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本文研究了大鼠脑缺血再灌流时［３Ｈ］—三磷酸肌醇（［３Ｈ］－ＩＰ３）放射活性及突触体游离Ｃａ２＋（［Ｃａ２＋］ｉ）的变化，并用苯甲基磺酰氟化物（ＰＭＳＦ）治疗，观察其对［３Ｈ］－ＩＰ３放射活性及突触体［Ｃａ２＋］ｉ的影响。结果：脑缺血１ｍｉｎ［３Ｈ］－ＩＰ３放射活性非常显著地增高。缺血２０ｍｉｎ、缺血２０ｍｉｎ再灌流１ｈ、６ｈ、２ｄ［３Ｈ］－ＩＰ３放射活性非常显著地降低。缺血２０ｍｉｎ突触体［Ｃａ２＋］ｉ非常显著地增高，至再灌流６ｈ达到最高水平。应用ＰＭＳＦ治疗能显著地抑制突触体［Ｃａ２＋］ｉ的升高。
In this paper, we investigated the radioactivity of [3H] -IPI3 and the change of synaptosomal free Ca2 + ([Ca2 +] i) during cerebral ischemia-reperfusion in rats. The effects of phenylmethylsulfonyl fluoride (PMSF) treatment to observe its [3H] -IP3 radioactivity and synaptosome [Ca2] i impact. Results: The radioactivity of [3H] -IP3 in cerebral ischemia was significantly increased. Ischemia 20min, ischemia 20min reperfusion 1h, 6h, 2d [3H] -IP3 radioactivity was significantly reduced. The synaptosome [Ca2 +] i increased significantly at 20 min after ischemia and reached the highest level at 6 h after reperfusion. Treatment with PMSF significantly inhibited the elevation of synaptosomal [Ca2 +] i.