The negative inotropic effects of gaseous sulfur dioxide and its derivatives in the isolated perfused rat heart
The negative inotropic effects of gaseous sulfur dioxide and its derivatives in the isolated perfused rat heart
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DOI：
10.1002/tox.20628
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发表时间：
2012-03-01
影响因子：
4.5
通讯作者：
Meng, Ziqiang
中科院分区：
文献类型：
--
作者：
Zhang, Quanxi;Meng, Ziqiang
流行病学调查显示，二氧化硫（SO2）暴露与心血管疾病有关。本研究旨在探讨气态SO2及其衍生物对离体灌流大鼠心脏的负性肌力作用及其可能的机制。结果表明，SO2和SO2衍生物均能引起负性肌力作用，且呈剂量依赖性，SO2的负性作用强于SO2衍生物。低浓度和高浓度SO2引起的负性肌力作用机制不同。在低浓度下，SO2的负性肌力作用机制可能是通过促进蛋白激酶C（PKC）、环氧化酶（COX）和cGMP的活性而实现的，而SO2衍生物的负性肌力作用机制可能与开放ATP敏感性K+通道（KATP）和抑制L型钙通道的Ca ~（2+）内流有关。在高浓度时，SO2和SO2衍生物的负性肌力作用机制相似，可能与KATP通道和L型钙通道以及PKC、环氧化酶和cGMP的改变有关。需要进一步的工作，以确定SO2介导的变力作用中每个途径的相对贡献。(c)2010 Wiley Periodicals，Inc.环境毒理学，2012年。
Epidemiological investigations have revealed that sulfur dioxide (SO2) exposure is linked to cardiovascular diseases. The present study was designed to investigate the negative inotropic effects of gaseous SO2 and its derivatives in the isolated perfused rat heart and the possible mechanisms involved in their effects. The results showed that both SO2 and SO2 derivatives elicited a negative inotropic effect in a dose-dependent manner, and SO2 produced a higher negative effect than SO2 derivatives. The mechanism of SO2-induced negative inotropic effects at low concentrations was different from that at high concentrations. At low concentrations, the mechanism of SO2-induced negative inotropic effects might occur through promoting the activities of protein kinase C (PKC), cycloxygenase, and cGMP, while the mechanism of SO2 derivatives-induced effects might be related to the opening of ATP-sensitive K+ (KATP) channel and the inhibition of Ca2+ influx via L-type calcium-channel. At high concentrations, the mechanisms of SO2 and SO2 derivatives-induced negative inotropic effects were similar, which might be related to the KATP channel and L-type calcium-channel as well as the possible alterations in PKC, cycloxygenase, and cGMP. Further work is needed to determine the relative contribution of each pathway in SO2-mediated inotropic effect. (c) 2010 Wiley Periodicals, Inc. Environ Toxicol, 2012.