@article{oai:niigata-u.repo.nii.ac.jp:00016675,
 author = {木下, 秀則},
 issue = {6},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Jun},
 note = {The effects of the commonly-used intravenous anesthetics, ketamine and thiopental (10^<-5>, 3x10.^<-5>, and 10^<-4>M), on vasorelaxation induced by polymorphonuclear leukocytes(PMNLs) were investigated using the porcine coronary artery. Ketamine, 10^<-4>M, enhanced the PMNLs-induced vasorelaxation, whereas thiopental had no effect. Katamine in concentrations over 10^<-4> M increased the appearance of a cell adhesion molecule, L-selectin(CD62L) on PMNLs measured by flow cytometer. Concanavalin A(Con-A) and lens culinarins agglutinin (LCA), which are kinds of lectin, caused endothelium-dependent vasorelaxation. The PMNLs-induced vasorelaxation was abolished in KCI(25mM)-contracted and ouabain(10^<-5> M)-treated preparation s, and was attenuated by 10^<-2> M tetreathylammonium(TEA), 10^<-2> M tetrabutylammonium (TBA), and 10^<-7> M charybdotoxin(ChTx), but not by 10^<-3> M 4-aminopyridine and  10^<-6> M glibenclamide. The relaxation by Con-A and LCA was also attenuated by TEA and TBA. The findings suggest that PMNLs-induced vasorelaxation is at least in part produced through the calcium dependent potassium channel. However, the facilitation of Na^+ pump cannot be excluded in the mechanism of vasodilation by PMNLs. Oxygen free radical scavengers, superoxide dismutase (150 U/ml), catalase (1200 U/ml), and manittol (80mM) had no influence on the PMNLs-induced  vasorelaxation. These findings suggest that lectins induce vasorelaxation partly through calcium dependent potassium channel, and also that ketamine-induced enhancement of the relaxation by PMNLs is produced by increased appearance of L-selectin.},
 pages = {344--350},
 title = {白血球による血管弛緩に及ぼす静脈麻酔薬ケタミン及びサイオペンタールの影響},
 volume = {112},
 year = {1998}
}