Nishida M
First Department of Medicine, Osaka University School of Medicine, Japan.
Med J Osaka Univ. 1990 Mar;39(1-4):5-11.
To assess how polymorphonuclear leukocytes act on coronary vasomotion, we measured the changes in isometric tension of isolated canine coronary arterial rings by adding autologous polymorphonuclear leukocytes to the organ chamber. Ring preparations of the left circumflex coronary artery developed isometric tension with a maximum of 80 +/- 21% of PGF2 alpha (5 muM)-induced contraction at the addition of polymorphonuclear leukocytes (5 x 10(5) cells/ml) isolated by the Percoll gradient method. This increase in tension was dependent on the amount of added polymorphonuclear leukocytes (10(4)-5 x 10(6) cells/ml). The integrity of endothelial cells was not disrupted after the addition of polymorphonuclear leukocytes, because the developed tension was reversed by the addition of acetylcholine in an endothelium-dependent manner. The mechanical rubbing of endothelium completely abolished this polymorphonuclear leukocyte-induced vasoconstriction, which was regained by placing an endothelium-unrubbed ring inside the rubbed ring ("sandwich preparation"). The supernatant of either polymorphonuclear leukocyte suspension or polymorphonuclear leukocyte incubation medium with A23187 could not induce the development of vascular tension. Lipoxygenase inhibitors partially suppressed polymorphonuclear leukocyte-induced vasoconstriction. These findings indicate that polymorphonuclear leukocytes and endothelial cells. This polymorphonuclear leukocyte-induced vasoconstriction is not an increase in resting tension due to endothelial injury caused by added polymorphonuclear leukocytes, but the development of active tension. Lipoxygenase product(s) of arachidonate may partially mediate this contraction.
