College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, UK.
University of Birmingham Institute of Cardiovascular Sciences, City Hospital, Birmingham, UK.
J Physiol. 2018 Oct;596(20):4847-4861. doi: 10.1113/JP276644. Epub 2018 Sep 12.
A surge in cortisol during acute physiological and pathophysiological stress may precipitate ventricular arrhythmia and myocardial infarction. Reduced cardiovagal baroreflex sensitivity and heart rate variability are observed during acute stress and are associated with an increased risk of acute cardiac events. In the present study, healthy young men received either a single iv bolus of saline (placebo) or hydrocortisone, 1 week apart, in accordance with a randomized, placebo-controlled, cross-over study design. Hydrocortisone acutely increased heart rate and blood pressure and reduced cardiovagal baroreflex sensitivity and heart rate variability in young men. These findings suggest that, by reducing cardiovagal baroreflex sensitivity and heart rate variability, acute surges in cortisol facilitate a pro-arrhythmic milieu and provide an important mechanistic link between stress and acute cardiac events ABSTRACT: Surges in cortisol concentration during acute stress may increase cardiovascular risk. To better understand the interactions between cortisol and the autonomic nervous system, we determined the acute effects of hydrocortisone administration on cardiovagal baroreflex sensitivity (BRS), heart rate variability (HRV) and cardiovascular reactivity. In a randomized, placebo-controlled, single-blinded cross-over study, 10 healthy males received either a single iv bolus of saline (placebo) or 200 mg of hydrocortisone, 1 week apart. Heart rate (HR), blood pressure (BP) and limb blood flow were monitored 3 h later, at rest and during the sequential infusion of sodium nitroprusside and phenylephrine (modified Oxford Technique), a cold pressor test and a mental arithmetic stress task. HRV was assessed using the square root of the mean of the sum of the squares of differences between successive R-R intervals (rMSSD). Hydrocortisone markedly increased serum cortisol 3 h following infusion and also compared to placebo. In addition, hydrocortisone elevated resting HR (+7 ± 4 beats min ; P < 0.001) and systolic BP (+5 ± 5 mmHg; P = 0.008); lowered cardiovagal BRS [geometric mean (95% confidence interval) 15.6 (11.1-22.1) ms/mmHg vs. 26.2 (17.4--39.5) ms/mmHg, P = 0.011] and HRV (rMSSD 59 ± 29 ms vs. 84 ± 38 ms, P = 0.004) and increased leg vasoconstrictor responses to cold pressor test (Δ leg vascular conductance -45 ± 20% vs. -23 ± 26%; P = 0.023). In young men, an acute cortisol surge is accompanied by increases in HR and BP, as well as reductions in cardiovagal BRS and HRV, potentially providing a pro-arrhythmic milieu that may precipitate ventricular arrhythmia or myocardial infarction and increase cardiovascular risk.
在急性生理和病理生理学应激期间皮质醇的激增可能会引发室性心律失常和心肌梗死。在急性应激期间观察到心脏迷走神经压力反射敏感性和心率变异性降低，并且与急性心脏事件的风险增加相关。在本研究中，健康的年轻男性按照随机、安慰剂对照、交叉设计，每周接受一次静脉内推注生理盐水（安慰剂）或氢化可的松。氢化可的松可使年轻男性的心率和血压急性升高，并降低心脏迷走神经压力反射敏感性和心率变异性。这些发现表明，急性皮质醇激增通过降低心脏迷走神经压力反射敏感性和心率变异性，促进心律失常环境，并为应激和急性心脏事件之间提供重要的机制联系。
急性应激期间皮质醇浓度的激增可能会增加心血管风险。为了更好地了解皮质醇和自主神经系统之间的相互作用，我们确定了氢化可的松给药对心脏迷走神经压力反射敏感性（BRS）、心率变异性（HRV）和心血管反应性的急性影响。在一项随机、安慰剂对照、单盲交叉研究中，10 名健康男性每周接受一次静脉内推注生理盐水（安慰剂）或 200mg 氢化可的松。 3 小时后，在休息时和连续输注硝普钠和苯肾上腺素（改良牛津技术）、冷加压试验和心算应激任务期间监测心率（HR）、血压（BP）和肢体血流量。使用连续 R-R 间期之间差异的均方根的平方根（rMSSD）评估心率变异性。氢化可的松输注后 3 小时血清皮质醇明显升高，与安慰剂相比也是如此。此外，氢化可的松还升高了静息心率（+7±4 次/分钟；P<0.001）和收缩压（+5±5mmHg；P=0.008）；降低了心脏迷走神经压力反射敏感性[几何平均值（95%置信区间）为 15.6（11.1-22.1）ms/mmHg，而 26.2（17.4-39.5）ms/mmHg，P=0.011]和心率变异性（rMSSD 59±29ms，而 84±38ms，P=0.004），并增加了冷加压试验时腿部血管收缩反应（Δ腿部血管传导率-45±20%，而-23±26%；P=0.023）。在年轻男性中，急性皮质醇激增伴随着心率和血压升高，以及心脏迷走神经压力反射敏感性和心率变异性降低，这可能提供一种促心律失常环境，从而引发室性心律失常或心肌梗死并增加心血管风险。
