摘要
目的：探讨内毒素性脑水肿心房肽（ANP）和血管紧张素Ⅱ（ANGⅡ）的变化及其意义。方法：30只新西兰白兔，分内毒素组（25只）和对照组（5只），内毒素组于每只兔脑池内注射内毒素400μg，对照组注入等量生理盐水。于不同时间收集血液、脑脊液和脑组织，用放射免疫法测定ANP和ANGⅡ含量，干燥法测定脑组织含水量。结果：注射内毒素6h后，脑组织（海马区）、脑脊液和血浆中ANP和ANGⅡ含量显著高于对照组和注射前（P＜0．05或P＜0．01），12h后脑组织和脑脊液ANP逐渐降低，24h后明显低于对照组，而ANGⅡ仍然持续增高。脑组织含水量明显高于对照组（P＜0．05或P＜0．01），24h后脑含水量达到高峰。结论：中枢神经系统在内毒素作用下，中枢和周围组织ANP／ANGⅡ平衡失调，早期ANP升高可能是代偿性机制，持续性ANGⅡ增高可加剧脑水肿和炎症损害。
Aim: To investigate the changes of atrial natriuretic peptide (ANP) and angiotensin Ⅱ (ANG Ⅱ) in brain edema induced by endotoxin. Methods: 400μg of endotoxin was intraventricularly injected in 25 New Zealand white rabbits and the same volume of normal saline was injected in 5 rabbits as control.ANP and ANG Ⅱ concentrations were detected by radioimmunoassay in various periods in the plasma, cerebrospinal fluid (CSF) and brain tissue (hippocampus area). Brain water content was measured by drying method. Results: Compared to the control group and before endotoxin injection, ANP and ANG Ⅱconcentrations on 6 hours after endotoxin injection were significantly higher in brain tissue, CSF and plasma (P < 0.05 or P < 0.01). ANP began to decrease gradually in brain tissue and CSF on 12 hours after injection, but ANG Ⅱ levels kept going up continuously. Brain water levels were also significantly higher (P < 0.05 or P < 0.01 )and reached peak levels on 24 hours after injection. Conclusion: ANP/ANG Ⅱ imbalance emerged during inflammation of central nervous system. The early high ANP expression may be a protective mechanism and ANG Ⅱ continuous increaseing could worsen the process of brain edema and inflammation.
出处
《急诊医学》
CSCD
1998年第6期376-378,共3页
关键词
心房肽
血管紧张素Ⅱ
脑水肿
内毒素
Atrial natriuretic peptide Angiotensin Ⅱ Brain edema Endotoxin
