Low-dose Carbicarb improves cerebral outcome after asphyxial cardiac arrest in rats

作     者：Katz, LM Wang, YF Rockoff, S Bouldin, TW 

作者机构：Univ N Carolina Sch Med Dept Emergency Med Chapel Hill NC USA Univ N Carolina Sch Med Dept Pathol & Lab Med Chapel Hill NC USA Lake Erie Coll Osteopath Med Erie PA USA 

出 版 物：《ANNALS OF EMERGENCY MEDICINE》 (急救医学纪事)

年 卷 期：2002年第39卷第4期

页      面：359-365页

核心收录：

学科分类：1002[医学-临床医学] 10[医学] 

基　　金：American Heart Association  AHA  (9601408) 

主　　题：酸中毒/药物疗法 酸中毒/病因学 窒息/并发症 脑/代谢 脑缺血/药物疗法 脑缺血/病因学 脑缺血/代谢 碳酸盐类/治疗应用 细胞死亡/药物作用 疾病模型 动物 复方合剂 谷氨酸/药物作用 谷氨酸/代谢 心脏停搏/并发症 海马/代谢 神经元/药物作用 功能恢复/药物作用 再灌注损伤/药物疗法 再灌注损伤/病因学 碳酸氢钠/治疗应用 治疗结果 动物 大鼠 

摘      要：Study 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: Bats 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). Conclusion: 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.