Division of Cardiovascular and Diabetes Research, Leeds Institute of Genetics Health and Therapeutics, LIGHT Laboratories, Clarendon Way, University of Leeds, Leeds, United Kingdom.
Can J Cardiol. 2013 Feb;29(2):236-42. doi: 10.1016/j.cjca.2012.03.020. Epub 2012 May 30.
In normal individuals, carbohydrate ingestion increases sympathetic vasoconstrictor activity but causes net vasodilatation in the same vascular bed. This study quantified the effects of carbohydrate ingestion on muscle sympathetic nerve activity (MSNA) and vasoregulation in patients with congestive heart failure (CHF). We hypothesized that high resting levels of MSNA in patients with CHF would blunt further increases in MSNA following carbohydrate ingestion and that their sympathetic activation would restrain vasodilatation.
Eleven patients with treated severe CHF and 11 age- and body mass index-matched normal controls (NCs) were studied for 2 hours after a high-carbohydrate meal. MSNA was measured by peroneal microneurography and calf blood flow by venous occlusion plethysmography.
Patients with CHF had higher (P < 0.03) baseline MSNA (67 ± 4.0 bursts/100 beats) than NCs (51 ± 5.8 bursts/100 beats) and lower (P < 0.001) baroreflex sensitivity (2.1 ± 0.58 ms/mm Hg) than NCs (7.4 ± 1.2 ms/mm Hg). Carbohydrate ingestion was associated with a significant increase in MSNA (P < 0.05) and calf blood flow (P < 0.01) with unchanged blood pressure in CHF patients. The magnitude of responses in CHF patients was not significantly different from that in NCs, but vasodilatation was delayed significantly (by 30 minutes).
Despite considerable resting sympathoexcitation and reduced baroreflex sensitivity, patients with CHF exhibited further increases in MSNA after carbohydrate ingestion, achieving levels similar to those after myocardial infarction. They also had temporally delayed vasodilatation, which could contribute to cachexia and muscle weakness in CHF patients. These observations suggest that high-carbohydrate meals may adversely affect CHF patients via altered autonomic tone and blood-flow patterns.
在正常个体中，碳水化合物摄入会增加交感神经血管收缩活性，但会导致同一血管床的净血管舒张。本研究量化了碳水化合物摄入对充血性心力衰竭（CHF）患者肌肉交感神经活动（MSNA）和血管调节的影响。我们假设 CHF 患者的 MSNA 静息水平较高会使碳水化合物摄入后 MSNA 的进一步增加减弱，并且他们的交感神经激活会抑制血管舒张。
研究了 11 名接受过治疗的严重 CHF 患者和 11 名年龄和体重指数匹配的正常对照组（NCs），在高碳水化合物餐后 2 小时进行研究。通过腓肠肌微神经记录法测量 MSNA，并通过静脉闭塞体积描记法测量小腿血流。
CHF 患者的基线 MSNA （67 ± 4.0 次/ 100 次搏动）高于 NCs （51 ± 5.8 次/ 100 次搏动）（P < 0.03），并且他们的压力反射敏感性（2.1 ± 0.58 ms / mmHg）低于 NCs （7.4 ± 1.2 ms / mmHg）（P < 0.001）。碳水化合物摄入与 MSNA （P < 0.05）和小腿血流（P < 0.01）的显著增加相关，而 CHF 患者的血压没有变化。CHF 患者的反应幅度与 NCs 没有显著差异，但血管舒张明显延迟（延迟 30 分钟）。
尽管存在相当大的静息交感兴奋和降低的压力反射敏感性，CHF 患者在碳水化合物摄入后仍会出现 MSNA 的进一步增加，达到与心肌梗死后相似的水平。他们也有时间上延迟的血管舒张，这可能导致 CHF 患者的恶病质和肌肉无力。这些观察结果表明，高碳水化合物餐可能通过改变自主神经张力和血流模式对 CHF 患者产生不利影响。
