Studies on the role of arachidonic acid metabolites in airways contraction inducedin vitro by antigen and calcium ionophore A23187

1983 ◽  
Vol 13 (4) ◽  
pp. 318-326 ◽  
Author(s):  
J. F. Burka
Keyword(s):  
Arachidonic Acid ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Platelet Contribution to Leukotriene Production in Inflammation: In Vivo Evidence in the Rabbit

1999 ◽  
Vol 81 (03) ◽  
pp. 442-448 ◽  
Author(s):  
Antonio Celardo ◽  
Giuseppe Dell’Elba ◽  
Stefano Manarini ◽  
Alexander Mironov ◽  
Giovanni Gaetano ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Plasma Concentrations ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Circulating Cells ◽  
Important Pathway

SummaryThe contribution of platelets to arachidonic acid transcellular metabolism may represent an important pathway of leukotriene (LT) production. The aim of this study was to investigate the role of platelets on LT production in an acute inflammatory model in the rabbit. Preliminary experiments showed that rabbit whole blood (5 ml) stimulated in vitro with the calcium ionophore A23187 produced LTB4 (52.7 ± 13.9 ng) and the mixed 5,12-DiHETE (7.25 ± 0.75 ng). In A23187-stimulated thrombocytopenic blood, LTB4 was significantly reduced to 19.5 ± 8.6 ng and 5,12-DiHETE was undetectable. Peptido-LTs were undetectable in both conditions. In experiments using washed cells, addition of thrombin-activated platelets to fMLP-activated PMN resulted in the appearance of 5,12-DiHETE and in more than twofold increase of LTB4 synthesis. When 3H-arachidonic acid-labelled platelets were mixed with unlabelled PMN and challenged with fMLP and thrombin, radioactive LTB4 and 5,12-DiHETE were produced, indicating that platelet-derived arachidonic acid was utilized by PMN 5-lipoxygenase. Intravenous infusion of fMLP (2.5 nmol/kg/min) in the rabbit induced marked granulocytopenia, thrombocytopenia and increased TxB2 plasma concentrations within 3 min. Electron microscopy of lungs showed morphologically activated and aggregated platelets occluding the capillary lumen. Activation and recruitment of circulating cells was accompanied by the production of LTB4 (peak levels at 1 min: 30.0 ± 9.5 ng/ml) and LTE4 (peak levels at 10 minutes: 77.8 ± 11.6 ng/ml). The areas under the blood concentrationtime curve (AUC, ng min/ml) corresponded to 812 ± 182 and 3692 ± 658 for LTB4 and LTE4, respectively. In immunologically thrombocytopenic rabbits, the AUC for LTB4 (86.0 ± 23.0) and LTE4 (1165 ± 542) were both significantly different from controls while in rabbits treated with an anti-leukocyte antiserum, both LTB4 and LTE4 were similar to controls. This experimental model provides in vivo evidence that platelets, involved in an acute inflammatory event contribute to the transcellular production of LTs.

The Role of Arachidonic Acid Metabolites in the Pathophysiology of Bartter’s Syndrome

1983 ◽  
pp. 353-364 ◽  
Author(s):  
Jeffrey S. Stoff ◽  
David M. Clive ◽  
Diane Leone ◽  
D. Euan MacIntyre ◽  
Robert S. Brown ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Bartter’S Syndrome ◽  
Bartter's Syndrome ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

Reduced prostacyclin formation after reoxygenation of anoxic endothelium

1990 ◽  
Vol 259 (5) ◽  
pp. C738-C745 ◽  
Author(s):  
S. L. Hempel ◽  
D. L. Haycraft ◽  
J. C. Hoak ◽  
A. A. Spector
Keyword(s):  
Arachidonic Acid ◽  
Umbilical Vein ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
High Rate ◽  
Ionophore A23187 ◽  
Arachidonic Acid Release ◽  
Cyclooxygenase Activity ◽  
Platelet Adherence ◽  
Acid Release

Human umbilical vein endothelial cells subjected to 24 h of anoxia followed by reoxygenation released less prostacyclin (PGI2) in response to thrombin, calcium ionophore A23187, or arachidonic acid. This was associated with a substantial increase in stimulated platelet adherence. Increased lactate dehydrogenase and 51Cr release occurred after 1 h of reoxygenation, but the high rate of release did not persist during the subsequent 23 h of reoxygenation. The changes in platelet adherence and PGI2 release partially resolved over 24 h. PGI2 formation from prostaglandin H2 was not reduced, suggesting that cyclooxygenase activity, but not prostacyclin synthase, is affected by reoxygenation. A decrease in arachidonic acid release from cellular lipids also occurred. The reduction in cyclooxygenase activity, but not arachidonic acid release, was prevented by the presence of ibuprofen during reoxygenation. Addition of catalase or superoxide dismutase during reoxygenation increased PGI2 release but did not completely overcome the reduction relative to control cultures. These findings suggest that the increase in platelet adherence during reoxygenation may be mediated in part by a change in cyclooxygenase activity. This is only partly overcome by extracellular oxygen species scavengers but is prevented by the presence of a reversible cyclooxygenase inhibitor during reoxygenation.

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