Identification of myosin isoenzymes in rat cardiac muscle after long-term methamphetamine administration.

长期服用甲基苯丙胺后大鼠心肌中肌球蛋白同工酶的鉴定。

• 批准号: 01570335
• 负责人: FUJITANI Noboru
• 金额: $ 0.77万
• 依托单位: Saga Medical School
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1989
• 资助国家: 日本
• 起止时间: 1989 至 1990
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-01570335/
• 关键词: Methamphetamine; Heart; Myosin isozyme; Actomyosin ATPase; Methampletamine; Myosinisoenzym; Methamphetamino

We have reported that long-term administration of methamphetamine (MA) of which main pharmacologic reaction is releasing catecholamine from nerve endings induces rat cardiac lesions such as hypertrophy, myolysis, contraction band necrosis and disarray of myofibers. To further investigate the mechanism of MA induced cardiac injury we examined the myosin isozyme pattern and the actomyosin ATPase activity of the heart. The histological examination of r-at heart administered MA 1 mg/kg b. w. /day for 8 weeks and 12 weeks revealed hypertrophy, atrophy, myolysis and disarray of myofibers. Isozyme patterns of myosin were investigated by polyacrylamide gel electrophoresis in the presence of pyrophosphate as described by Hoh et al. and were estimated by densitometry. Though there was a significant difference between VI value of controls which were injected saline same volume for 8 w and 12 w (69.3 +- 8.0 % vs 56.2 +- 5.7 %, respectively), no significant difference was observed between controls and MA treated rat hearts in both groups. Mg^2-ATPase activity in the presence of 10 or 0.1muM Ca^<2+> were measured by previously reported method. In result, there were no significant differences in Mg^<2+>-ATPase activity at 10muM Ca^<2+> between 8 w and 12 w controls and each MA treated rats, but there was a significant increase of Mg^<2+>-ATPase activity at 0.1muM Ca^<2+> in 12 w HA treated rats compared with controls. The result suggest that there may be some changes in cardiac function after long-term MA administration as well as histologic changes.

我们已报道，长期给予以神经末梢释放儿茶酚胺为主要药理反应的甲基苯丙胺(MA)可引起大鼠心脏肥大、肌溶解、收缩带坏死和肌纤维紊乱等损害。为了进一步探讨MA所致心脏损伤的机制，我们检测了心脏肌球蛋白同工酶和肌动球蛋白ATPase活性。连续给药8周和12周后，心肌组织学检查显示心肌纤维肥大、萎缩、溶解、紊乱。根据Hoh等人的描述，在焦磷酸盐存在下，用聚丙烯酰胺凝胶电泳法研究了肌球蛋白的同工酶图谱。并用密度法进行了估算。注射等量生理盐水8周和12周的对照组大鼠心脏VI值分别为69.3±8.0%和56.2±5.7%，差异有统计学意义(P<0.05)，而MA组和对照组大鼠心脏VI值差异无统计学意义。用文献报道的方法测定了10或0.1muM Ca~(2+)和Gt~(2+)存在下的Mg~(2+)-ATPase活性。结果表明，8周组、12周组和各MA处理组大鼠心肌组织中10µM Ca~(2+)&gt；-ATPase活性无显著差异，而12周HA组大鼠心肌组织中0.1µM Ca~(2+)&gt；-ATPase活性显著高于对照组。结果提示，长期服用MA后心功能可能有一定的变化，组织学上也有一定的变化。