The negative inotropic effects of gaseous sulfur dioxide and its derivatives in the isolated perfused rat heart

• Published in: Environmental toxicology 2012-03, Vol.27 (3), p.175-184
• Main Authors: Zhang, Quanxi, Meng, Ziqiang
• Format: Article
• Language: English
• Subjects: Air Pollutants - metabolism; Air Pollutants - toxicity; Animal, plant and microbial ecology; Animals; Applied ecology; Biological and medical sciences; Calcium Channels - metabolism; Calcium Channels, L-Type - metabolism; Ecotoxicology, biological effects of pollution; Fundamental and applied biological sciences. Psychology; General aspects; Guanylate Cyclase - metabolism; Heart - drug effects; Heart - physiology; In Vitro Techniques; inotropic effect; Male; Myocardial Contraction - drug effects; Myocardium - metabolism; Nitric Oxide Synthase - metabolism; Potassium Channels - metabolism; Protein Kinase C - antagonists & inhibitors; Protein Kinase C - metabolism; rat; Rats; Rats, Wistar; Signal Transduction - drug effects; signaling pathways; sulfur dioxide; Sulfur Dioxide - metabolism; Sulfur Dioxide - toxicity; sulfur dioxide derivatives
• ISSN: 1520-4081; 1522-7278
• DOI: 10.1002/tox.20628

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. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2012.