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高血压和血压正常的睡眠呼吸暂停患者的血小板功能和纤溶活性

Platelet function and fibrinolytic activity in hypertensive and normotensive sleep apnea patients.

作者信息

Rångemark C, Hedner J A, Carlson J T, Gleerup G, Winther K

机构信息

Department of Clinical Pharmacology, Sahlgrens and Renströmska Hospital, University of Göteborg, Sweden.

出版信息

Sleep. 1995 Apr;18(3):188-94. doi: 10.1093/sleep/18.3.188.

Abstract

Platelet function and fibrinolytic activity was studied during rest and after ergometric exercise in 13 hypertensive or normotensive patients with obstructive sleep apnea (OSA) and in 10 sex- and weight-matched controls. All patients had undergone a complete polysomnography for the diagnosis of OSA. The controls did not undergo any sleep investigation but had no history of snoring or witnessed apneas during sleep. On antihypertensive drug wash-out, two of the patients were normotensive, whereas 11 had mild to moderate hypertension. Platelet aggregation measured by adenosine 5'-diphosphate- or adrenaline-induced aggregation, platelet factor-4 or beta-thromboglobulin did not differ between patients and controls. During exercise beta-thromboglobulin decreased significantly in both OSA patients and controls. Plasma tissue plasminogen activator activity was similar in OSA patients and controls and increased significantly in both groups after exercise. Plasminogen activator inhibitor type 1 (PAI-1) was 18.4 +/- 3.6 IU/ml in OSA patients compared with 8.2 +/- 1.7 IU/ml in controls (p < 0.029) during rest, indicating decreased fibrinolytic activity. The difference between groups remained after exercise (p < 0.017). Blood pressure elevation was more common and body mass index (BMI) was higher in patients with OSA, but there was no direct relation between blood pressure level or BMI and PAI-1. Nevertheless, differences between groups were smaller when blood pressure and obesity were accounted for. It is concluded that patients with OSA may exhibit decreased fibrinolytic activity. Low fibrinolytic activity may represent a confounding pathophysiological mechanism behind the high incidence of myocardial infarction and stroke in patients with OSA.

摘要

在13例患有阻塞性睡眠呼吸暂停(OSA)的高血压或血压正常患者以及10例性别和体重匹配的对照组中,研究了静息状态和运动负荷试验后血小板功能和纤溶活性。所有患者均接受了完整的多导睡眠图检查以诊断OSA。对照组未进行任何睡眠调查,但无打鼾史或睡眠中呼吸暂停的记录。在停用抗高血压药物后,2例患者血压正常,而11例有轻度至中度高血压。通过5'-二磷酸腺苷或肾上腺素诱导的聚集、血小板因子4或β-血小板球蛋白测量的血小板聚集在患者和对照组之间没有差异。运动期间,OSA患者和对照组的β-血小板球蛋白均显著下降。血浆组织纤溶酶原激活物活性在OSA患者和对照组中相似,且两组运动后均显著增加。静息时,OSA患者的纤溶酶原激活物抑制剂1(PAI-1)为18.4±3.6 IU/ml,而对照组为8.2±1.7 IU/ml(p<0.029),表明纤溶活性降低。运动后两组之间的差异仍然存在(p<0.017)。OSA患者血压升高更为常见,体重指数(BMI)更高,但血压水平或BMI与PAI-1之间没有直接关系。然而,考虑到血压和肥胖因素后,两组之间的差异较小。结论是,OSA患者可能表现出纤溶活性降低。低纤溶活性可能是OSA患者心肌梗死和中风高发背后的一种混杂病理生理机制。

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