title: Global cerebral ischemia in piglets under conditions of mild and deep hypothermia.
abstract: OBJECTIVE
  To investigate the effects of hypothermia on the rate of change and degree of recovery of brain adenosine triphosphate and phosphocreatine concentrations and intracellular pH, we have developed a model that allows phosphorus nuclear magnetic resonance spectroscopy of the intact piglet brain during circulatory arrest.
  
  
  METHODS
  Three groups of piglets were studied. Three control animals underwent cardiopulmonary bypass at normothermia for 1 hour; five group 1 animals underwent bypass at a brain temperature of 15 degrees C, followed by a period of circulatory arrest such that adenosine triphosphate was absent for 21 minutes, followed by 1 hour of reperfusion; and five group 2 animals underwent bypass at a brain temperature of 37 degrees C, followed by a period of circulatory arrest such that adenosine triphosphate was absent for 21 minutes, followed by reperfusion for 1 hour.
  
  
  RESULTS
  Control animals showed no significant metabolic effects of bypass. Group 1 animals showed a slower decay of the adenosine triphosphate and phosphocreatine concentrations than group 2 animals, consistent with a lower metabolic rate, and had a higher pH at the onset of ischemia. Recovery of the adenosine triphosphate concentration was significantly better in group 1 animals (95%) than in group 2 animals (30%) (p less than 0.02), and recovery of the phosphocreatine concentration was also better in group 1 animals (93%) than in group 2 animals (32%) (p less than 0.02). Intracellular pH recovered in group 1 animals, but not in group 2 animals. Regional biochemical assays of metabolites performed in the group 2 piglets and in five pilot piglets exposed to deep hypothermia generally confirmed the spectroscopic findings but demonstrated considerable regional variation, specially in the group 2 piglets' brains.
  
  
  CONCLUSIONS
  We conclude that hypothermia exerts a protective effect on the piglet brain during global ischemia even after the adenosine triphosphate pool has been completely depleted.
authors.affiliation: Department of Neurosurgery, Children's Hospital of Philadelphia, PA 19104.
authors.forename: L N
authors.initials: LN
authors.lastname: Sutton
authors.forename: B J
authors.initials: BJ
authors.lastname: Clark
authors.forename: C R
authors.initials: CR
authors.lastname: Norwood
authors.forename: E J
authors.initials: EJ
authors.lastname: Woodford
authors.forename: F A
authors.initials: FA
authors.lastname: Welsh
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D006324:Heart Arrest, Induced; D006863:Hydrogen-Ion Concentration; D007036:Hypothermia, Induced; D010725:Phosphocreatine / Q000378:metabolism; D013552:Swine
chemical_list: D010725:Phosphocreatine; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate