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采用兔肾缺血模型,用放免方法测定血浆及组织内6-keto-PGF_(1α)和TXB_2的变化。结果提示肾缺血再灌流早期内、外髓质6-keto-PGF_(1α)及全肾组织TXB_2显著增加,6-keto-PGF_(1α)/TXB_2比值则显著下降。6-keto-PGF_(1α),TXB_2的异常代谢可能是缺血再灌流早期肾血流量减少和血流再分布的重要原因。
Rabbit kidney ischemia model was used to determine the changes of 6-keto-PGF_(1α) and TXB_2 in plasma and tissues by radioimmunoassay. The results suggest that the 6-keto-PGF_(1α) and TXB_2 in the whole kidney of the medulla significantly increase in the early stage of renal ischemia/reperfusion, and the ratio of 6-keto-PGF_(1α)/TXB_2 decreases significantly. The abnormal metabolism of 6-keto-PGF_(1α) and TXB_2 may be an important cause of the decrease of renal blood flow and redistribution of blood in the early stage of ischemia and reperfusion.