Human Neurotransmitters, Baker IDI Heart and Diabetes Institute Melbourne, VIC, Australia.
Front Physiol. 2011 Aug 26;2:52. doi: 10.3389/fphys.2011.00052. eCollection 2011.
Sympathetic activation in subjects with the metabolic syndrome (MS) plays a role in the pathogenesis of cardiovascular disease development. Diet-induced weight loss decreases sympathetic outflow. However the mechanisms that account for sympathetic inhibition are not known. We sought to provide a detailed description of the sympathetic response to diet by analyzing the firing behavior of single-unit sympathetic nerve fibers. Fourteen subjects (57 ± 2 years, nine men, five females) fulfilling ATP III criteria for the MS underwent a 3-month low calorie diet. Metabolic profile, hemodynamic parameters, and multi-unit and single-unit muscle sympathetic nerve activity (MSNA, microneurography) were assessed prior to and at the end of the diet. Patients' weight dropped from 96 ± 4 to 88 ± 3 kg (P < 0.001). This was associated with a decrease in systolic and diastolic blood pressure (-12 ± 3 and -5 ± 2 mmHg, P < 0.05), and in heart rate (-7 ± 2 bpm, P < 0.01) and an improvement in all metabolic parameters (fasting glucose: -0.302.1 ± 0.118 mmol/l, total cholesterol: -0.564 ± 0.164 mmol/l, triglycerides: -0.414 ± 0.137 mmol/l, P < 0.05). Multi-unit MSNA decreased from 68 ± 4 to 59 ± 5 bursts/100 heartbeats (P < 0.05). Single-unit MSNA indicated that the firing rate of individual vasoconstrictor fibers decreased from 59 ± 10 to 32 ± 4 spikes/100 heart beats (P < 0.05). The probability of firing decreased from 34 ± 5 to 23 ± 3% of heartbeats (P < 0.05), and the incidence of multiple firing decreased from 14 ± 4 to 6 ± 1% of heartbeats (P < 0.05). Cardiac and sympathetic baroreflex function were significantly improved (cardiac slope: 6.57 ± 0.69 to 9.57 ± 1.20 ms·mmHg(-1); sympathetic slope: -3.86 ± 0.34 to -5.05 ± 0.47 bursts/100 heartbeats·mmHg(-1), P < 0.05 for both). Hypocaloric diet decreased sympathetic activity and improved hemodynamic and metabolic parameters. The sympathoinhibition associated with weight loss involves marked changes, not only in the rate but also in the firing pattern of active vasoconstrictive fibers.
患有代谢综合征 (MS) 的患者体内交感神经激活在心血管疾病发展的发病机制中发挥作用。饮食诱导的体重减轻会降低交感神经输出。然而，导致交感神经抑制的机制尚不清楚。我们试图通过分析单个交感神经纤维的放电行为，对饮食引起的交感神经反应进行详细描述。14 名符合 ATP III 代谢综合征标准的受试者（57 ± 2 岁，9 名男性，5 名女性）接受了为期 3 个月的低热量饮食。在饮食前和饮食结束时评估代谢特征、血流动力学参数以及多单位和单单位肌肉交感神经活动（MSNA，微神经记录）。患者体重从 96 ± 4 降至 88 ± 3 kg（P < 0.001）。这与收缩压和舒张压降低（-12 ± 3 和-5 ± 2 mmHg，P < 0.05）以及心率降低（-7 ± 2 bpm，P < 0.01）和所有代谢参数改善有关（空腹血糖：-0.302.1 ± 0.118 mmol/l，总胆固醇：-0.564 ± 0.164 mmol/l，甘油三酯：-0.414 ± 0.137 mmol/l，P < 0.05）。多单位 MSNA 从 68 ± 4 降至 59 ± 5 次/100 次心跳（P < 0.05）。单单位 MSNA 表明，单个血管收缩纤维的放电率从 59 ± 10 降至 32 ± 4 次/100 次心跳（P < 0.05）。放电的概率从 34 ± 5 降至 23 ± 3%的心跳（P < 0.05），多发性放电的发生率从 14 ± 4 降至 6 ± 1%的心跳（P < 0.05）。心脏和交感神经压力反射功能显著改善（心脏斜率：6.57 ± 0.69 至 9.57 ± 1.20 ms·mmHg(-1)；交感斜率：-3.86 ± 0.34 至-5.05 ± 0.47 次/100 次心跳·mmHg(-1)，两者均 P < 0.05）。低热量饮食降低了交感神经活动，并改善了血流动力学和代谢参数。与体重减轻相关的交感神经抑制不仅涉及速率，还涉及活性血管收缩纤维的放电模式的显著变化。
