脑缺血再灌流［~3H］—三磷酸肌醇放射活性及突触体游离Ca^（2＋）的变化

Changes of the radioactivity of [~3H]-IP_3 and [Ca^(2+)] i during cerebral ischemia and reperfusion

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 order to elucidate the role of phosphoinositide transduction system in ischemic brain damage,the changes of the radioactivity of[3H]-IP3 and [Ca2+]i in cerebral ischemia Wistar rat were observed and the effect of PLC inhibitor PMSF treatment were also studied.The results demonstrated that the radioactivity of[3H]-IP3 was increased significantly 1 min after cerebral ischemia and decreased significantly at 20 min after cerebral ischemia.The the activity of[3H]-IP3 increased slowly to that of control level as the reperfusion was prolonged.The level of[Ca2+]i increased significantly at 20 min after cerebral ischemia and reached to maxium after 6 hour reperfusion.Compared to the vehicle treatment,PMSF treatment could reduced the level of[Ca2+]i.