title: Cerebral effects of cold reperfusion after hypothermic circulatory arrest.
abstract: OBJECTIVE
  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 degrees C. Eight animals were rewarmed immediately after hypothermic circulatory arrest (controls), and 8 were reperfused for 20 minutes at 20 degrees 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 degrees C), before hypothermic circulatory arrest, after discontinuing circulatory arrest at 37 degrees 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 degrees C, suggesting that cold reperfusion may decrease cerebral edema and thereby improve outcome after prolonged hypothermic circulatory arrest.
authors.affiliation: Department of Cardiothoracic Surgery, Mount Sinai School of Medicine, One Gustave Levy Place, New York, NY 10029, USA.
authors.forename: M P
authors.initials: MP
authors.lastname: Ehrlich
authors.forename: J
authors.initials: J
authors.lastname: McCullough
authors.forename: D
authors.initials: D
authors.lastname: Wolfe
authors.forename: N
authors.initials: N
authors.lastname: Zhang
authors.forename: H
authors.initials: H
authors.lastname: Shiang
authors.forename: D
authors.initials: D
authors.lastname: Weisz
authors.forename: C
authors.initials: C
authors.lastname: Bodian
authors.forename: R B
authors.initials: RB
authors.lastname: Griepp
mesh_terms: D000818:Animals; D001831:Body Temperature; D001834:Body Water / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D002560:Cerebrovascular Circulation; D003080:Cold Temperature; D004569:Electroencephalography; D005071:Evoked Potentials; D006324:Heart Arrest, Induced; D007036:Hypothermia, Induced; D007427:Intracranial Pressure; D019344:Lactic Acid / Q000378:metabolism; D015425:Myocardial Reperfusion / Q000379:methods; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D013552:Swine
chemical_list: D019344:Lactic Acid; D010100:Oxygen