Sekiguchi S, Ozawa A, Hanafusa Y, Andou S, Inoue K, Takaba T
Department of First Surgery, Showa University, School of Medicine, Tokyo, Japan.
Jpn J Thorac Cardiovasc Surg. 1998 Jul;46(7):622-8. doi: 10.1007/BF03217791.
The effects of Ryanodine, an inhibitor of salcoplasmic reticulum function, was investigated in isolated hearts of the Wistar rat strain. The cytosolic calcium was measured with the intracellular Ca2+ fluorescent indicator Fura-2. After 3 minutes perfusion of various cardioplegic solution which were added potassium (the concentration; 20 mmol/L) and four Ryanodine groups (1, 4, 10, and 20 nmol/L), these were obtained cardiac arrest. The arrested hearts were kept at 37 degrees C (normothermia) measuring hemodynamic studies. Hemodynamic parameters were heart rate, LVDP, LV dp/dt, coronary flow, and the intracellular calcium fluorescents which were calculated intracellular Ca2+. The significant difference was not noted in LVDP, but comparable improvement was achieved with Ryanodine groups (p < 0.05; 20 nM vs 0 nM). Other cardiac functions were likely same as above. The cytosolic calcium concentration of Ryanodine groups was depressed during cardiac arrest, it was 97.4 +/- 17.2% at the end of cardiac arrest, and it was slowly increased to 161.9 +/- 46.9% after 40 minutes reperfusion. On the other hand, that of the control group was higher than Ryanodine groups at every measuring points about two times. There was significant difference between both groups (p < 0.01). Concequently these phenomena caused that Ca2+ handling in the salcoplasmic reticulum were supressed by Ryanodine and the contractile function was recovered for that reason.
研究了肌浆网功能抑制剂雷诺丁对Wistar大鼠品系离体心脏的影响。用细胞内Ca2+荧光指示剂Fura-2测量胞质钙。在灌注添加了钾(浓度为20 mmol/L)的各种心脏停搏液以及四个雷诺丁组(1、4、10和20 nmol/L)3分钟后,实现了心脏停搏。将停搏的心脏保持在37摄氏度(正常体温)进行血流动力学研究。血流动力学参数包括心率、左心室舒张末压(LVDP)、左心室dp/dt、冠状动脉血流量以及计算得出的细胞内钙荧光强度(即细胞内Ca2+)。LVDP未观察到显著差异,但雷诺丁组有类似的改善(p < 0.05;20 nM vs 0 nM)。其他心脏功能可能与上述情况相同。雷诺丁组在心脏停搏期间胞质钙浓度降低,在心脏停搏结束时为97.4 +/- 17.2%,再灌注40分钟后缓慢升高至161.9 +/- 46.9%。另一方面,对照组在每个测量点的胞质钙浓度约为雷诺丁组的两倍。两组之间存在显著差异(p < 0.01)。因此,这些现象表明雷诺丁抑制了肌浆网中的Ca2+处理,从而使收缩功能得以恢复。