Bachen Elizabeth A, Muldoon Matthew F, Matthews Karen A, Manuck Stephen B
Department of Psychology, Mills College, Oakland, CA 94613, USA.
Psychosom Med. 2002 Jul-Aug;64(4):587-94. doi: 10.1097/01.psy.0000021943.35402.8a.
Previous studies suggest that hemoconcentration may be one mechanism by which acute psychological stress causes elevations of serum total cholesterol and its subfractions. Alternatively, such elevations may result from sympathetically mediated changes in lipid metabolism. This study evaluated these two hypotheses by manipulation of sympathetically mediated responses to stress using a nonselective adrenoceptor antagonist, labetalol.
In a 2 x 2 factorial design, 52 healthy male participants were randomly assigned to a stress or no-stress condition and, within each condition, were administered either labetalol or saline. Participants assigned to stress completed three cognitive and evaluative tasks lasting a total of 18 minutes. Indices of hemoconcentration (hematocrit and hemoglobin), heart rate, blood pressure, and serum lipids (total, high-density lipoprotein (HDL), low-density lipoprotein (LDL), free fatty acids, and triglycerides) were assessed at preinfusion and infusion baselines and after mental stress (or rest).
Labetalol reduced sympathetic activation, as shown by a substantial reduction in heart rate elevation during stress, but did not alter changes in blood pressure or in hemoconcentration, as indicated by equivalent increases in hematocrit and hemoglobin in the two stressed groups. Labetalol blocked stress-induced increases in free fatty acid concentrations and lowered triglyceride levels but did not influence rises in total, HDL, or LDL cholesterol among stressed subjects. However, arithmetic correction for hemoconcentration eliminated the increases in total, HDL, and LDL cholesterol.
These findings suggest that elevations in total cholesterol and its HDL and LDL subfractions during acute stress are caused by accompanying hemoconcentration, whereas concomitant rises in free fatty acids and triglycerides result from the direct metabolic effects of sympathetic activation.
以往研究表明，血液浓缩可能是急性心理应激导致血清总胆固醇及其亚组分升高的一种机制。或者，这种升高可能是由交感神经介导的脂质代谢变化引起的。本研究通过使用非选择性肾上腺素能受体拮抗剂拉贝洛尔来操纵对压力的交感神经介导反应，评估了这两种假设。
采用2×2析因设计，将52名健康男性参与者随机分为应激组或非应激组，在每组中分别给予拉贝洛尔或生理盐水。分配到应激组的参与者完成了三项认知和评估任务，共持续18分钟。在输注前和输注基线以及心理应激（或休息）后，评估血液浓缩指标（血细胞比容和血红蛋白）、心率、血压和血清脂质（总胆固醇、高密度脂蛋白（HDL）、低密度脂蛋白（LDL）、游离脂肪酸和甘油三酯）。
拉贝洛尔降低了交感神经激活，表现为应激期间心率升高显著降低，但未改变血压或血液浓缩的变化，两组应激组的血细胞比容和血红蛋白等量增加表明了这一点。拉贝洛尔阻断了应激诱导的游离脂肪酸浓度升高并降低了甘油三酯水平，但未影响应激受试者中总胆固醇、HDL或LDL胆固醇的升高。然而，对血液浓缩进行算术校正消除了总胆固醇、HDL和LDL胆固醇的升高。
这些发现表明，急性应激期间总胆固醇及其HDL和LDL亚组分的升高是由伴随的血液浓缩引起的，而游离脂肪酸和甘油三酯的同时升高是由交感神经激活的直接代谢效应导致的。
