清醒大鼠内毒素休克时体内降钙素基因相关肽(CGRP)改变的进一步研究

FURTHER STUDY OF CHANGES OF CALCITONIN GENE-RELATED PEPTIDE (CGRP) DURING ENDOTOXIC SHOCK IN CONSCIOUS RATS

本文观察清醒大鼠内毒素休克时体内多种组织中CGRP含量的改变,比较门静脉和主动脉、腔静脉血浆中CGRP的浓度以及它们在内毒素休克时的改变;并观察地塞米松治疗对休克时血浆CGRP浓度的影响。由此揭示内毒素休克时血浆CGRP的可能来源以及血浆CGRP浓度升高在休克发病中的可能意义。

We observed CGRP changes in various tissues from rat given 16.7 mg/kg endotoxin (ET) and compared CGRP levels in plasma from portal vein with those from aortic artery and vena cava, respectively. In addition, effects of dexamethasone (dex.) on CGRP concentration in plasma of ET shock rats were observed. Male wistar rats were anethetized by ether. ET or/and dex. (10 mg/kg) were injected i. v. and i. p., respectively. The tissues and blood were taken for specific R1A of CGRP 30 or 180 min after the injections. The results showed that levels of CGRP in duodenum and vena cava were much higher than those in adrenal gland, atrium, ventricle and kidney. Thirty and 180 min after ET shock, the CGRP content in duodenum was elevated (p<0.05), while that in vena cava v/as decreased (P<0.05). There were no significant changes of CGRP levels in other tissues after ET shock. The CGRP concentration in all three kinds of plasma were elevated 180 min after ET shock. Meanwhile, the CGRP level in plasma from portal vein was significantly higher than that in plasma from aortic artery and vena cava (P<0.05). Dsx. could significantly inhibit the elevation of CGRP in three kinds of plasma afteer ET shock. The results suggest that during ET shock CGRP concentration in plasma in raised significantly, which is originated from releasing CGRP from the tissues containing high contents of CGRP. Dex can inhibit the elevation of CGRP concentration in plasma partially by reducing the release of CGRP from gut into circulatory blood, thus contributes to the therapeutic effects of dex. on ET shock.