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  • Articles: DFG German National Licenses  (2)
  • 1995-1999  (2)
  • Amino acids  (1)
  • Calcitonin gene-related peptide  (1)
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  • Articles: DFG German National Licenses  (2)
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Years
  • 1995-1999  (2)
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  • 1
    ISSN: 0942-0940
    Keywords: Calcitonin gene-related peptide ; slow-release tablet ; subarachnoid haemorrhage ; cerebral vasospasm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The calcitonin gene-related peptide (CGRP), a known potent intrinsic cerebral vasodilator, is contained in the sensory nerves from trigeminal ganglia that inervate the cerebral arteries. We previously reported that human α CGRP (hCGRP) dilates spastic cerebral arteries after experimental subarachnoid haemorrhage (SAH) in rabbits. In the present study, we investigated the prophylactic potential of a sustained higher cerebrospinal fluid level ofhCGRP against experimental cerebral vasospasm. AnhCGRP slow-release tablet (hCGRP s-r tablet) was developed for cisternal implantation. Experimental SAH was induced by percutaneous cisternal injection of autologous arterial blood. Angiography was initiated on day 1 (before SAH) and performed everyday. ThehCGRP s-r tablet was implanted into the cisterna magna on day 2 in the treated groups. The spastic response of the basilar artery was maximized on day 4 in the non-treated (80.7% of day 1) and the placebo-treated (79.3%) groups. In contrast, the arterial diameters on day 4 were 96.1% and 90.5% of day 1 in the groups implanted withhCGRP 24 μg and 153 μg s-r tablets, respectively. We also measured the concentration ofhCGRP in the cerebrospinal fluid (CSF) following implantation of thehCGRP 24 μg s-r tablet in the cisterna magna. The hCGRP concentration before implantation was below the dectable level. Following implantation, thehCGRP level in the CSF was 23.12 nmol/L on the second day and remained at elevated levels until the fifth day. These experiments suggest that the intrathecal single implantation of thehCGRP s-r tablet could produce an elevated concentration ofhCGRP in the CSF over five days and have prevented the cerebral vasospasm after SAH in the rabbit. ThehCGRP s-r tablet may be clinically applicable in the treatment of patients with SAH against cerebral vasospasm.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1438-2199
    Keywords: Amino acids ; Imidazole compound ; Mercaptopyruvic acid ; Urocanic acid ; Histidine ; Mass spectrometry ; Paper electrophoresis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary S-[2-Carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptopyruvic acid (I) was chemically synthesized in 15% yield by incubating a reaction mixture oftrans-urocanic acid and 3-fold excess of 3-mercaptopyruvic acid at 45°C for 6 days. The synthesized compound was characterized by fast-atom-bombardment mass spectrometry and high-voltage paper electrophoresis. CompoundI was identified with a product of an enzymatic reaction ofS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-l-cysteine (II) with rat liver homogenate in a phosphate buffer, pH 7.4. CompoundI was degraded toS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl]-3-mercaptolactic acid (III), a compound previously found in human urine [Kinuta et al. (1994) Biochem J 297: 475–478], by incubation with rat liver homogenate. From these results, we suggest that compoundI is a metabolic intermediate for the formation of compoundIII from compoundII. The present pathway follows a formation of compoundII fromS-[2-carboxy-1-(1H-imidazol-4-yl)ethyl] gluthathione [Kinuta et al. (1993) Biochim Biophys Acta 1157: 192–198], a proposed metabolite ofl-histidine.
    Type of Medium: Electronic Resource
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