高气压暴露对大鼠血浆内皮素-1含量、血清一氧化氮含量、一氧化氮合酶活性的影响

目的 探讨高气压暴露对大鼠血浆内皮素-1(endothelin-1,ET-1)含量、血清一氧化氮(nitric oxide,NO)含量、一氧化氮合酶(nitric oxide synthase,NOS)活性的影响.方法 40只SD大鼠随机分为5组.A组为对照组,B组0.7 MPa空气暴露后缓慢减压,C组0.7 MPa空气暴露后快速减压,D组0.147 MPa纯氧暴露后减压,E组0.250 MPa纯氧暴露后减压.各组暴露时间均为60 min.采用放射免疫方法测定血浆ET-1含量,硝酸还原酶法测定血清NO含量,比色法测定血清NOS活性.结果 与对照组相比,安全减压组和高压氧组的血浆ET-1含量明显升高(P<0.05),原因可能与高分压氧有关(PO2=0.147 MPa/0.250 MPa);快速减压组血清NO含量、NOS活性明显升高(P<0.05),与血浆ET-1含量升高的3个组相比,血清NO、NOS升高得更为显著(P<0.01).结论 NO与ET-1在机体对高气压暴露的反应中呈拮抗关系.高气压与高压氧暴露导致血浆ET-1的释放增加,但快速减压刺激血管内皮细胞产生更多的NO,这种机制可能是通过提高血浆中的NOS活性实现的,这个现象可能是血管内皮系统对血管内气泡产生的应激性反应之一.

Effects of hyperbaric exposure on the levels of plasma endothelin-1, serum nitric oxide and nitric oxide synthase activity in rats

Objective To explore effects of hyperbaric exposure on the levels of serum nitric oxide (NO) and plasma endothelin-1(ET-1), and nitric oxide synthase (NOS) activity in rats. Methods Forty SD rats were randomly divided into 5 groups, i.e. group A (the control group), group B (safe decompression to normal pressure following 0.7 MPa air exposure), group C (fast decompression to normal pressure following air exposure at the same pressure), group D (safe decompression to normal pressure following 0.147 MPa pure oxygen exposure), and group E (safe decompression to normal pressure after 0.250 MPa pure oxygen exposure). Exposure durations for all the groups were 60 minutes. Serum concentrations of NO were determined with the nitrate reductase method, activity of NOS in rats was determined with the coiorimetric method, and plasma concentrations of ET-1 were analyzed by using the radioimmunoassay (RIA) technique. Results When compared with that of the control group, plasma concentrations of ET-1 in the safe decompression groups and the HBO groups increased significantly(P<0.05), which might be due to exposure to high partial pressure of oxygen (PO2 = 0.147 MPa/0.250 MPa). Serum concentrations of NO and NOS activity of the fast decompression groups increased significantly (P<0.05). When compared with those of the 3 groups with increased ET-1 in plasma, serum NO and NOS increased more significantly (P<0.01). Conclusions Hyperbaric exposure might bring about an antagonistic effect on NO and ET-1, when animals were exposed to the hyperbaric environment. Hyperbaric and HBO exposure might induce more release of ET-1, and fast decompression load probably induced higher increase in NO. This phenomenon might be one of the stress responses of the vascular endothelial system to the endovascular bubbles.