Department of Chemical Defense Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, China.
J Cardiovasc Pharmacol. 2012 Apr;59(4):331-8. doi: 10.1097/FJC.0b013e318242baa1.
Previous studies in our laboratory have shown that the cardiotoxicity is the main reason for rat death caused by tentacle-only extract from jellyfish Cyanea capillata. However, the direct cardiotoxicity in vitro and its mechanisms of toxic action remain unclear. The current studies were performed by using the Langendorff-perfused isolated heart model, which showed a dose-dependent hemodynamic and electrocardiogram changes. Heart injury-related enzymes increased. Histopathological analysis showed early ischemic damage in the myocardium. The Ca channel blockers nifedipine and verapamil led to a marked improvement in recovery of cardiac function, including heart rate, left ventricular developed pressure, positive and negative first derivatives of intraventricular pressure, coronary flow, left ventricular end-diastolic pressure, and electrocardiogram changes. Tentacle-only extract-induced cardiac dysfunction could be partly improved by the pretreatments of both propranolol and phentolamine, but not by either atropine or neostigmine at all. In conclusion, we have verified the direct cardiotoxicity of tentacle-only extract from jellyfish C. capillata by the Langendorff isolated heart model, which consisted of 3 separate parts: sinoatrial node malfunction, cardiomyocyte injury, and coronary spasm. The potential mechanism might be attributed to the overactivation of L-type Ca channel, β- and α-adrenergic receptors, but not cholinergic receptors.
先前在我们实验室的研究表明，水母触手提取物的心脏毒性是导致水母（Cyanea capillata）提取物中毒的大鼠死亡的主要原因。然而，其体外直接心脏毒性及其作用机制尚不清楚。目前的研究是使用 Langendorff 灌流分离心脏模型进行的，该模型显示出剂量依赖性的血流动力学和心电图变化。与心脏损伤相关的酶增加。组织病理学分析显示心肌早期缺血性损伤。钙通道阻滞剂硝苯地平和维拉帕米可显著改善心脏功能的恢复，包括心率、左心室发展压、心室压力的正负一阶导数、冠状动脉流量、左心室舒张末期压和心电图变化。普萘洛尔和酚妥拉明预处理可部分改善水母触手提取物引起的心脏功能障碍，但阿托品和新斯的明预处理则完全无效。总之，我们通过 Langendorff 分离心脏模型验证了水母 C. capillata 触手提取物的直接心脏毒性，该模型包括 3 个独立部分：窦房结功能障碍、心肌细胞损伤和冠状动脉痉挛。潜在的机制可能归因于 L 型钙通道、β-和α-肾上腺素能受体过度激活，而不是胆碱能受体。
