摘要
目的探讨肾上腺髓质素(adrenomedulin,AM)和降钙素基因相关肽(calcitonin gene-related peptide,CGRP)在急性高原低氧中的作用。方法采用放射免疫法测定40名世居低海拔地区的健康男性青年在海拔1 100 m、进入海拔2 260m 3月、3 780 m 1 d、5 d和15 d AM和CGRP血浆含量。结果志愿者进入海拔2 260 m 3个月后,血浆AM浓度开始下降,进入海拔3 780 m 1 d时其值降至谷底,与此同时CGRP浓度则显著增加。随着在低氧环境停留时间的延长,从3 780 m 5 d起血浆AM浓度开始反弹,到高海拔15 d时达最高值(与海拔2 260 m、3 780 m 1 d相比,P<0.01)。与此相反,CGRP浓度则持续下降,海拔3 780 m 5和15 d时与海拔2 260 m相比差异显著(P<0.01)..AM与CGRP呈负相关(r=-7.897,P<0.01)。结论AM和CGRP作为血管扩张因子协同作用于人体高原缺氧时的生理调节过程。二者协同发挥其对肺循环的保护性调节作用。
Objective Recent experiment showed that adrenomedulin, (AM) and calcitonin gene-related peptide (CGRP) played an important role in vasodilation and inhibition of proliferation of pulmonary blood vessel smooth muscular cells in hypoxic animals. In order to study whether the same results occurr in human body when they are subjected to acute exposure to high altitude. Methods The blood samples of 40 young male volunteers who live permanently in a lower altitude (1100 m) were collected, on the spots of altitude of 1 100 m (control group), 2260 m (after 3 month) and 3 780 m (for 1 d, 5 d and 15 d). The contents of AM and CGRP were measured by radioimmunoassay. Results AM content continuously decreased 3 months after stay at 2 260 m and the content reached the lowest 1 day after stay at the altitude 3 780 m. Meanwhile, CGRP content increased significantly (P<0. 01, compared with control group). With increase of altitude and prolongation of hypoxic time the AM content gradually increased and began to rise 5 days after stay at altitude of 3 780 m and reached the highest (P<0. 01, when compared with those 1 d after stay at 2 260 m and 3 780). On the contrary, the CGRP content decreased continuously, and the differences in the content were significant between the CGRP content 5 days after stay at the altitude of 3 780 m and that after stay at the altitude of 2 260 m for 15 d. AM and CGRP showed a significant negative correlation (r=-7. 897, P<0. 01). Conclusion AM and CGRP, serving as co-factors of vasodilation, are involved in the regulation of pulmonary circulation and they work together to protect the lung circulation by such regulation.
出处
《医学分子生物学杂志》
CAS
CSCD
2005年第3期175-177,共3页
Journal of Medical Molecular Biology
