Division of Cardiology, Pulmonology and Vascular Medicine, University Duesseldorf, Duesseldorf, Germany.
Eur J Med Res. 2009 Dec 7;14 Suppl 4(Suppl 4):151-5. doi: 10.1186/2047-783x-14-s4-151.
Autonomic neuropathy is common in patients suffering from end-stage renal disease (ESRD). This may in part explain the high cardiovascular mortality in these patients. Chemosensory function is involved in autonomic cardiovascular control and is mechanistically linked to the sympathetic tone.
The aim of the present study was to assess whether sympathetic hyperactivity contributes to an altered chemosensory function in ESRD.
In a randomized, double-masked, placebo controlled crossover design we studied the impact of chemosensory deactivation on heart rate, blood pressure and oxygen saturation in 10 ESRD patients and 10 age and gender matched controls. The difference in the R-R intervals divided by the difference in the oxygen pressures before and after deactivation of the chemoreceptors by 5-min inhalation of 7 L oxygen was calculated as the hyperoxic chemoreflex sensitivity (CHRS). Placebo consisted of breathing room air. Baseline sympathetic activity was characterized by plasma catecholamine levels and 24-h time-domain heart rate variability (HRV) parameters.
Plasma norepinephrine levels were increased (1.6 +/- 0.4 vs. 5.8 +/- 0.6; P<0.05) while the SDNN (standard deviation of all normal R-R intervals: 126.4 +/- 19 vs. 100.2 +/- 12 ms), the RMSSD (square root of the mean of the squared differences between adjacent normal R-R intervals: 27.1 +/- 8 vs. 15.7 +/- 2 ms), and the 24-h triangular index (33.6 +/- 4 vs. 25.7 +/- 3; each P<0.05) were decreased in ESRD patients as compared to controls. CHRS was impaired in ESRD patients (2.9 +/- 0.9 ms/mmHg, P<0.05) as compared to controls (7.9 +/- 1.4 ms/mmHg). On multiple regression analysis 24 h-Triangular index, RMSSD, and plasma norepinephrine levels were independent predictors of an impaired hyperoxic CHRS.
Sympathetic hyperactivity influences chemosensory function in ESRD resulting in an impaired hyperoxic CHRS.
自主神经病变在终末期肾病(ESRD)患者中很常见。这在一定程度上可以解释这些患者心血管死亡率高的原因。化学感觉功能参与自主心血管控制,并且与交感神经张力在机制上相关。
本研究旨在评估自主神经活性亢进是否导致 ESRD 患者的化学感觉功能改变。
采用随机、双盲、安慰剂对照交叉设计,我们研究了 10 名 ESRD 患者和 10 名年龄和性别匹配的对照者在化学感受器通过 5 分钟 7 L 氧气吸入被激活和失活时心率、血压和氧饱和度的变化。化学感受器失活前后 R-R 间期的差值除以氧分压的差值除以 5 分钟,得出高氧化学反射敏感性(CHRS)。安慰剂为呼吸室内空气。基础交感神经活性通过血浆儿茶酚胺水平和 24 小时时域心率变异性(HRV)参数来描述。
与对照组相比,ESRD 患者的血浆去甲肾上腺素水平升高(1.6 ± 0.4 比 5.8 ± 0.6;P<0.05),而 SDNN(所有正常 R-R 间期的标准差:126.4 ± 19 比 100.2 ± 12 ms)、RMSSD(相邻正常 R-R 间期均方根的差值:27.1 ± 8 比 15.7 ± 2 ms)和 24 小时三角指数(33.6 ± 4 比 25.7 ± 3;每项 P<0.05)降低。与对照组相比,ESRD 患者的 CHRS 受损(2.9 ± 0.9 ms/mmHg,P<0.05)。多元回归分析显示,24 小时三角指数、RMSSD 和血浆去甲肾上腺素水平是 CHRS 受损的独立预测因子。
自主神经活性亢进影响 ESRD 患者的化学感觉功能,导致高氧 CHRS 受损。