title: Neonatal ischemic neuroprotection by modest hypothermia is associated with attenuated brain acidosis.
abstract: OBJECTIVE
  A 2.9 degrees C reduction in the intraischemic rectal temperature of neonatal piglets is associated with less brain damage compared with animals with normothermic rectal temperatures. This investigation studied one potential mechanism for this observation: better maintenance of energy stores and less brain acidosis secondary to reduced metabolic activity associated with modest hypothermia.
  
  
  METHODS
  31P MR spectroscopy was used to study piglets before, during, and after 15 minutes of partial brain ischemia with intraischemic rectal temperatures of either 38.3 +/- 0.4 degrees C (n = 10, normothermic) or 35.4 +/- 0.5 degrees C (n = 10, hypothermic). Animals were followed up for up to 72 hours after ischemia and were evaluated clinically and by brain histology.
  
  
  RESULTS
  Values for pHi remained 0.15 to 0.20 pH units greater in modestly hypothermic than in normothermic piglets during ischemia and the initial 30 minutes after ischemia (P = .049, group effect). Phosphocreatine, beta-ATP, and inorganic phosphorus were similar between groups. The relationship between the intraischemic energy state and subsequent clinical evidence of brain damage (irrespective of group assignment) revealed lower pHi over the last 7 minutes of ischemia for abnormal compared with normal piglets (5.98 +/- 0.22 versus 6.39 +/- 0.24, respectively; P = .002). In contrast, intraischemic beta-ATP (41 +/- 19% versus 57 +/- 21% of control) and inorganic phosphorus (273 +/- 31% versus 224 +/- 92% of control) for abnormal and normal piglets, respectively, did not differ between groups.
  
  
  CONCLUSIONS
  Intraischemic modest hypothermia attenuates the severity of brain acidosis during and 30 minutes after ischemia compared with normothermic animals and supports the concept that attenuated brain acidosis is a potential mechanism by which hypothermia may reduce ischemic brain damage.
authors.affiliation: Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas 75235-9063, USA.
authors.forename: A R
authors.initials: AR
authors.lastname: Laptook
authors.forename: R J
authors.initials: RJ
authors.lastname: Corbett
authors.forename: D
authors.initials: D
authors.lastname: Burns
authors.forename: R
authors.initials: R
authors.lastname: Sterett
mesh_terms: D000138:Acidosis / Q000378:metabolism / Q000517:prevention & control*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001831:Body Temperature; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001925:Brain Damage, Chronic / Q000517:prevention & control; D001927:Brain Diseases / Q000378:metabolism / Q000517:prevention & control*; D002545:Brain Ischemia / Q000473:pathology / Q000517:prevention & control*; D004734:Energy Metabolism; D005500:Follow-Up Studies; D006863:Hydrogen-Ion Concentration; D007036:Hypothermia, Induced; D009682:Magnetic Resonance Spectroscopy; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D010759:Phosphorus Isotopes; D013552:Swine; D013997:Time Factors
chemical_list: D010710:Phosphates; D010759:Phosphorus Isotopes; D010725:Phosphocreatine; D000255:Adenosine Triphosphate