Yamamoto H, Yamamoto F
Department of Cardiovascular Surgery, National Cardiovascular Center, Osaka, Japan.
Nihon Kyobu Geka Gakkai Zasshi. 1995 Jul;43(7):966-72.
Myocardial rapid cooling is known to result in sarcoplasmic reticular (SR) calcium release. SR calcium release during an infusion of cold cardioplegic solution may contribute to myocardial protection against hypothermic global ischemia. We have, therefore, investigated using the isolated working rat heart preparation to determine the effect of cold cristalloid cardioplegic solution (K+ = 16 mmol/L) containing ryanodine on myocardial injury due to hypothermic global ischemia. Hearts (n = 6-12/group) from male Wistar rats were aerobically (37 degrees C) perfused (20 min) with bicarbonate buffer (Ca2+ = 2.4 mmol/L). This was followed by a 3 min infusion of St. Thomas' Hospital cardioplegic solution (20 degrees C) containing various concentrations of ryanodine. Hearts were then subjected to 180 min of hypothermic (20 degrees C) global ischemia and 35 min of normothermic (37 degrees C) reperfusion (15 min Langendorff, 20 min working). The recoveries of aortic flow were 46.4 +/- 3.7% in the ryanodine free controls versus 50.8 +/- 5.1, 50.6 +/- 4.8, 53.1 +/- 5.9, 59.4 +/- 1.9, 50.5 +/- 3.2 and 31.8 +/- 6.1% in the 0.18, 0.88, 1.31, 1.75, 10.00 and 100.00 nmol/L ryanodine groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
已知心肌快速冷却会导致肌浆网(SR)钙释放。在输注冷心脏停搏液期间,SR钙释放可能有助于心肌抵御低温性全心缺血。因此,我们使用离体工作大鼠心脏标本进行研究,以确定含有ryanodine的冷晶体心脏停搏液(K + = 16 mmol/L)对低温性全心缺血所致心肌损伤的影响。将雄性Wistar大鼠的心脏(每组n = 6 - 12)在37℃下用碳酸氢盐缓冲液(Ca2 + = 2.4 mmol/L)进行有氧灌注(20分钟)。随后输注含不同浓度ryanodine的圣托马斯医院心脏停搏液(20℃)3分钟。然后使心脏经历180分钟的低温(20℃)全心缺血和35分钟的常温(37℃)再灌注(15分钟Langendorff灌注,20分钟工作)。在无ryanodine的对照组中,主动脉血流恢复率为46.4±3.7%,而在0.18、0.88、1.31、1.75、10.00和100.00 nmol/L ryanodine组中分别为50.8±5.1%、50.6±4.8%、53.1±5.9%、59.4±1.9%、50.5±3.2%和31.8±6.1%。(摘要截断于250字)