Pernet A, Hammond V A, Blesa-Malpica G, Burrin J, Orskov H, Alberti K G, Johnston D G
Eur J Clin Pharmacol. 1984;26(1):23-8. doi: 10.1007/BF00546703.
The metabolic effects of dopamine have been investigated by its infusion in normal man with and without simultaneous somatostatin administration. Dopamine was infused into overnight fasted men at 1.5 microgram/kg/min (n = 6) and 3.0 micrograms/kg/min (n = 5) for 120 min. Plasma dopamine concentrations at 120 min were 78 +/- 9 nmol/l and 117 +/- 17 nmol/l respectively, associated with a marginal rise in plasma noradrenaline. Dopamine (1.5 microgram/kg/min) induced an early and sustained rise in plasma glucagon (48 +/- 9 pg/ml versus 19 +/- 6 pg/ml in saline controls at 10 min, p less than 0.01) and a transient elevation in serum growth hormone which peaked to 17.7 (range 4.5-71.8) mU/l at 60 min (7.2 (range 0.6-37.7) mU/l with saline, p less than 0.05) but did not alter serum insulin, blood glucose or other metabolite levels. At 3.0 micrograms/kg/min, dopamine in addition provoked mild and transient elevations in blood glucose and serum insulin. Somatostatin (250 micrograms/h) suppressed circulating insulin, glucagon, and growth hormone levels and abolished the small hyperglycaemic effect seen with the higher dopamine dose. Somatostatin alone induced a progressive rise in circulating non-esterified fatty acid and 3-hydroxybutyrate levels reflecting insulin deficiency. This rise in NEFA and 3-hydroxybutyrate was increased by dopamine particularly at the higher dosage (plasma NEFA; somatostatin alone, 1.08 +/- 0.13 mmol/l; somatostatin plus dopamine 3 micrograms/kg/min, 1.44 +/- 0.17 mmol/l at 120 min, p less than 0.01: blood 3-hydroxybutyrate; somatostatin alone, 0.32 +/- 0.04 mmol/l; somatostatin plus dopamine 3 micrograms/kg/min, 0.56 +/- 0.12 mmol/l at 120 min, p less than 0.05). Thus: 1) dopamine at pharmacological dosage has minor effects when other endocrine mechanisms are intact, 2) it enhances lipolysis and ketogenesis during somatostatin-induced insulin deficiency; 3) the hyperglycaemia effect of the higher dopamine dose is probably mediated through stimulated glucagon secretion.
通过在正常男性中输注多巴胺(同时给予或不给予生长抑素),对多巴胺的代谢作用进行了研究。将多巴胺以1.5微克/千克/分钟(n = 6)和3.0微克/千克/分钟(n = 5)的速度输注到过夜禁食的男性体内,持续120分钟。120分钟时血浆多巴胺浓度分别为78±9纳摩尔/升和117±17纳摩尔/升,同时血浆去甲肾上腺素略有升高。多巴胺(1.5微克/千克/分钟)导致血浆胰高血糖素早期持续升高(10分钟时为48±9皮克/毫升,而生理盐水对照组为19±6皮克/毫升,p<0.01),血清生长激素短暂升高,60分钟时峰值达到17.7(范围4.5 - 71.8)毫国际单位/升(生理盐水组为7.2(范围0.6 - 37.7)毫国际单位/升,p<0.05),但未改变血清胰岛素、血糖或其他代谢物水平。以3.0微克/千克/分钟的速度输注时,多巴胺还引起血糖和血清胰岛素轻度短暂升高。生长抑素(250微克/小时)抑制循环中的胰岛素、胰高血糖素和生长激素水平,并消除了较高剂量多巴胺引起的轻微高血糖效应。单独使用生长抑素会导致循环中非酯化脂肪酸和3 - 羟基丁酸水平逐渐升高,反映出胰岛素缺乏。多巴胺会加剧这种非酯化脂肪酸和3 - 羟基丁酸的升高,尤其是在较高剂量时(血浆非酯化脂肪酸;单独使用生长抑素时为1.08±0.13毫摩尔/升;生长抑素加3微克/千克/分钟多巴胺时,120分钟时为1.44±0.17毫摩尔/升,p<0.01;血液3 - 羟基丁酸;单独使用生长抑素时为0.32±0.04毫摩尔/升;生长抑素加3微克/千克/分钟多巴胺时,120分钟时为0.56±0.12毫摩尔/升,p<0.05)。因此:1)当其他内分泌机制完整时,药理剂量的多巴胺作用较小;2)在生长抑素诱导的胰岛素缺乏期间,它会增强脂肪分解和生酮作用;3)较高剂量多巴胺的高血糖效应可能是通过刺激胰高血糖素分泌介导的。