgery,b and Biomathematics,c Mount Sinai School of Medicine, New York, NY.

This work was supported by grant HL 45636 from the National Institutes of Health and by the Nat Lapkin Foundation.

Received for publication May 4, 2000. Revisions requested Aug 11, 2000; revisions received Oct 6, 2000. Accepted for publication Nov 27, 2000. Address for reprints: Randall B. Griepp, MD, Department of Cardiothoracic Surgery, Mount Sinai School of Medicine, One Gustave Levy Place, Box 1028, New York, NY 10029.

Objectives: This study was undertaken to explore whether an interval of cold reperfusion can improve cerebral outcome after prolonged hypothermic circulatory arrest.
Methods: Sixteen pigs (27-30 kg) underwent 90 minutes of circulatory arrest at a brain temperature of 20°C. Eight animals were rewarmed immediately after hypothermic circulatory arrest (controls), and 8 were reperfused for 20 minutes at 20°C and then rewarmed (cold reperfusion). Electrophysiologic recordings, fluorescent microsphere determinations of cerebral blood flow, calculations of cerebral oxygen consumption, and direct measurements of intracranial pressure (millimeters of mercury) were obtained at baseline (37°C), before hypothermic circulatory arrest, after discontinuing circulatory arrest at 37°C deep brain temperature, and at 2, 4, and 6 hours thereafter. Histopathologic features and percent brain water were determined after the animals were sacrificed.
Results: Cerebral blood flow and oxygen consumption decreased during cooling: cerebral oxygen consumption returned to baseline levels after 4 hours, but cerebral blood flow remained depressed until 6 hours in both groups. Cold reperfusion failed to improve electrophysiologic recovery or to reduce brain weight, but median intracranial pressure increased significantly less after cold reperfusion than in controls (P = .02). Although no significant difference in the incidence of histopathologic abnormalities between groups was found, all 3 animals with an intracranial pressure of more than 15 mm Hg after immediate rewarming had histopathologic lesions, and high intracranial pressure was more prevalent among all animals with subsequent histopathologic lesions (P = .03).
Conclusions: Cold reperfusion significantly inhibited the rise in intracranial pressure seen in control pigs after 90 minutes of circulatory arrest at 20°C, suggesting that cold reperfusion may decrease cerebral edema and thereby improve outcome after prolonged hypothermic circulatory arrest.




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