| Autor: |
Sjakste, Nikolajs, Baumane, Larisa, Boucher, Jcan-Luc, Dzintare, Maija, Meirena, Dainuvite, Sjakste, Jelizaveta, Lauberte, Lasma, Kalvinsh, Ivars |
| Předmět: |
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| Zdroj: |
Basic & Clinical Pharmacology & Toxicology; Jan2004, Vol. 94 Issue 1, p46-50, 5p |
| Abstrakt: |
Production of nitric oxide was measured in lipopolysaccharide-treated rats (10 mg/kg, 4 hr) using the electron paramagnetic resonance method. As compared to the control animals, the nitric oxide level in liver of lipopolysaccharide-treated rats increased from 27.6±4.7 to 1485±129 ng/g tissue, in heart from 4.8±0.7 to 271±26 ng/g tissue, in blood from 33.6±12.4 to 638±136 ng/g tissue, in kidney from 3.3±0.5 to 356±31 ng/g tissue, in brain cortex from 46.0±3.4 to 227±27 ng/g tissue, in cerebellum from 27.7±2.6 to 218±30 ng/g tissue, and in testes from 13.8±1.1 to 86±8 ng/g tissue. Administration of the antiischaemic drug, mildronate (120 mg/kg) caused a significant twofold decrease of the nitric oxide level in brain cortex and cerebellum 1 hr after drug administration. Its natural analogue γ-butyrobetaine (30 mg/kg) triggered a twofold decrease of the nitric oxide concentration in all studied tissues 30 min. after the administration. Nitric oxide reached the initial level 2 hr later. Neither mildronate nor γ-butyrobetaine could inhibit the inducible nitric oxide synthase in vitro. Analogues of γ-butyrobetaine appear to be prospective drugs for the treatment of circulatory complications of sepsis. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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