佐剂性关节炎大鼠尿硝酸盐排泄增加。
Increased urinary nitrate excretion in rats with adjuvant arthritis.
作者信息
Stichtenoth D O, Gutzki F M, Tsikas D, Selve N, Bode-Böger S M, Böger R H, Frölich J C
机构信息
Department of Clinical Pharmacology, Hannover Medical School, Germany.
出版信息
Ann Rheum Dis. 1994 Aug;53(8):547-9. doi: 10.1136/ard.53.8.547.
OBJECTIVES
In rats with adjuvant arthritis measurements were taken of the urinary excretion of nitrate, reflecting endogenous nitric oxide (NO) formation, and cyclic guanosine monophosphate (cGMP).
METHODS
Urinary nitrate was determined by gas chromatography, cGMP by radioimmunoassay.
RESULTS
A significant (p < 0.001), more than three fold increase of urinary nitrate excretion was found in rats 20 days after induction of adjuvant arthritis compared with non-arthritic rats. There was no significant difference in urinary cGMP excretion between arthritic rats and control animals.
CONCLUSION
The data suggest that the dramatic increase of urinary nitrate excretion is due to increase of NO synthesis by the inducible form of NO synthase.
目的
在佐剂性关节炎大鼠中，测定反映内源性一氧化氮（NO）生成的尿硝酸盐排泄量以及环磷酸鸟苷（cGMP）。
方法
尿硝酸盐通过气相色谱法测定，cGMP通过放射免疫分析法测定。
结果
与非关节炎大鼠相比，佐剂性关节炎诱导20天后的大鼠尿硝酸盐排泄量显著增加（p < 0.001），增加了三倍多。关节炎大鼠与对照动物的尿cGMP排泄量无显著差异。
结论
数据表明，尿硝酸盐排泄量的显著增加是由于诱导型一氧化氮合酶合成NO增加所致。
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