title: Low-dose Carbicarb improves cerebral outcome after asphyxial cardiac arrest in rats.
abstract: OBJECTIVE
  Controversy surrounds the use of buffers during cardiac arrest to correct acidosis. The objective of this study was to determine whether attenuation or neutralization of cerebral acidosis by Carbicarb alters hippocampal glutamate levels, neuronal cell death, and neurologic deficits after reperfusion from asphyxial cardiac arrest in rats.
  
  
  METHODS
  Rats were prospectively randomized to either a control (n=45), low-dose Carbicarb (LDC; 3 mL/kg, n=45), or high-dose Carbicarb (HDC; 6 mL/kg, n=45) group in a blinded fashion during resuscitation after 8 minutes of asphyxial cardiac arrest. Microdialysis was used to assess brain pH and glutamate. A neurologic deficit score and neuronal cell death in the hippocampus were determined at day 7.
  
  
  RESULTS
  Resuscitation was greatest in LDC rats (42/45) and least in HDC rats (28/45) versus that in control rats (34/45). Brain pH was higher in the LDC and HDC rats 10 minutes after resuscitation and remained higher than that of control rats for 120 minutes after resuscitation. Glutamate levels at 10 to 120 minutes after reperfusion were lowest in the LDC rats. LDC rats had the lowest neurologic deficit score (1+/-2) versus that of control rats (13+/-8) and HDC rats (19+/-6). Hippocampal neuronal cell death was lowest in LDC rats (30+/-20) versus that in control rats (86+/-47) and HDC rats (233+/-85).
  
  
  CONCLUSIONS
  LDC administered during resuscitation from asphyxial cardiac arrest attenuated acidosis, improved resuscitation, and reduced neurologic deficits and the number of dead hippocampal neurons. Neutralization of cerebral acidosis with HDC increased the number of dead hippocampal neurons and neurologic deficits after resuscitation from cardiac arrest in rats.
authors.affiliation: Department of Emergency Medicine, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA. LKatz@med.unc.edu
authors.forename: Laurence M
authors.initials: LM
authors.lastname: Katz
authors.forename: Yuanfan
authors.initials: Y
authors.lastname: Wang
authors.forename: Steve
authors.initials: S
authors.lastname: Rockoff
authors.forename: Thomas W
authors.initials: TW
authors.lastname: Bouldin
mesh_terms: D000138:Acidosis / Q000188:drug therapy / Q000209:etiology; D000818:Animals; D001237:Asphyxia / Q000150:complications*; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D002254:Carbonates / Q000627:therapeutic use*; D016923:Cell Death / Q000187:drug effects; D004195:Disease Models, Animal; D004338:Drug Combinations; D018698:Glutamic Acid / Q000187:drug effects / Q000378:metabolism; D006323:Heart Arrest / Q000150:complications*; D006624:Hippocampus / Q000378:metabolism; D009474:Neurons / Q000187:drug effects; D051381:Rats; D020127:Recovery of Function / Q000187:drug effects; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000209:etiology; D017693:Sodium Bicarbonate / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D002254:Carbonates; D004338:Drug Combinations; C046283:sodium bicarbonate, sodium carbonate drug combination; D018698:Glutamic Acid; D017693:Sodium Bicarbonate