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|Title:||Inhibition by a stable factor derived from neutrophils of endothelium-dependent relaxation in rat aorta.|
|Authors:||Liu, J J;Chen, J R;Wiley, J;Johnston, C C;Buxton, Brian F|
|Affiliation:||Department of Cardiac Surgery, University of Melbourne Austin Hospital, Heidelberg, Victoria, Australia.|
|Citation:||The American Journal of Physiology; 265(4 Pt 2): H1454-9|
|Abstract:||Polymorphonuclear leukocytes (PMNs) may play an important role in many pathophysiological states. The effect of a factor derived from PMNs on endothelium-dependent relaxation was studied using rat aortic rings in organ chambers. PMNs were obtained from cardiac surgical patients and healthy volunteers. After incubation in Krebs solution for 3 h, supernatants of PMN suspensions were isolated and used to pretreat the aortic rings for 30 min. The results showed that the supernatants derived from 1 x 10(4) to 5 x 10(6) cells/ml PMNs produced a concentration-dependent inhibition of endothelium-dependent relaxation to acetylcholine but not endothelium-independent relaxation to sodium nitroprusside. The effect could not be prevented by oxygen free radical scavenger superoxide dismutase (150 U/ml), catalase (1,200 U/ml), or mannitol (20 mM) used alone or in combination. Heating the supernatants at 95 degrees C for 30 min did not reduce the inhibitory effect. L-Arginine at 3 x 10(-5) to 3 x 10(-3) M did not significantly reverse the inhibitory effect of the PMN-derived factor. In conclusion, this study reveals that a heat-stable factor derived from human PMNs potently inhibits acetylcholine-induced endothelium-dependent relaxation but not sodium nitroprusside-induced endothelium-independent relaxation in rat aorta. This inhibitory effect is not caused by oxygen free radicals, a limitation of nitric oxide precursor or other unstable factors.|
|Internal ID Number:||8238434|
Endothelium, Vascular.drug effects
In Vitro Techniques
|Appears in Collections:||Journal articles|
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