[Blood oxygen transport in rats during lipopolysaccharide administration combined with modification of L-arginine-No system].
Lipopolysacharide from Escherichia coli was intravenously administered to rats (5.0 mg/kg). L-arginine-No system was modified by intravenous injection of L-arginine, N(G)-nitro-L-arginine methyl ester or L-lysine-N(G)-acetamidine (nitric oxide synthase (NOS) substrate, nonselective NOS inhibitor, and selective inducible NOS inhibitor, respectively.) Lipopolysacharide-induced disorders of blood oxygen transport were the least during the selective inducible NOS inhibition. The protective effects of L-arginine and N(G)-nitro-L-arginine methyl ester were less prominent. Such features of NOS modification effect on the blood oxygen transport suggest that activation of inducible NOS may change the hemoglobin-oxygen affinity during the lipopolysacharide treatment.
Glebov
A N
AN
Zinchuk
V V
VV
D000818:Animals; D001120:Arginine / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006454:Hemoglobins / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D018384:Oxidative Stress; D010100:Oxygen / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains
D004791:Enzyme Inhibitors; D006454:Hemoglobins; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D010100:Oxygen; D019331:NG-Nitroarginine Methyl Ester