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[Relationship of leukotriene C4 and ischemic brain edema in stroke-resistant spontaneously hypertensive rats].

The effects on eicosanoid levels were investigated in the stroke-resistant spontaneously hypertensive rat (SHRSR) brain and the relation of eicosanoid to the progression of cerebral edema was studied. The effects of dexamethasone, indomethacin and AA-861 on the induction of eicosanoids and cerebral edema were also studied in this model. Global cerebral ischemia was induced by occluding the bilateral common carotid arteries (BLCO) with clips. After two hours of BLCO the blood was reperfused by removing the clips. After each period of reperfusion the rat brain was used for the radioimmunoassay of eicosanoids. The time period of cerebral edema was also investigated by measuring the water content of the brain after the reperfusion. The TXB2 (stable metabolite of TXA2) was elevated significantly 5 minutes after reperfusion and the 6-keto PGF1a (stable metabolite of PGI2) was also markedly increased at the same time and returned to control levels at 15 minutes. In contrast, the LTC, levels showed an increase at the end of BLCO and the beginning of reperfusion and reached a peak at 30 minutes. Furthermore, the high levels persisted until 60 minutes after reperfusion. Indomethacin did not fully suppress the increase of brain water content. However, dexamethasone and AA-861 completely suppressed brain water content and the production of LTC4 This fact may indicate that these compounds have the function of suppressing the ischemic cerebral edema. It has been previously reported that in the BLCO model the procedure can produce a sudden elevation of prostaglandins. The results of the present investigation are consistent with the previous observation. TXB2 and 6-keto PGF1a in the ischemic brain were significantly increased only 5 minutes after reperfusion and decreased in 15 minutes to almost the same level as that of 0 time. This time phase did not correspond to the time phase of cerebral edema. The 6-keto PGF1a and TXB2 concentration may correlate with platelet and vascular endothelial cell response in the early stage of reperfusion. By reperfusion of the ischemically injured tissue, LTC4 level elevated significantly and its time phase corresponded to the progression of the cerebral edema showing the induction of brain water contents during BLCO and the significant increase 30 and 60 minutes after the reperfusion. These results indicate a close relationship between LTC4 and ischemic brain edema.