Balazs T
Arch Toxicol Suppl. 1986;9:171-7. doi: 10.1007/978-3-642-71248-7_22.
The most commonly occurring cardiotoxic reactions in humans are due to over-exposure to chemicals that affect physiological function of the heart. These effects, which are usually receptor-mediated, are dose related and can generally be predicted from safety studies in animals. Direct chemical toxicity is initiated by an interaction of a reactive metabolite of the xenobiotic with cellular macromolecules. The incidence of such cardiotoxicity is low because few of these chemicals are metabolized in the heart. The concentration of cellular protective substances influences the development of such toxicity, and therefore species variation should be considered in safety studies. Chemically induced immune system-mediated reactions can develop in the heart, and may occur in anaphylaxis. Antibody mediated cytotoxic or immune complex reactions are rare events, and the predictability is poor. In some instances sensitivity is immunogenetically controlled. Cardiotoxic effects can also develop after prenatal exposure to chemicals, and thus consideration should be given to examining the offspring for those effects in teratology studies.
人类中最常见的心脏毒性反应是由于过度接触影响心脏生理功能的化学物质。这些效应通常是受体介导的，与剂量相关，并且通常可以从动物安全性研究中预测出来。直接化学毒性是由外源性物质的反应性代谢产物与细胞大分子相互作用引发的。这种心脏毒性的发生率较低，因为这些化学物质很少在心脏中代谢。细胞保护物质的浓度会影响这种毒性的发展，因此在安全性研究中应考虑物种差异。化学诱导的免疫系统介导的反应可在心脏中发生，可能发生在过敏反应中。抗体介导的细胞毒性或免疫复合物反应是罕见事件，且可预测性较差。在某些情况下，敏感性受免疫遗传学控制。产前接触化学物质后也可能产生心脏毒性作用，因此在致畸学研究中应考虑检查后代是否有这些影响。
