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THE VARIATION OF ARACHIDONIC ACID METABOLISM OF PMN LEUKOCYTES IN CEREBRAL THROMBOSIS

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It was suggested that there is a transfer of metabolites between leukocytes,paltelets and endothelial cells,and that the leukocytes might take part in thrombosis and haemostasis. In order to ascertain whether the arachidonic acid metabolism of PMN leukocytes changes when cerebral thrombosis occurs, we studied this metabolism using isolated human PMN leukocytes, stimulated by ionophor A23187. PGE2 and TXB2 were measured with the method of radioimmunoassay, while leukotrienes(LT) were separated and measured by HPLC. The amount of PGE2, TXB2 and LTs produced by PMN leukocytes of 8 normal volunteers was compared with that of 8 patients suffering from cerebral thrombosis. All these patients were confirmed by CT examination. We found that the production of TXB2, LTB4 and its derivative 20-0H-LTB4 of PMN leukocytes of patients was significantly enhanced. The PGE2 production of PMN leukocytes of patients was also higher than that 0? the volunteers, but without statistically significant difference.These results demonstrate that leukocytes and their arachi donic acid metabolites might play some role in the pathogenetic sequence of cerebral thrombosis. And it is possible that LTB4 is not only a potent inducer of neutrophil chemotaxis and leukocyte aggregation, but also an associated factor in the ischemic vascular disease. It seems that the increasing production of TXB2 and LTB4 by PMN leukocytes is not the main reason of cerebral thrombosis. Hoever, it might accelerate the degree of brain tissue ischemia. We observed that corticosteroids, as an inhibitor of phosphoIipase A2,strikingly reduced the production of arachidonic acid metabolites by leukocytes. Therefore, it is probable that the efficacy of corticosteroids on cerebral thrombosis is, in part, due to inhibit the production of these arachidonic acid metabolites of leukocytes.
Title: THE VARIATION OF ARACHIDONIC ACID METABOLISM OF PMN LEUKOCYTES IN CEREBRAL THROMBOSIS
Description:
It was suggested that there is a transfer of metabolites between leukocytes,paltelets and endothelial cells,and that the leukocytes might take part in thrombosis and haemostasis.
In order to ascertain whether the arachidonic acid metabolism of PMN leukocytes changes when cerebral thrombosis occurs, we studied this metabolism using isolated human PMN leukocytes, stimulated by ionophor A23187.
PGE2 and TXB2 were measured with the method of radioimmunoassay, while leukotrienes(LT) were separated and measured by HPLC.
The amount of PGE2, TXB2 and LTs produced by PMN leukocytes of 8 normal volunteers was compared with that of 8 patients suffering from cerebral thrombosis.
All these patients were confirmed by CT examination.
We found that the production of TXB2, LTB4 and its derivative 20-0H-LTB4 of PMN leukocytes of patients was significantly enhanced.
The PGE2 production of PMN leukocytes of patients was also higher than that 0? the volunteers, but without statistically significant difference.
These results demonstrate that leukocytes and their arachi donic acid metabolites might play some role in the pathogenetic sequence of cerebral thrombosis.
And it is possible that LTB4 is not only a potent inducer of neutrophil chemotaxis and leukocyte aggregation, but also an associated factor in the ischemic vascular disease.
It seems that the increasing production of TXB2 and LTB4 by PMN leukocytes is not the main reason of cerebral thrombosis.
Hoever, it might accelerate the degree of brain tissue ischemia.
We observed that corticosteroids, as an inhibitor of phosphoIipase A2,strikingly reduced the production of arachidonic acid metabolites by leukocytes.
Therefore, it is probable that the efficacy of corticosteroids on cerebral thrombosis is, in part, due to inhibit the production of these arachidonic acid metabolites of leukocytes.

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