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短暂性低钙再灌注并不能改善用圣托马斯医院心脏停搏液保存后的大鼠心脏缺血后恢复情况。

Transient hypocalcemic reperfusion does not improve postischemic recovery in the rat heart after preservation with St. Thomas' Hospital cardioplegic solution.

作者信息

Chambers D J, Harvey D M, Braimbridge M V, Hearse D J

机构信息

Department of Cardiovascular Research, Rayne Institute, St. Thomas' Hospital, London, United Kingdom.

出版信息

J Thorac Cardiovasc Surg. 1992 Aug;104(2):344-56.

PMID:1495296
Abstract

We used the isolated perfused working rat heart to investigate the effects of transient hypocalcemic reperfusion after cardioplegic arrest with the St. Thomas' Hospital cardioplegic solution and 25 minutes of global normothermic (37 degrees C) ischemia. Hearts were reperfused (Langendorff mode) transiently (20 minutes) with solutions containing various concentrations of calcium; this was followed by 30 minutes of reperfusion with standard (1.4 mmol/L, the physiologic concentration) calcium buffer (10 minutes in the Langendorff mode and 20 minutes in the working mode). Recovery of cardiac output in control hearts (calcium concentration 1.4 mmol/L throughout) was 51.7% +/- 4.6%; in hearts transiently reperfused with hypocalcemic buffer (0.25, 0.5, 0.75, or 1.0 mmol/L) the recoveries of cardiac output were 49.3% +/- 6.4%, 52.2% +/- 7.2%, 58.7% +/- 3.2%, and 47.2 +/- 4.7%, respectively (all not significant), whereas recovery was only 14.7% +/- 2.8% (p less than 0.05) in hearts transiently reperfused with calcium 0.1 mmol/L. Creatine kinase leakage was significantly (p less than 0.05) greater in the group reperfused with calcium 0.1 mmol/L, but it did not vary significantly between the other groups. Tissue high-energy phosphate content was similar and in the normal range in all groups except for the group reperfused with calcium 0.1 mmol/L. In further experiments, the duration of hypocalcemic (0.5 mmol/L) reperfusion was varied (0, 5, 10, 15, 20, or 30 minutes). No significant differences in recovery of cardiac output were observed (58.2% +/- 5.0%, 52.3% +/- 5.7%, 52.0% +/- 8.2%, 61.2% +/- 5.0%, 62.2% +/- 4.3%, and 66.2% +/- 3.2%, respectively). In additional studies, the standard calcium concentration (1.4 mmol/L) used before and after ischemia was replaced by hypercalcemic solution (2.5 mmol/L). Despite this, transient (10 minutes) hypocalcemic (0.5 mmol/L) reperfusion did not improve recovery. Finally, studies were undertaken with a longer duration of ischemia (40 minutes), and although recovery of cardiac output in the hypocalcemic group (0.5 mmol/L for 10 minutes) tended to be higher than in the control group (29.7% +/- 4.8% versus 18.5% +/- 4.9%, respectively), statistical significance was not achieved. We conclude that in these studies transient hypocalcemic reperfusion did not afford any additional protection over and above that afforded by cardioplegia alone.

摘要

我们使用离体灌注的工作大鼠心脏,研究在采用圣托马斯医院心脏停搏液进行心脏停搏以及25分钟全心常温(37摄氏度)缺血后,短暂低钙再灌注的影响。心脏先使用含有不同钙浓度的溶液进行短暂(20分钟)再灌注(Langendorff模式);随后使用标准(1.4 mmol/L,生理浓度)钙缓冲液进行30分钟再灌注(Langendorff模式10分钟,工作模式20分钟)。对照心脏(全程钙浓度1.4 mmol/L)的心输出量恢复率为51.7%±4.6%;用低钙缓冲液(0.25、0.5、0.75或1.0 mmol/L)短暂再灌注的心脏,心输出量恢复率分别为49.3%±6.4%、52.2%±7.2%、58.7%±3.2%和47.2%±4.7%(均无显著差异),而用0.1 mmol/L钙短暂再灌注的心脏,恢复率仅为14.7%±2.8%(p<0.05)。0.1 mmol/L钙再灌注组的肌酸激酶漏出显著更高(p<0.05),但其他组之间无显著差异。除0.1 mmol/L钙再灌注组外,所有组的组织高能磷酸含量相似且处于正常范围内。在进一步实验中,改变低钙(0.5 mmol/L)再灌注的持续时间(0、5、10、15、20或30分钟)。未观察到心输出量恢复有显著差异(分别为58.2%±5.0%、52.3%±5.7%、52.0%±8.2%、61.2%±5.0%、62.2%±4.3%和66.2%±3.2%)。在另外的研究中,缺血前后使用的标准钙浓度(1.4 mmol/L)被高钙溶液(2.5 mmol/L)替代。尽管如此,短暂(10分钟)低钙(0.5 mmol/L)再灌注并未改善恢复情况。最后,进行了更长缺血时间(40分钟)的研究,虽然低钙组(0.5 mmol/L,持续10分钟)的心输出量恢复率倾向于高于对照组(分别为29.7%±4.8%和18.5%±4.9%),但未达到统计学显著性。我们得出结论,在这些研究中,短暂低钙再灌注并未提供比单纯心脏停搏更多的额外保护。

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