| Autor: |
Sjakste N; Faculty of Medicine, University of Latvia, and Latvian Institute of Organic Synthesis, Riga. sjakste@osi.lv, Baumane L, Boucher JL, Dzintare M, Meirena D, Sjakste J, Lauberte L, Kalvinsh I |
| Jazyk: |
angličtina |
| Zdroj: |
Basic & clinical pharmacology & toxicology [Basic Clin Pharmacol Toxicol] 2004 Jan; Vol. 94 (1), pp. 46-50. |
| 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 gamma-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 gamma-butyrobetaine could inhibit the inducible nitric oxide synthase in vitro. Analogues of gamma-butyrobetaine appear to be prospective drugs for the treatment of circulatory complications of sepsis. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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