* Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, North Carolina 27599;
Toxicol Sci. 2013 Oct;135(2):425-36. doi: 10.1093/toxsci/kft155. Epub 2013 Jul 19.
Cardiac disease exacerbation is associated with short-term exposure to vehicular emissions. Diesel exhaust (DE) might impair cardiac performance in part through perturbing efferent sympathetic and parasympathetic autonomic nervous system (ANS) input to the heart. We hypothesized that acute changes in ANS balance mediate decreased cardiac performance upon DE inhalation. Young adult heart failure-prone rats were implanted with radiotelemeters to measure heart rate (HR), HR variability (HRV), blood pressure (BP), core body temperature, and pre-ejection period (PEP, a contractility index). Animals pretreated with sympathetic antagonist (atenolol), parasympathetic antagonist (atropine), or saline were exposed to DE (500 µg/m(3) fine particulate matter, 4h) or filtered air and then treadmill exercise challenged. At 1 day postexposure, separate rats were catheterized for left ventricular pressure (LVP), contractility, and lusitropy and assessed for autonomic influence using the sympathoagonist dobutamine and surgical vagotomy. During DE exposure, atenolol inhibited increases in HR, BP, and contractility, but not body temperature, suggesting a role for sympathetic dominance. During treadmill recovery at 4h post-DE exposure, HR and HRV indicated parasympathetic dominance in saline- and atenolol-pretreated groups that atropine inhibited. Conversely, at treadmill recovery 21h post-DE exposure, HRV and PEP indicated sympathetic dominance and subsequently diminished contractility that only atenolol inhibited. LVP at 1 day postexposure indicated that DE impaired contractility and lusitropy while abolishing parasympathetic-regulated cardiac responses to dobutamine. This is the first evidence that air pollutant inhalation both causes time-dependent oscillations between sympathetic and parasympathetic dominance and decreases cardiac performance via aberrant sympathetic dominance.
心脏疾病恶化与短期暴露于机动车排放物有关。柴油废气（DE）可能通过干扰心脏的传出交感神经和副交感自主神经系统（ANS）输入来部分损害心脏功能。我们假设，ANS 平衡的急性变化介导了 DE 吸入后心脏功能的下降。年轻的易患心力衰竭的大鼠被植入无线电遥测仪，以测量心率（HR）、心率变异性（HRV）、血压（BP）、核心体温和射血前期（PEP，收缩性指数）。用交感神经拮抗剂（阿替洛尔）、副交感神经拮抗剂（阿托品）或生理盐水预处理的动物暴露于 DE（500μg/m³细颗粒物，4 小时）或过滤空气，然后进行跑步机运动挑战。在暴露后 1 天，单独的大鼠被进行左心室压力（LVP）、收缩性和舒张性评估，并使用拟交感神经激动剂多巴酚丁胺和手术迷走神经切断术评估自主神经的影响。在 DE 暴露期间，阿替洛尔抑制了 HR、BP 和收缩性的增加，但不影响体温，这表明交感神经优势的作用。在 DE 暴露后 4 小时进行跑步机恢复期间，HR 和 HRV 表明在生理盐水和阿替洛尔预处理组中副交感神经优势，而阿托品抑制了这种优势。相反，在 DE 暴露后 21 小时进行跑步机恢复时，HRV 和 PEP 表明交感神经优势，随后收缩性下降，只有阿替洛尔抑制了这种下降。暴露后 1 天的 LVP 表明，DE 损害了收缩性和舒张性，同时取消了副交感神经调节的心脏对多巴酚丁胺的反应。这是第一个证据，表明空气污染物吸入既会引起交感神经和副交感神经优势之间的时间依赖性振荡，又会通过异常的交感神经优势降低心脏功能。
