Hazari Mehdi S, Griggs Jennifer, Winsett Darrell W, Haykal-Coates Najwa, Ledbetter Allen, Costa Daniel L, Farraj Aimen K
Environmental Public Health Division, United States Environmental Protection Agency (USEPA), 109 Alexander Drive, B105, Research Triangle Park, NC, 27711, USA,
Cardiovasc Toxicol. 2014 Mar;14(1):52-63. doi: 10.1007/s12012-013-9228-9.
Short-term exposure to air pollutants has been linked to acute cardiovascular morbidity and mortality. Even in the absence of overt signs or symptoms, pollutants can cause subtle disruptions to internal compensatory mechanisms, which maintain homeostatic balance in response to various environmental and physiological stressors. We hypothesized that a single exposure to acrolein, a ubiquitous gaseous air pollutant, would decrease the sensitivity of baroreflex (BRS), which maintains blood pressure by altering heart rate (HR), modify cardiac electrophysiological properties and increase arrhythmia in rats. Wistar-Kyoto normotensive (WKY) and spontaneously hypertensive (SH) rats implanted with radiotelemeters and a chronic jugular vein catheter were tested for BRS using phenylephrine and sodium nitroprusside 2 days before and 1 h after whole-body exposure to 3 ppm acrolein (3 h). HR and electrocardiogram (ECG) were continuously monitored for the detection of arrhythmia in the pre-exposure, exposure and post-exposure periods. Whole-body plethysmography was used to continuously monitor ventilation in conscious animals. SH rats had higher blood pressure, lower BRS and increased frequency of AV block as evidence by non-conducted p-waves when compared with WKY rats. A single exposure to acrolein caused a decrease in BRS and increased incidence of arrhythmia in both WKY and SH rats. There were minimal ECG differences between the strains, whereas only SH rats experienced irregular breathing during acrolein. These results demonstrate that acrolein causes immediate cardiovascular reflexive dysfunction and persistent arrhythmia in both normal and hypertensive animals. As such, homeostatic imbalance may be one mechanism by which air pollution increases risk 24 h after exposure, particularly in people with underlying cardiovascular disease.
短期接触空气污染物已被证明与急性心血管疾病的发病率和死亡率有关。即使没有明显的体征或症状，污染物也可能对内部代偿机制造成细微干扰，这些机制会对各种环境和生理应激源做出反应以维持体内平衡。我们假设，单次接触丙烯醛（一种普遍存在的气态空气污染物）会降低压力反射（BRS）的敏感性，压力反射通过改变心率（HR）来维持血压，还会改变心脏电生理特性并增加大鼠的心律失常。对植入无线电遥测仪和慢性颈静脉导管的Wistar-Kyoto正常血压（WKY）大鼠和自发性高血压（SH）大鼠，在全身暴露于3 ppm丙烯醛（3小时）之前2天和之后1小时，使用去氧肾上腺素和硝普钠测试其BRS。在暴露前、暴露期间和暴露后持续监测HR和心电图（ECG）以检测心律失常。使用全身体积描记法持续监测清醒动物的通气情况。与WKY大鼠相比，SH大鼠血压更高，BRS更低，且非传导p波证明房室传导阻滞频率增加。单次接触丙烯醛导致WKY和SH大鼠的BRS降低，心律失常发生率增加。两品系之间的ECG差异极小，而只有SH大鼠在接触丙烯醛期间出现呼吸不规则。这些结果表明，丙烯醛会导致正常和高血压动物立即出现心血管反射功能障碍和持续性心律失常。因此，体内平衡失衡可能是空气污染在接触后24小时增加风险的一种机制，尤其是在患有潜在心血管疾病的人群中。
