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Ann Thorac Surg 2001;71:1325-1334
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Histopathologic consequences of hyperglycemic cerebral ischemia during hypothermic cardiopulmonary bypass in pigs

^a Department of Anesthesiology (Division of Cardiothoracic Anesthesiology), University of Texas Medical Branch, Galveston, Texas, USA
^b Department of Pathology, The University of Texas Medical Branch, Galveston, Texas, USA
^c Department of Neurosurgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

Accepted for publication December 13, 2000.

Address reprint requests to Dr Johnston, Department of Anesthesiology, The University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555-0591
e-mail: william.johnston{at}utmb.edu

Background. This study examined whether 34°C or 31°C hypothermia during global cerebral ischemia with hyperglycemic cardiopulmonary bypass (CPB) in surviving pigs improves electroencephalographic (EEG) recovery and histopathologic scores when compared with normothermic animals.

Methods. Anesthetized pigs were placed on CPB and randomly assigned to 37°C (n = 9), 34°C (n = 10), or 31°C (n = 8) management. After increasing serum glucose to 300 mg/dL, animals underwent 15 minutes of global cerebral ischemia by temporarily occluding the innominate and left subclavian arteries. Following reperfusion, rewarming, and termination of CPB, animals were recovered for 24 (37°C animals) or 72 hours (34°C and 31°C animals). Daily EEG signals were recorded, and brain histopathology from cortical, hippocampal, and cerebellar regions was graded by an independent observer.

Results. Before ischemia, serum glucose concentrations were similar in the 37°C (307 ± 9 mg/dL), 34°C (311 ± 14 mg/dL), and 31°C (310 ± 15) groups. By the first postoperative day, EEG scores in 31°C animals (4.2 ± 0.6) had returned to baseline and were greater than those in the 34°C (3.4 ± 0.5) and 37°C (2.5 ± 0.4) groups (p < 0.05, respectively, between groups). Cooling to 34°C showed selective improvement over 37°C in hippocampal, temporal cortical, and cerebellar regions, but the greatest improvement in all regions occurred with 31°C. Cumulative neuropathology scores in 31°C animals (13.5 ± 2.2) exceeded 34°C (6.8 ± 2.2) and 37°C (1.9 ± 2.1) animals (p < 0.05, respectively, between groups).

Conclusions. Hypothermia during CPB significantly reduced the morphologic consequences of severe, temporary cerebral ischemia under hyperglycemic conditions, with the greatest protection at 31°C.

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