Carmignani M, Boscolo P, Iannaccone A
Br J Ind Med. 1983 Aug;40(3):280-4. doi: 10.1136/oem.40.3.280.
Cardiovascular function was studied in anaesthetised male rats which received 50 micrograms/ml of arsenic (as sodium arsenate) in deionised drinking water for 320 days. High urinary excretion of arsenic was found at the end of treatment and the metal accumulated considerably in the kidneys and liver, which both presented slight alterations. No histopathological modifications were evident in other organs. Base line blood pressure, cardiac inotropism, and chronotropism and cardiovascular reactivity to noradrenaline, acetylcholine, angiotensin II, bradykinin, histamine, and serotonin did not differ in exposed or in control animals. In the exposed group, however, there was potentiation of the effects of vascular beta-adrenoceptor stimulation and a reduction in the vascular responsiveness to angiotensin I. Chronic arsenic exposure did not affect the baroreflex sensitivity but was able to induce sympathetic hyperactivity or hypersensitivity, or both, possibly associated with an antivagal action. Our results might help to explain the cardiovascular alterations seen in people chronically exposed to high concentrations of arsenic.
对麻醉的雄性大鼠的心血管功能进行了研究,这些大鼠在去离子饮用水中摄入50微克/毫升的砷(以砷酸钠形式),持续320天。在治疗结束时发现尿砷排泄量很高,并且该金属在肾脏和肝脏中大量蓄积,两者均出现轻微改变。其他器官未发现明显的组织病理学改变。暴露组和对照组动物的基线血压、心肌收缩性、变时性以及对去甲肾上腺素、乙酰胆碱、血管紧张素II、缓激肽、组胺和5-羟色胺的心血管反应性没有差异。然而,在暴露组中,血管β-肾上腺素能受体刺激的作用增强,对血管紧张素I的血管反应性降低。慢性砷暴露不影响压力反射敏感性,但能够诱导交感神经活动亢进或过敏,或两者兼有,可能与抗迷走神经作用有关。我们的结果可能有助于解释长期暴露于高浓度砷的人群中出现的心血管改变。