神经肽Y与阻塞性睡眠呼吸暂停低通气综合征所致高血压的相关性

目的 初步探讨神经肽Y(neuropeptide Y,NPY)在阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)所致高血压的病理生理过程中的意义.方法 实验1.随机选择OSAHS患者31例,正常对照组30人,所有受试者均接受整夜多导睡眠图监测并于晨起前测量右上肢肱动脉血压,检测血浆NPY水平.分析两组受试者睡眠呼吸紊乱指数、平均动脉压(mean arterial pressure,MAP)与NPY浓度的关系.实验2.选择患者26例给予经鼻持续气道正压通气(nasal continuous positive airway pressure,nCPAP)治疗3个月后复查多导睡眠图、平均动脉压、血浆NPY浓度.比较治疗前后患者的呼吸暂停低通气指数(apnea-hypopnea index,AHI)、最低血氧饱和度(MinSpO2)、夜间血氧饱和度低于90%时间百分比(T-SaO2＜90%)、MAP与血浆NPY浓度的变化.结果 OSAHS患者组MAP、血浆NPY浓度较正常对照组显著升高(P＜0.01),且血浆NPY水平与MAP呈正相关(P＜0.01).经过3个月nCPAP治疗,患者MAP及血浆NPY浓度均有下降(P＜0.01).且MAP下降幅度、血浆NPY下降幅度均与AHI下降幅度呈正相关(P值分别为0.042,0.006),且MAP下降幅度与血浆NPY下降幅度亦呈正相关(P=0.034).所有实验对象NPY、MAP与AHI、T-SaO2＜90%均呈正相关,与MinSpO2呈负相关(P值均＜0.01).MAP与NPY呈正相关(P＜0.01).逐步回归方程为:NPY＝2.229×AHI-2.928×MinSpO2+1.729×MAP+279.321.结论 OSAHS可引起血浆NPY浓度的升高.NPY与OSAHS所致血压升高的发生、发展有关.有效治疗OSAHS可以预防或减缓OSAHS所致高血压的发生、发展.

Study on the relationship between blood pressure and plasma neuropeptide Y among patients with obstructive sleep apnea-hypopnea syndrome

Objective To investigate the role of plasma neuropeptide Y (NPY) in physiopathologic process of obstructive sleep apnea-hypopnea syndrome (OSAHS) accompanied by hypertension. Methods Thirty-one patients with OSAHS were placed into the OSAHS group,and 30 normal subjects into the control group. First, the plasma concentrations of NPY, right upper extremity arteria brachialis blood pressure,apnea-hypopnea index ( AHI) , minimal saturation of pulse oxygen ( MinSpO2 ) and time when percent of nocturnal oxygen saturation lower than 90% (T-SaO2＜90%) were measured respectively. And the relationship between NPY and the other variables were analyzed in both groups. Second,26 OSAHS patients accepted nasal continuous positive airway pressure (nCPAP) therapy. After 3-month treatment with nCPAP,plasma concentration of NPY,right upper extremity arteria brachialis blood pressure, AHI,MinSpO2 and T-SaO2＜90% were remeasured and compared with the OSAHS group. Results Our study indicated that compared to the control subjects the patients with OSAHS had higher mean arterial pressure (MAP) and the NPY level in plasma ( P ＜0. 01). After the 3-month nCPAP therapy both MAP and the NPY level were significantly decreased(P ＜0. 01). And the decrease of MAP and the plasma level of NPY had positive correlation with AHI ( P ＜0. 01). The decrease of MAP also had positive correlation with the decrease of the plasma level of NPY ( P ＜0. 05). In all groups. MAP and the plasma level of NPY both had positive correlation with AHI, T-SaO2 ＜ 90% (P ＜ 0. 01), and negative correlation with MinSpO2 ( P ＜0. 01). MAP exhibited positive correlation with the plasma level of NPY in all groups (P＜0. 01). Stepwise multiple regression analysis showed that regression equation was: NPY= 2. 229 X AHI-2. 928 X MinSpO2 + 1. 729 X MAP+ 279. 321. Conclusions Our research suggests that there is a close relationship between the plasma NPY level and the OSAHS combined with hypertension. nCPAP therapy could not only decrease the MAP but also the plasma NPY level in OSAHS patients. Correct treatment was effective not only on OSAHS but also on coexisting hypertension.