Pre-ischaemic administration of procaine suppresses ischaemic glutamate release and reduces neuronal damage in the gerbil hippocampus.
The effects of intracerebroventricular administration of procaine 2 mumol on ischaemic release of neurotransmitter amino acids in the gerbil hippocampal CAI region were investigated using a microdialysis-high-performance liquid chromatography procedure. Histological outcome was examined by comparing delayed neuronal death between animals treated with procaine before ischaemia and animals treated after ischaemia. Transient forebrain ischaemia for 3 min produced increases in dialysate amino acid concentrations. Aspartate, glutamate and glycine reached 331%, 394% and 233% of pre-ischaemic values. Basal concentrations were restored immediately by reperfusion. Pre-ischaemic administration of procaine suppressed peak release and improved histological outcome. However, post-ischaemic administration did not protect against ischaemic neuronal death. Improvement in ischaemic neuronal damage by pre-ischaemic administration of procaine may be related to suppression of excitatory amino acid release.
Adachi
N
N
Department of Anaesthesiology and Resuscitology, Ehime University School of Medicine, Japan.
Chen
J
J
Nakanishi
K
K
Arai
T
T
D000596:Amino Acids / Q000378:metabolism*; D000779:Anesthetics, Local / Q000627:therapeutic use*; D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D005849:Gerbillinae; D018698:Glutamic Acid / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D008297:Male; D018377:Neurotransmitter Agents / Q000378:metabolism; D011343:Procaine / Q000627:therapeutic use*
D000596:Amino Acids; D000779:Anesthetics, Local; D018377:Neurotransmitter Agents; D018698:Glutamic Acid; D011343:Procaine