Paramore D S, Fanelli C G, Shah S D, Cryer P E
Division of Endocrinology, Diabetes, and Metabolism, General Clinical Research Center and the Diabetes Research and Training Center, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Am J Physiol. 1998 Nov;275(5):E872-81. doi: 10.1152/ajpendo.1998.275.5.E872.
Plasma norepinephrine (NE) concentrations are a fallible index of sympathetic neural activity because circulating NE can be derived from sympathetic nerves, the adrenal medullas, or both and because of regional differences in sympathetic neural activity. We used isotope dilution measurements of systemic and forearm NE spillover rates (SNESO and FNESO, respectively) to study the sympathochromaffin system during prolonged standing, hyperinsulinemic euglycemia, and hyperinsulinemic hypoglycemia in healthy humans. Prolonged standing led to decrements in blood pressure without increments in heart rate, the pattern of incipient vasodepressor syncope. FNESO was not increased (0.58 +/- 0.20 to 0. 50 +/- 0.21 pmol. min-1. 100 ml tissue-1), suggesting that the approximately twofold increments in plasma NE and SNESO were derived from sympathetic nerves other than those in the forearm (with a possible contribution from the adrenal medullas). Hyperinsulinemia per se (euglycemia maintained) stimulated sympathetic neural activity, as evidenced by increments in FNESO (0.57 +/- 0.11 to 1.25 +/- 0.25 pmol. min-1. 100 ml tissue-1, P < 0.05), but not adrenomedullary activity. Hypoglycemia per se stimulated adrenomedullary activity (plasma epinephrine from 190 +/- 70 to 1720 +/- 320, pmol/l, P < 0.01). Although SNESO (P < 0.05) and perhaps plasma NE (P < 0.06) were raised to a greater extent during hyperinsulinemic hypoglycemia than during hyperinsulinemic euglycemia, FNESO was not. Thus these data do not provide direct support for the concept that hypoglycemia per se also stimulates sympathetic neural activity.
血浆去甲肾上腺素（NE）浓度是交感神经活动的一个不可靠指标，因为循环中的NE可来源于交感神经、肾上腺髓质或两者，还因为交感神经活动存在区域差异。我们采用同位素稀释法分别测量全身和前臂的NE溢出率（分别为SNESO和FNESO），以研究健康人在长时间站立、高胰岛素正常血糖和高胰岛素低血糖状态下的交感嗜铬系统。长时间站立导致血压下降但心率未增加，这是血管减压性晕厥初期的模式。FNESO未增加（从0.58±0.20降至0.50±0.21 pmol·min⁻¹·100 ml组织⁻¹），这表明血浆NE和SNESO大约两倍的增加来源于前臂以外的交感神经（肾上腺髓质可能有一定贡献）。高胰岛素血症本身（维持正常血糖）刺激了交感神经活动，这可通过FNESO增加得到证明（从0.57±0.11增至1.25±0.25 pmol·min⁻¹·100 ml组织⁻¹，P<0.05），但未刺激肾上腺髓质活动。低血糖本身刺激了肾上腺髓质活动（血浆肾上腺素从190±70升至1720±320 pmol/l，P<0.01）。尽管高胰岛素低血糖期间SNESO（P<0.05）以及可能血浆NE（P<0.06）升高的幅度比高胰岛素正常血糖期间更大，但FNESO并非如此。因此，这些数据并不直接支持低血糖本身也刺激交感神经活动这一概念。
