Mery P, Riou B, Chemla D, Lecarpentier Y
Institut National de la Santé et de la Recherche Médicale, Unité 275, LOA-ENSTA-Ecole Polytechnique, Palaiseu, France.
Intensive Care Med. 1994;20(2):119-23. doi: 10.1007/BF01707666.
Colchicine poisoning may be lethal and a decrease in cardiac function has been reported in several case reports, but the precise cardiotoxicity of colchicine remains unknown.
The experimental in vitro study assessed the intrinsic contractility of left ventricular papillary muscle in rats, 24 h after administration of intraperitoneal colchicine or saline.
The administration of colchicine (2 or 4 mg.kg-1) in adult Wistar rats markedly impaired intrinsic myocardial contractility, as shown by a decrease in maximum shortening velocity (-32 and -61%, respectively), active isometric force (-47 and -65%, respectively), and peak power output (-57 and -69%, respectively) of left ventricular papillary muscle. Colchicine impaired isotonic relaxation and load dependence of relaxation, suggesting a decrease in sarcoplasmic reticulum function. Conversely, colchicine significantly accelerated isometric relaxation, suggesting a decrease in calcium myofilament sensitivity. Myothermal economy was markedly impaired only in some rats (3/10 in each group), in which the negative inotropic effect of colchicine appeared to be more particularly pronounced.
The results indicate that the administration of high doses of colchicine induced intrinsic cardiotoxic effects. Due to its amplitude, such cardiotoxic action may participate in the fatal outcome of acute colchicine poisoning.
秋水仙碱中毒可能致死，已有数例病例报告称其会导致心脏功能下降，但秋水仙碱的确切心脏毒性仍不清楚。
本实验性体外研究评估了成年大鼠腹腔注射秋水仙碱或生理盐水24小时后左心室乳头肌的内在收缩性。
成年Wistar大鼠腹腔注射秋水仙碱（2或4mg·kg-1）后，左心室乳头肌的最大缩短速度（分别降低32%和61%）、主动等长力（分别降低47%和65%）以及峰值功率输出（分别降低57%和69%）均显著受损，表明心肌内在收缩性明显受损。秋水仙碱损害了等张舒张和舒张的负荷依赖性，提示肌浆网功能下降。相反，秋水仙碱显著加速了等长舒张，提示钙肌丝敏感性降低。仅在部分大鼠（每组3/10）中，热经济性明显受损，秋水仙碱的负性肌力作用似乎更为明显。
结果表明，高剂量秋水仙碱给药会诱发内在心脏毒性作用。鉴于其作用程度，这种心脏毒性作用可能是急性秋水仙碱中毒致死的原因之一。
