- 作者: Chien Ming Hu; Yu Wen Cheng; Jiunn Wang Liao; Huei Wen Cheng; Jaw Jou Kang
- 作者服務機構: a Institute of Pharmaceutical Sciences, Taipei Medical University, Taipei, Taiwan; ; b Graduate Institute of Veterinary Pathology, National Chung-Hsing University, Taichung, Taiwan;; c Institute of Toxicology, College of Medicine, National Taiwan University, No. 1 Jen-Ai Road, Section 1, Taipei, Taiwan; d Current address: Division of Cardiovascular Research, Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
- 中文摘要: --
- 英文摘要: 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 45Ca2+ influx, which could be inhibited by pretreatment with La3+ . However, the SANG-induced 45Ca2+ 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.
- 中文關鍵字: --
- 英文關鍵字: Ca2+ permeability, cardiac, contracture, sanguinarine