摘要
目的:探讨阻塞性睡眠呼吸暂停低通气综合(OSAHS)患者体循环高血压的机制。方法:正常对照组[呼吸暂停/低通气指数(AHI)>5次/h],男性25名(年龄55±9.9岁),OSAHS组(AHI≥20次/h)男性25名(年龄56.8±12.3岁)分别行多导睡眠图(PSG),彩色超声心动图,心钠素(ANF),肾小球滤过率(GFR)测定,24小时动态血压检查。结果:OSAHS患者AHI越大,氧饱和度低于90%的时间占总睡眠时间的百分数(TSaO2)越大(P<0.001),舒张压越高(P<0.001),ANF分泌越多(P<0.001);OSAHS患者GFR较对照组显著下降(P<0.05),年龄越大,GFR越低(P<0.001)。结论:OSAHS引起高血压的机制可能为:AHI增大引起TSaO2扩大,舒张压升高,肺动脉压升高,肺动脉口径扩大,ANF分泌增加,进一步升高血压;GFR下降也促进了血压的升高。
Objective: To explore the mechanism of developing syslematic hypertension in patients with obstructive sleep apnea/hypopnea syndrome (OSAHS). Methods: Atotal of 25 normal males (55. 0±9. 9 years) as control group [Apnea/Hypopnea index (AHI) <5次/h], 25 male patients (56. 8±12. 3 years) with OSAHS (AHI≥20 times/h) as OSAHS group were examined with polysomnography (PSG). color ultrasoniccardiogram, and for level of ANF. GFR (ECT method), ambulatory blood pressure recording in 24 hours respectively. Results: For OSAHS patient, the more the AHI, the higher the percent of the time of oxygen saturation below 90% in the total time (TSaO2), P <0. 001. diastolic blood pressure (DBP). P<0. 001, the higher the level of plasma ANF (P<0. 001). Compared with control group, the GFR significantly decreased in OSAHS patients (P<0. 05); the older the age, the lower the GFR (P<0. 001), Conclusion: The mechanism caused hypertension in OSAHS patients may be that, recurrent sleep apnea and hypoxemia in OSAHS patients can result in hypoxemia, increasing diastolic pressure, further increasing pulmonary hypertension, increasing the level of ANF secretion and further develop hypertension; Decreased GFR facilitate hypertension also.
出处
《心血管康复医学杂志》
CAS
2004年第2期109-112,共4页
Chinese Journal of Cardiovascular Rehabilitation Medicine
关键词
阻塞性睡眠呼吸暂停低通气综合征
高血压
发病机制
并发症
多导睡眠图
Obstructive sleep apnea/hypopnea syndrome
Glomerular filtration rate
Pulmonary hypertension
Atrial natriuretic peptide
Hypertension
