title: Effect of lidocaine on improving cerebral protection provided by retrograde cerebral perfusion: a neuropathologic study.
abstract: OBJECTIVE
  To determine whether lidocaine can improve the neuropathologic results in canine brains after retrograde cerebral perfusion (RCP).
  
  
  METHODS
  Randomized, blinded, experimental study.
  
  
  METHODS
  University animal laboratory.
  
  
  METHODS
  Mongrel dogs.
  
  
  METHODS
  Fourteen mongrel dogs were placed on 120 minutes of hypothermic (20 degrees C) RCP. Following the RPC, they then resumed cardiopulmonary bypass and rewarming for 60 minutes. In the lidocaine group (n = 8), lidocaine was administered continuously; in the control group (n = 6), normal saline was administered. Cerebral perfusion fixation was performed at the end of the experiment.
  
  
  RESULTS
  The number of ischemic cells in 200 neurons was counted in the parietal cortex, CA1 sector of the hippocampus, CA3 sector of the hippocampus, ventral posterolateral nucleus of the thalamus, and Purkinje cells of the cerebellar cortex. Those in the parietal cortex, CA1 sector of the hippocampus, and ventral posterolateral nucleus of the thalamus were significantly less in the lidocaine group than in the control group (25.8+/-17.3 v 53.7+/-12.0; p < 0.01; 17.0+/-8.5 v 54.7+/-22.1; p < 0.01; and 16.9+/-17.8 v 49.7+/-28.4; p < 0.05, respectively). The total number of ischemic cells in the five examined regions was also significantly less in the lidocaine group than in the control group (89.5+/-19.4 v 219.5+/-45.5; p < 0.01).
  
  
  CONCLUSIONS
  Continuous lidocaine significantly alleviated the ischemic neuropathologic injury after RCP and thus possibly improved cerebral protection.
authors.affiliation: Department of Anesthesiology, the First School of Clinical Medicine, China.
authors.forename: D
authors.initials: D
authors.lastname: Wang
authors.forename: X
authors.initials: X
authors.lastname: Wu
authors.forename: Y
authors.initials: Y
authors.lastname: Zhong
authors.forename: Y
authors.initials: Y
authors.lastname: Zhou
authors.forename: G
authors.initials: G
authors.lastname: Shan
authors.forename: X
authors.initials: X
authors.lastname: Hu
authors.forename: J
authors.initials: J
authors.lastname: Li
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
authors.forename: X
authors.initials: X
authors.lastname: Qin
authors.forename: Z
authors.initials: Z
authors.lastname: Xia
mesh_terms: D000779:Anesthetics, Local / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D002545:Brain Ischemia / Q000209:etiology / Q000473:pathology; D002315:Cardiopulmonary Bypass; D002531:Cerebellum / Q000473:pathology; D002560:Cerebrovascular Circulation / Q000187:drug effects*; D004285:Dogs; D006324:Heart Arrest, Induced; D006624:Hippocampus / Q000473:pathology; D007036:Hypothermia, Induced; D008012:Lidocaine / Q000008:administration & dosage / Q000494:pharmacology*; D009474:Neurons / Q000473:pathology; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000494:pharmacology*; D010296:Parietal Lobe / Q000473:pathology; D011689:Purkinje Cells / Q000473:pathology; D011897:Random Allocation; D017694:Rewarming; D016037:Single-Blind Method; D012965:Sodium Chloride; D013787:Thalamic Nuclei / Q000473:pathology
chemical_list: D000779:Anesthetics, Local; D001786:Blood Glucose; D018696:Neuroprotective Agents; D012965:Sodium Chloride; D008012:Lidocaine