Effects of methylphenidate (Ritalin) on mammalian myocardial ultrastructure.

T A Henderson, V W Fischer
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Abstract

Previous observations have indicated lamellated ultrastructural lesions in the myocardium of a patient treated with methylphenidate (Ritalin) hydrochloride (MPH). A causal relationship between MPH exposure and these membranous changes was tested in the myocardium of rats and mice. Following injection of varying doses of MPH for different periods, myocardial ultrastructure was examined and lesions were quantified by stereological techniques. Myocardial tissue also was stained using techniques selective for acid phosphatase and for sarcoplasmic reticulum to identify possible pathogenetic mechanisms. MPH induced membrane accumulations and lamellations which were not membrane-bound and did not react for acid phosphatase, but stained positively for sarcoplasmic reticulum. Both lesions were highly focal, surrounded by normal appearing myocardial tissue. Lamellations were evident at the earliest timepoints examined and appeared to occur without lysosomal involvement. Lesions were still apparent 12 weeks after terminating MPH. These data suggest that MPH may have persistent, cumulative effects on the myocardium.

哌甲酯对哺乳动物心肌超微结构的影响。
先前的观察表明,在接受盐酸哌甲酯(利他林)(MPH)治疗的患者心肌中存在层状超微结构病变。在大鼠和小鼠心肌中测试了MPH暴露与这些膜变化之间的因果关系。在不同时间注射不同剂量的MPH后,观察心肌超微结构,并用体视学技术对病变进行量化。心肌组织也采用选择性酸性磷酸酶和肌浆网染色技术,以确定可能的发病机制。MPH诱导了非膜结合的膜堆积和层状,对酸性磷酸酶没有反应,但对肌浆网染色呈阳性。两个病变都是高度局灶性的,周围是正常的心肌组织。在检查的最早时间点上,层状瘤很明显,似乎没有溶酶体的参与。在终止MPH后12周,病变仍然明显。这些数据表明,MPH可能对心肌有持续的、累积的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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