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Experimental Myocardial Preservation Study of adding Perfluorochemicals (FC43) in Lidocaine Cardioplegia

利多卡因停搏液中添加全氟化合物(FC43)的心肌保护实验研究

基本信息

批准号：
11671340
负责人：
INOUE Koichi
金额：
$ 0.7万
依托单位：
Showa University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671340/
关键词：
Perfluorochemicals Lidocaine intracellular Ca reperfusion injury myocardial protection 心保存 Langendorff灌流

项目摘要

Objective :Lidocaine exhibits a cardioplegic action via acute inhibition of sodium influx into the myocardial cells. In terms of the cardiac function and calcium dynamics in the myocardial cells, we investigated the myocardial protective effect of addition of FC43 of perfluorochemicals, which has an excellent oxygen transport function to meet the myocardial oxygen demand, on lidocaine induced cardioplegia.Methods :Isolated rat hearts were perfused with Langendorff mode and were divided to three experimental groups. During of preservation, these hearts were perfused continuously with the next three solution, potassium chloride was added to Krebs-Henseleit bicarbonate buffer to make potassium concentration of 20 mM in the first group (Group A), 2 mM lidocaine was added to Krebs-Henseleit bicarbonate buffer in the second group (Group B), and 2 mM lidocaine and 20% FC43 were added to Krebs-Henseleit bicarbonate buffer in the third group (Group C). After 60 minutes of continuous perfusion, the cardiac function and the intracellular calcium concentration in Groups A and B during cardioplegia were measured, Furthermore, after 360 minutes of continuous coronary perfusion, the cardiac function were measured in Group B and Group C.Results and Conclusions :Lidocaine cardioplegia showed a good recovery of cardiac function, because lidocaine induced prompt cardiac arrest by blocking sodium influx and inhibited the intracellular calcium overload by the following inhibition of sodium calcium channels. Moreover, our results suggested that combining perfluorochemicals with lidocaine produced a more effective myocardial preservation that meets the myocardial oxygen demand during long term cardiac arrest.

目的：利多卡因通过急性抑制钠流入心肌细胞而发挥心脏停搏作用。从心脏功能和心肌细胞钙动态方面，我们研究了添加全氟化合物FC43对利多卡因诱导的心肌停跳液的心肌保护作用，FC43具有良好的氧运输功能，满足心肌需氧量。方法：离体大鼠心脏采用Langendorff模式灌注，分为3个实验组。保存期间，连续灌注以下三种溶液，第一组（A组）向Krebs-Henseleit碳酸氢盐缓冲液中加入氯化钾使钾浓度为20 mM，第二组（B组）向Krebs-Henseleit碳酸氢盐缓冲液中加入2 mM利多卡因，向Krebs-Henseleit碳酸氢盐缓冲液中加入2 mM利多卡因和20% FC43。第三组（C 组）中的 Krebs-Henseleit 碳酸氢盐缓冲液。连续灌注60分钟后，测量A组和B组心脏停跳期间的心功能和细胞内钙浓度，此外，连续冠脉灌注360分钟后，测量B组和C组的心功能。结果与结论：利多卡因心脏停跳液显示出良好的心功能恢复，因为利多卡因通过阻断钠流入而导致即时心脏骤停。并通过抑制钠钙通道来抑制细胞内钙超载。此外，我们的结果表明，将全氟化合物与利多卡因结合可产生更有效的心肌保护，满足长期心脏骤停期间的心肌需氧量。