晶体停搏液中钙离子浓度对幼兔未成熟心肌的保护作用

Crystalloid cardioplegia at different calcium concentration: its effect on immature rabbit myocardium

目的探讨含不同Ｃａ２＋浓度的ＳｔＴｈｏｍａｓⅡ停搏液对未成熟心肌的保护作用。方法采用幼兔离体心脏灌注模型，根据停搏液中不同的Ｃａ２＋浓度，将实验分为三组（１）［Ｃａ２＋］０６ｍｍｏｌ／Ｌ；（２）［Ｃａ２＋］１２ｍｍｏｌ／Ｌ；（３）［Ｃａ２＋］２４ｍｍｏｌ／Ｌ。离体灌注心脏经２０℃９０分钟缺血后，３７℃再灌注３０分钟。结果再灌注１０分钟，高Ｃａ２＋组左室功能恢复亢进，左心室形成压（ＬＶＤＰ），±ｄｐ／ｄｔｍａｘ恢复率分别高于低Ｃａ２＋及中Ｃａ２＋组（Ｐ＜００５，Ｐ＜００１），再灌注２０分钟，该高Ｃａ２＋组左室功能恢复呈下降的趋势。３０分钟再灌注末，与其他两组相比无显著差异。高Ｃａ２＋组心肌组织Ｃａ２＋ＡＴＰ酶活性显著高于中Ｃａ２＋及低Ｃａ２＋组（Ｐ＜００１，Ｐ＜０００１），而心肌ＡＴＰ含量却明显低于其它两组。结论低温缺血期间，高Ｃａ２＋组细胞外滞留的Ｃａ２＋在再灌注期间经Ｃａ２＋通道和Ｃａ２＋／Ｎａ＋交换途径进入心肌细胞内，激活Ｃａ２＋ＡＴＰ酶而加速由Ｃａ２＋所诱导的ＡＴＰ耗能过程。从未成熟心肌细胞能量代谢的角度分析，高Ｃａ２＋浓度的Ｓｔ．ＴｈｏｍａｓⅡ停搏液对未成熟心肌不能提供满意的心肌?

Objective To determine the myocardial protective effect of St.Thomas Ⅱ cardioplegia at different calcium concentration on immature myocardium. Methods Isolated perfused neonatal rabbit hearts from three groups (the calcium concentration of St.Thomas Ⅱ cardioplegia was modified: [Ca 2+ ] 0.6 mmol/L; [Ca 2+ ]1.2 mmol/L; [Ca 2+ ]2.4 mmol/L) were subjected to 20℃ hypothermia, 90 minutes of global ischemia followed by 30 minutes reperfusion in Langendorff mode. Results Although the recovery of LVDP, ±dp/dt max at calcium content of 2.4 mmol/L after 10 minutes of reperfusion was significantly higher than that at 0 6 and 1.2 mmol/L calcium ( P <0.05, P <0.01, respectively), the declined tendency of left ventricular hemodynamics in this group was detected after 20 minutes of reperfusion. By the end of 30 minute reperfusion, the left ventricular hemodynamic recovery at 2.4 mmol/L calcium did not differ from those at 0.6 mmol/L and 1.2 mmol/L calcium. Conversely, postischemic left ventricular functions at 0.6 and 1.2 mmol/L calcium were gradually improved during the 30 minutes reperfusion. Ca 2+ ATPase activity at 2.4 mmol/L calcium showed significant increase ( P <0.01, P <0.001), whereas ATP content was lower than that of other groups. Conclusion Calciun accumulated in extracellular space during ischemia enters myocardial cell via Ca 2+ channel and Ca 2+ /Na + exchange after reperfusion, activates Ca 2+ ATPase, and finally accelerates adenosinetriphosphate (ATP) consumption induced by calcium, which would be responsible for the results of our study. We conclude that, from the point of view of myocardial cell energy metabolism, St. Thomas Ⅱ cardioplegia at high calcium concentration can not provide immature myocardium with optimal myocardial protection.