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

发布时间：2019-06-29 16:37

【摘要】： 目的: 初步探讨神经肽Y(neuropeptide Y)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,进一步阐述OSAHS所致高血压的发生发展机制,为寻找防治OSAHS并发症的途径提供思路。方法: 实验1.将经过多导睡眠监测仪(polysomnography,PSG)检查并被确诊为阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的患者31人及正常对照组30人纳入研究对象,所有受试者均接受整夜多导睡眠图监测(7小时)并于晨起前测量右上肢肱动脉血压,计算平均动脉压,抽取静脉血,以酶联免疫吸附测定法(enzyme-linked immunosorbent assay,ELISA)检测血浆中的NPY水平。分析两组受试者呼吸暂停低通气指数(apnea-hypopnea index,AHI)、最低血氧饱和度(minimal saturation of pulse oxygen,MinSpO2)、夜间血氧饱和度低于90%时间百分比(time when percent of nocturnal oxygen saturation lower than 90%,T-SaO290%)、平均动脉压(mean arterial pressure,MAP)与血浆神经肽Y(NPY)浓度的关系。实验2.开展干预实验,OSAHS患者组中选择愿意接受夜间经鼻持续气道正压通气(nasal continuous positive air pressure,nCPAP)治疗的患者26例给予nCPAP治疗。每晚治疗至少超过5小时,持续3个月。3个月之后再复查多导睡眠图、平均动脉压、血浆NPY浓度。比较治疗前后患者的AHI、MinSpO2、T-SaO290%、MAP与血浆NPY浓度的变化。结果: 1. OSAHS患者组MAP较正常对照组高,且差别有统计学意义(分别为111.96±8.86mmHg,98.71±12.15mmHg,t值-4.85,P0.01)。 2. OSAHS患者组血浆NPY浓度较正常对照组高,且差别有统计学意义(分别为322.82±52.56ng/L,187.08±39.32ng/L,t值-11.39,P0.01)。 3. OSAHS患者组血浆NPY水平与MAP呈正相关(r=0.463,P0.01)。 4.经过3个月nCPAP治疗,复测患者MAP(103.68±6.55mmHg),与3个月前比较有明显下降,差异有统计学意义(t值14.54,P0.01)。复查血浆NPY浓度(200.69±38.88ng/L),与3个月前比较,差异有统计学意义(t值11.84,P0.01)。 5.经nCPAP治疗后患者MAP下降幅度(6.17±2.16mmHg )与AHI下降幅度(24.64±13.46次/h)呈正相关(r=0.401,P=0.042),血浆NPY下降幅度(116.57±50.19ng/L)与AHI下降幅度呈正相关(r=0.587,P=0.006),且MAP下降幅度与血浆NPY下降幅度亦呈正相关(r=0.418,P=0.034)。 6.所有实验对象NPY、MAP与AHI、T-SaO290%均呈正相关,与MinSpO2呈负相关。MAP与AHI、MinSpO2、T-SaO290%的相关系数分别为(0.596、-0.531、0.527,P均0.01)。NPY与AHI、MinSpO2、T-SaO290%的相关系数分别为(0.850、-0.827、0.762,P均0.01)。 7.所有实验对象MAP与NPY呈正相关(r=0.631,P0.01)。 8.逐步回归分析显示AHI、MinSpO2和MAP是NPY水平的预测因素,t值分别为3.83(P0.01)、-3.48(P0.01)、2.15(P=0.035),回归方程为:NPY=2.229×AHI-2.928×MinSpO2+1.729×MAP+279.321 (F=43.21)。结论: 1. OSAHS患者血浆NPY浓度较正常对照组高,且与睡眠呼吸暂停现象的严重程度相关,考虑OSAHS可引起血浆NPY浓度的升高。 2.所有观察对象的血压水平与血浆NPY浓度呈正相关,推测NPY与OSAHS所致血压升高的发生发展有关。 3.经nCPAP治疗后, OSAHS患者血浆NPY浓度及平均动脉压均较治疗前有下降,提示有效治疗OSAHS可以预防或减缓OSAHS所致高血压的发生、发展。
[Abstract]:Purpose: The significance of neuropeptide Y in the pathophysiological process of high blood pressure induced by obstructive sleep apnea-hypopnea syndrome (OSAHS) was discussed. The mechanism of the exhibition is to find ways to prevent and control the complications of OSAHS. supply of thought . Methods:1. The patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) were examined by polysomnography (PSG) and diagnosed as obstructive sleep apnea-hypopnea syndrome (OSAHS). A group of 30 subjects were included in the study, all subjects were monitored for multiple sleep patterns all night (7 hours) and the right upper limb brachial artery blood pressure was measured before the morning and the mean arterial pressure was calculated and the venous blood was extracted and the enzyme-linked immunosorbent assay (ELISA) was used. The NPY level in the plasma was detected. The two groups of subjects were analyzed for apnea-hypoventilation index (AHI), minimum blood oxygen saturation (MinSpO2), and at night, the blood oxygen saturation was lower than 90% time percentage (T-SaO 290%), mean arterial pressure (mean artery pressure). (MAP) and plasma neuropeptide Y (NP Y) The relationship of concentration. Experiment 2. In the intervention experiment, the patients in the OSAHS group were selected to be treated with continuous positive airway pressure (nCPAP) during the night. The patient was treated with nCPAP for at least 5 hours per night for 3 months. Multiple sleep after 3 months Figure, mean arterial pressure, plasma NPY concentration. Comparison of AHI, MinSpO2, T-SaO 290% of patients before and after treatment ,MA Results:1. The MAP of the patients with OSAHS was higher than that in the normal control group, and the difference was statistically significant (111.96, 8.86mmHg, 98.71-1, respectively). The plasma NPY concentration in the OSAHS group was higher than that in the normal control group, and the difference was significant (322.82, 52.56 ng/ L, 187.0, respectively). 8 (39.32 ng/ L, t-value-11.39, P0.01).3. OSAHS patients The plasma NPY level in the group was positively correlated with MAP (r = 0.463, P0.01).4. After 3-month nCPAP treatment, the MAP of the patient (103.68, 6.55 mmHg) was re-measured. There was a statistically significant difference in the three months (t-value 14.54, P0.01). The plasma NPY concentration (200.69-38.88 ng) was reviewed. The decrease of MAP (6.17-2.16 mmHg) was positively correlated with the decrease of AHI (24.64-13.46 times/ h) after nCPAP treatment (r = 0.401, P = 0.042), and plasma NPY decreased (116.57). 50.19 ng/ L was positively correlated with the decrease of AHI (r = 0.587, P = 0.006), and The decrease of MAP was positively correlated with the decrease of plasma NPY (r = 0.418, P = 0.034).6. The NPY, MAP and AHI and T-SaO 290% of the experimental subjects were positively correlated and negatively correlated with MinSpO2. MAP and AHI, MinSpO2, T -The correlation coefficient of-SaO 290% was (0.596,-0.531, 0.527, P 0.01). NPY and AHI, MinSpO2, T -The correlation coefficient of-SaO 290% is (0.850,-0.827, 0.762, respectively). (P <0.01).7. The MAP of all experimental subjects was positively correlated with NPY (r = 0.631, P0.01).8. The stepwise regression analysis showed that AHI, MinSpO2 and MAP were the predictors of NPY level, t-values were 3.83 (P0.01),-3.48 (P0.01), 2.15 (P = 0.035), and the regression equation was: NPY. = 2. 229-AHI-2.928-MinSpO2 + 1.729-MAP + 279.321 (F = 43.21). Conclusion: 1.O The plasma NPY concentration in the SAHS patients is higher than that of the normal control group, and is related to the severity of the sleep apnea, and the OSAHS can cause plasma 2. The level of blood pressure of all observed subjects was positively correlated with the plasma NPY concentration, and it was estimated that NPY was related to the development of blood pressure increase caused by OSAHS.3. nCPAP
【学位授予单位】：福建医科大学
【学位级别】：硕士
【学位授予年份】：2010
【分类号】：R766;R544.1

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