To study a role of leukotrienes (LTs) in bronchial asthma, we measured LTC₄ and LTD₄ in plasma of 16 asthmatics during wheezing attack and of 4 normal subjects. Plasma of arterial blood was processed by extraction using the SEP-PAK, followed by high-performance liquid chromatography (HPLC). Fractions from HPLC with elution times which corresponded to synthetic LTC₄ and LTD₄ were used for quantification of LTs by radioimmunoassay (RIA) and bioassay. LTC₄ was detected in 13 out of 16 asthmatics by RIA (mean ± SD, 410 ± 630 pg/ml) and in 5 by bioassay. LTD₄ was detected in 10 out of 16 asthmatics by RIA (mean ± SD, 540 ± 290 pg/ml) and in 7 by bioassay. No LTs were detected by either method in the normal subjects. The present study shows that LTC₄ and LTD₄ play a role as chemical mediators during asthmatic attack.

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The free radical scavenger edaravone is able to stimulate prostacyclin release and inhibit the lipoxygenase pathway in the arachidonic acid cascade. The effect of edaravone administration on myocardial damage in rabbit hearts subjected to ischaemia-reperfusion was examined at different times relative to reperfusion. All rabbits underwent sustained coronary artery occlusion for 30 min followed by 3 h of reperfusion. Rabbits were divided into the following groups: control; early (3 mg/kg edaravone IV 10 min before reperfusion); immediate (3 mg/kg edaravone IV immediately after the start of reperfusion); and late (3, 6 or 10 mg/kg edaravone IV 5 min after the start of reperfusion). Single bolus administration of edaravone 10 min before reperfusion or immediately upon initiation of reperfusion appears to be associated with reductions in infarction size and the percentage of apoptotic cells, but treatment with edaravone 5 min after initiation of reperfusion does not appear to have this protective effect.

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