EFFECTS OF VOLATILE ANESTHETICS ON SODIUM/CALCIUM EXCHANGER ACTIVITY IN ISCHEMIC-REPERFUSION INJURY

本文研究了吸入麻醉药对缺血再灌注损伤时钠/钙交换体活性的影响。在这项研究中，我们研究了Na +/Ca+交换活性，Ca2+瞬变，和收缩性在离体兔心室肌细胞。分别用荧光Na指示剂SBFL和fluo 3测量细胞内Na（[Na +] i）和Ca2+浓度（[Ca2 +] i），并根据场刺激期间细胞缩短的变化评估收缩性。结果表明：（1）氟烷能显著降低心肌细胞内Ca~（2+）瞬变和心肌收缩力，（2）缺血再灌注引起心肌细胞内[Ca~（2+）] i和[Na~+] i升高，（3）氟烷能减弱再灌注时[Ca~（2+）] i升高的幅度，（4）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（5）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（6）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（7）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（8）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（10）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（10）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（10）氟烷能抑制心肌细胞内[Ca~（2+）] i升高，（10）氟烷能抑制心肌细胞内[（4）氟烷对缺血期心肌[Na +] i的变化无明显影响，提示氟烷可降低再灌注后心肌细胞内过多的钙离子，对心肌再灌注后的功能可能有一定的保护作用。

We studied that effects of volatile anesthetics on sodium/calcium exchanger activity under ischemic-reperfusion injury. In this study, we examined Na+/Ca+ exchange activity, Ca2+ transients, and contractility in isolated rabbit ventricular myocytes. Intracellular Na ([Na+]i) and Ca2+ concentration ([Ca2+]i) were measured with the fluorescent Na indicators SBFL and fluo 3, respectively, and contractility was assessed from changes in cell shortening during field stimulation. Experiments were performed at extracellular pH 7.4 in the presence of HEPES buffer.Our findings demonstrate that I) halothane significantly decreased Ca2+ transients and contractility, 2) ischemic-reperfusion caused increases in [Ca2+]i and [Na+]i, 3) halothane attenuate the magnitude in increases in [Ca2+]i during reperfusion, 4) halothane did not alter the changes in [Na+]i during ischemic period.It is suggested that a reduction of excessive intracellular calcium after reperfusion caused by halothane may be beneficial on myocardial function following reperfusion in the intact rabbit myocardium.