Kopp S J, Barron J T, Tow J P
Department of Physiology, Chicago College of Osteopathic Medicine, IL 60615.
Environ Health Perspect. 1988 Jun;78:91-9. doi: 10.1289/ehp.887891.
Chronic and acute lead poisoning cause overt, clinical symptoms of cardiac and vascular damage with potentially lethal consequences. Morphological, biochemical, and functional derangements of the heart have all been described in patients following exposure to excessive lead levels. Disturbances in cardiac electrical and mechanical activity and postmortem evidence of morphological and biochemical derangements of the myocardium have all been reported following excessive exposure to lead in humans. In addition, signs of vascular degeneration, abnormal vascular smooth muscle function, and altered vessel compliance have been described in humans chronically and acutely exposed to toxic lead levels. Similar cardiovascular complications have been detected following excessive lead exposure in experimental animals. Myocarditis, electrocardiographic disturbances, heightened catecholamine arrhythmogenicity, altered myocardial contractile responsiveness to inotropic stimulation, degenerative structural and biochemical changes affecting the musculature of the heart and vasculature, hypertension, hypercholesterolemia, atherosclerosis, and increased vascular reactivity to alpha-adrenergic agonists have been among the reported cardiovascular disturbances linked to lead poisoning. Less certain are the cardiovascular effects of subclinical lead poisoning. Although controversial, chronic low-level lead exposure has been linked to hypertension and other cardiovascular disturbances in both clinical and experimental studies. In general, it can be concluded that lead over a wide range of exposure intensities can induce significant changes in the function of the cardiovascular system. Evidence points to the involvement of multiple sites of action. Cardiac and vascular sites, as well as sites within the central nervous system, have all been implicated in the sequelae of cardiovascular effects. The exact pathogenic mechanisms that underlie the actions of lead in the cardiovascular system, however, have yet to be elucidated definitively.(ABSTRACT TRUNCATED AT 250 WORDS)
慢性和急性铅中毒会引发明显的心脏和血管损伤临床症状，可能导致致命后果。接触过量铅的患者出现了心脏的形态学、生物化学和功能紊乱。人体接触过量铅后，已报告出现心脏电活动和机械活动紊乱，以及心肌形态学和生物化学紊乱的尸检证据。此外，长期和急性接触有毒铅水平的人群中，出现了血管退化迹象、血管平滑肌功能异常和血管顺应性改变。实验动物接触过量铅后也检测到了类似的心血管并发症。已报告的与铅中毒相关的心血管紊乱包括心肌炎、心电图紊乱、儿茶酚胺致心律失常性增强、心肌对变力刺激的收缩反应性改变、影响心脏和血管肌肉组织的退行性结构和生物化学变化、高血压、高胆固醇血症、动脉粥样硬化以及血管对α-肾上腺素能激动剂的反应性增加。亚临床铅中毒对心血管的影响尚不确定。尽管存在争议，但临床和实验研究均表明，慢性低水平铅暴露与高血压和其他心血管紊乱有关。总体而言，可以得出结论，在广泛的暴露强度范围内，铅均可诱导心血管系统功能发生显著变化。有证据表明涉及多个作用位点。心脏和血管位点以及中枢神经系统内的位点均与心血管效应的后遗症有关。然而，铅在心血管系统中作用的确切致病机制尚未完全阐明。（摘要截选至250词）
