论文部分内容阅读
目的探讨阻塞性睡眠呼吸暂停低通气综合征(obstruotive sleep apnea hypopnea syndrom e,OSAHS)及阻塞性睡眠呼吸暂停低通气综合征合并高血压(Hypertension)患者血浆中血管紧张素Ⅱ(AngiotensinⅡ,AngⅡ)和内皮素-1(p lasm a,ET-1)的变化。方法将符合入选条件的中、重度OSAHS患者分为OSAHS并发高血压组、OSAHS血压正常组,另设正常对照组,每组30例,3组均行PSG监测。采用放射免疫法测定血浆中AngⅡ和ET-1水平,并对比分析3组血浆中AngⅡ和ET-1水平及其相关性,评价血浆中AngⅡ和ET-1变化与检测价值。结果 OSAHS合并高血压与OSAHS血压正常组血清ET-1质量浓度(x±s下同)分别是(58.94±16.37)和(44.75±15.68)ng/L,明显高于正常对照组(33.89±20.12)ng/L(P<0.01);同时OSAHS合并高血压组与OSAHS血压正常组之间比较血清ET-1质量浓度也明显增高(P<0.05)。两组患者血清ET-1水平与AH I呈明显的正相关(r=0.334,P<0.01)。OSAHS及合并高血压患者血浆AngⅡ和ET-1水平与正常对照组相比差异有统计学意义(P<0.01)。结论 OSAHS患者存在着明显的睡眠结构紊乱,但合并高血压者并没有特异性改变。ET-1可能在OSAHS合并高血压的发病中起一定作用。
Objective To investigate the effects of obstructive sleep apnea hypopnea syndrom e (OSAHS) and plasma levels of angiotensin Ⅱ (AngⅡ) in patients with obstructive sleep apnea hypopnea syndrome and hypertension (Hypertension) Endothelin-1 (p lasm a, ET-1) changes. Methods Patients with moderate and severe OSAHS who met the inclusion criteria were divided into OSAHS complicated hypertension group and OSAHS normal blood pressure group. Another 30 cases of normal OSAHS patients were enrolled in this study. The levels of AngⅡ and ET-1 in plasma were determined by radioimmunoassay. The levels of AngⅡ and ET-1 in plasma were compared and analyzed. The changes of AngⅡ and ET-1 in plasma and the detection value were evaluated. Results The serum concentration of ET-1 in OSAHS patients with OSAHS and OSAHS was 58.94 ± 16.37 and 44.75 ± 15.68 ng / L, respectively, which was significantly higher than that of the normal controls (33.89 ± 20.12 ) ng / L (P <0.01). At the same time, the serum ET-1 concentration in OSAHS patients with hypertension and OSAHS patients with normotension were also significantly increased (P <0.05). There was a significant positive correlation between serum ET-1 level and AHI in both groups (r = 0.334, P <0.01). The plasma levels of AngⅡ and ET-1 in patients with OSAHS and those with hypertension were significantly lower than those in normal controls (P <0.01). Conclusion OSAHS patients have obvious sleep structural disorder, but there is no specific change in those with hypertension. ET-1 may play a role in the pathogenesis of OSAHS complicated by hypertension.