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1 in similarly infected mice not administered N-monomethyl-L-arginine).
2 n of NO because it was entirely inhibited by N-monomethyl-L-arginine.
3 is using the competitive substrate inhibitor N-monomethyl-L-arginine (100 micromol/L) did not alter t
7 of 0.5 mM S-methyl-isothio-uronium or 0.5 mM N-monomethyl-L-arginine, both competitive inhibitors of
8 dministration of the NO synthetase inhibitor N-monomethyl-L-arginine did not significantly inhibit cl
11 n T. gondii-infected mice and treatment with N-monomethyl-L-arginine (L-NMMA), a nitric oxide synthas
12 sion plethysmography using acetylcholine and N-monomethyl-L-arginine (L-NMMA), with sodium nitropruss
14 ular dialysis with the NO synthase inhibitor N-monomethyl-L-arginine (L-NMMA, 0.5 mmol/L) blocked CCh
15 brogated when NO production was inhibited by N-monomethyl-L-arginine (NMA), a competitive inhibitor o
16 her a nitric oxide synthase (NOS) inhibitor (N-monomethyl-L-arginine (NMMA); 300 or 500 microM) or a
17 the nitric oxide synthase inhibitor L-NAME (N-monomethyl-L-arginine) or the xanthine oxidase inhibit
18 time-dependent manner, and administration of N-monomethyl-L-arginine reduced NO release and increased
21 ficient mice treated with the iNOS inhibitor N-monomethyl-l-arginine were largely unable to resolve g
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