内皮素、降钙素基因相关肽及钙离子在缺血再灌流肾损伤中的作用研究

目的：研究内皮素（ET）、降钙素基因相关肽（CGRP）和钙离子（Ca2＋）对缺血再灌流所致肾损伤的影响及机理。方法：20只大耳白兔随机分成对照组和缺血再准流（IR）肾损伤组，观察肾缺血再池流24h时家兔肾组织中的ET、CGRP、Ca2＋含量和超微结构的变化。结果：IR组肾组织中的ET、CGRP、Ca2＋含量均较对照组显著升高（P＜0．05）；肾组织结构损伤较重。结论：缺血再泛流可刺激ET、CGRP和Ca2＋的产生和释放。ET可能通过强烈的缩血管作用，使缺血后产生无复流现象而致肾损伤；同时，ET通过多途径激活Ca2＋通道，Ca2＋大量内流，细胞内钙超载（CAO）而加重肾损伤；CGRP则可能通过拮抗ET缩血管和本身扩血管的效应而参与减轻肾损伤的作用。

THE ROLES OF ENDOTHELIN, CALCITONIN GENE-RELATED PEPTIDE AND CALCIUM IN RENAL INJURY OF ISCHEMIC REPERFUSION

Objective: To inrestigate the action of endothelin (ET), calcitonin gene-related peptide (CGRP) and calcium (Ca2 ) in the injury of the renal tissue in ischemia reperfusion. Method: The changes of contents of ET, CGRP and Ca2 and the renal ultrastructure of rabbit were observed in control group and ischemia reperfusion (IR) group. Result: There are considerable increase in ET, CGRP and Ca2 at the 24th hour after reperfusion in IR group as compared with the control group. Conclusion: It is suggested that ischemia reperfusion can stimulate the production and release of ET and CGRP. ET could result in the injury of the renal tissue from vasoconstriction and increase in the Ca2 inflow phenomena. Therefore, the damage of renal hssue is more serious in IR group than in control group. On the other hand, CGRP may-be involved in alleviating the renal injury by counteracting the vasoconstriction of ET and the vasodilation of itself.