Schulz Richard, Flötotto Christiane, Jahn Andreas, Eisele Hans Joachim, Weissmann Norbert, Seeger Werner, Rose Frank
Division of Pulmonary & Critical Care Medicine, Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany.
J Sleep Res. 2006 Mar;15(1):89-95. doi: 10.1111/j.1365-2869.2006.00498.x.
Adrenomedullin (AM) is a potent endothelial-derived vasodilator secreted under the influence of various stimuli such as hypoxia, shear stress and cytokines. As all of these stimuli might be active under the conditions of obstructive sleep apnoea (OSA), we hypothesized that vascular AM production is increased in these patients. The study included 41 consecutive OSA patients and 28 control subjects without sleep-disordered breathing who were recruited from a pool of patients hospitalized for other reasons. Both groups were matched for anthropometric and comorbid factors. In all patients, i.e. OSA and controls, peripheral venous blood samples were taken at 07:00 hours after diagnostic polysomnography. In subsets of OSA patients, this was repeated after two nights of continuous positive airway pressure (CPAP) therapy (n = 28) and after several months of constant CPAP use (n = 11). The controls and the untreated OSA patients did not have serial blood sampling. In all blood samples, plasma AM levels were measured by an enzyme immunoassay kit. At baseline, the OSA patients had markedly elevated AM concentrations when compared to the controls. There were no differences between normo- and hypertensive OSA patients. After two nights of CPAP therapy, AM levels significantly decreased. Patients on long-term CPAP treatment showed complete normalization of plasma AM concentrations. In conclusion, this pilot study suggests that circulating AM is increased in untreated OSA irrespective of coexistent arterial hypertension and declines after CPAP therapy. AM upregulation might be considered as an adaptive mechanism to counteract the emergence of OSA-related cardiovascular disease.
肾上腺髓质素(AM)是一种由内皮细胞分泌的强效血管舒张剂,在缺氧、剪切应力和细胞因子等各种刺激作用下分泌。由于所有这些刺激在阻塞性睡眠呼吸暂停(OSA)情况下可能都很活跃,我们推测这些患者的血管AM生成会增加。该研究纳入了41例连续的OSA患者和28例无睡眠呼吸障碍的对照受试者,这些对照受试者是从因其他原因住院的患者中招募的。两组在人体测量学和合并症因素方面进行了匹配。在所有患者(即OSA患者和对照者)中,诊断性多导睡眠图检查后于07:00采集外周静脉血样本。在OSA患者亚组中,在持续气道正压通气(CPAP)治疗两晚后(n = 28)以及持续使用CPAP几个月后(n = 11)重复采血。对照组和未经治疗的OSA患者未进行系列采血。在所有血样中,使用酶免疫分析试剂盒测量血浆AM水平。基线时,与对照组相比,OSA患者的AM浓度显著升高。正常血压和高血压的OSA患者之间没有差异。CPAP治疗两晚后,AM水平显著下降。长期接受CPAP治疗的患者血浆AM浓度完全恢复正常。总之,这项初步研究表明,未经治疗的OSA患者无论是否并存动脉高血压,循环AM都会升高,且CPAP治疗后会下降。AM上调可能被视为一种适应性机制,以对抗OSA相关心血管疾病的出现。