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標題: Induction of contracture and extracellular Ca2+ influx in cardiac muscle by sanguinarine: a study on cardiotoxicity of sanguinarine
作者: Hu, C.M.
Cheng, Y.W.
Liao, J.W.
Cheng, H.W.
Kang, J.J.
關鍵字: Ca2+ permeability;cardiac;contracture;sanguinarine;ventricular myocytes;ryanodine receptors;calcium-release;argemone;oil;biochemical toxicology;sarcoplasmic-reticulum;channel blockers;epidemic dropsy;cation channel;heart-muscle
Project: Journal of Biomedical Science
期刊/報告no:: Journal of Biomedical Science, Volume 12, Issue 2, Page(s) 399-407.
In this study, the toxic effect of sanguinarine (SANG) on heart was studied with isolated cardiac muscle strip isolated from Wistar rat. SANG induced positive inotropic action followed by contracture on the left ventricle and both atria strips. In addition, SANG dose-dependently inhibited spontaneous beat of the right atrium. SANG-induced contracture was completely suppressed by pretreatment with La3+ or in a Ca2+ free Tyrode solution containing 2.5 mM EGTA. Incubating isolated cardiomyocytes with SANG enhanced the Ca-45(2+) influx, which could be inhibited by pretreatment with La3+. However, the SANG-induced Ca-45(2+) influx could not be inhibited by pretreatment with other Ca2+ channel blockers, such as nifedipine, verapamil, diltiazem, nickel and manganese, and amiloride. Although antioxidants can inhibit the SANG-induced lipid peroxidation, they could not prevent the SANG-induced contracture. N-acetylcysteine and dithiothreitol, the sulfhydryl reducing agents, were shown to be effective in preventing the SANG-induced contracture. These data suggested that the SANG-induced contracture is caused by the influx of extracellular Ca2+ through a La3+-sensitive Ca2+ channel.
ISSN: 1021-7770
DOI: 10.1007/s11373-005-3007-y
Appears in Collections:獸醫病理生物學所

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