Open AccessEffect of Systemic Administration of L-Kynurenine on Corticocerebral Blood Flow under Normal and Ischemic Conditions of the Brain in Conscious Rabbits
Author(s) -
Katalin Sas,
Klára Csete,
László Vécsei,
Julius Gy. Papp
Publication year - 2003
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-200309000-00012
Subject(s) - kynurenic acid , neuroprotection , ischemia , pharmacology , nitric oxide , medicine , anesthesia , cholinergic , antagonist , endogeny , saline , cerebral blood flow , chemistry , endocrinology , receptor
Kynurenic acid, the only known endogenous antagonist of the excitatory amino acid receptors, exerts neuroprotective effect in focal cerebral ischemia. Kynurenic acid poorly while its bioprecursor, l-kynurenine (L-KYN) completely crosses the blood-brain barrier. The aim of our study was to investigate the effect of intravenous l-KYN (0.3, 1, and 3 mg/kg) on the normal and the unilateral carotid artery occlusion induced ischemic corticocerebral blood flow (cCBF) measured by hydrogen polarography in conscious rabbits. Administration of l-KYN produced a significant increase in the normal cCBF; the peak values were recorded at the dose of 1 mg/kg (187% at 120 and 150 mins. respectively). The cCBF-improving effect of l-KYN was immediate and highly pronounced also in rabbits with carotid occlusion (peak value was 192% at 120 mins. at the dose of 1 mg/kg). Pretreatment with either atropine or Nomega-nitro-L-arginine-methyl-ester (L-NAME) prevented the l-KYN induced enhancement of the normal and the ischemic cCBF alike. It is suggested that the cCBF-increasing effect of l-KYN might be mediated by activation of cholinergic and nitric oxide pathways.