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腺苷增强冷血心肌保护液在瓣膜置换患者术中初步应用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第6期
页码:
678-681,687
栏目:
临床研究
出版日期:
2006-12-25

文章信息/Info

Title:
Application of adenosine enriched cold blood cardioplegia in valve replacement patients
作者:
金振晓1; 周京军2; 辛梅1; 陈涛1; 顾春虎1; 薛卫斌1; 易定华1
第四军医大学：1.西京医院心血管外科，2.基础部生理学教研室，陕西 西安 710032
Author(s):
JIN Zhen-xiao1;  ZHOU Jing-jun2;  XIN Mei1;  CHEN Tao1;  GU Chun-hu1;  XUE Wei-bin1;  YI Ding-hua1
1.Department of Cardiovascular Surgery, Xijing Hospital, 2.Department of Physiology, Fourth Military Medical University, Xi′an,Shaanxi 710032, China
关键词:
心肌保护液; 腺苷; 瓣膜置换
Keywords:
cardioplegia;  adenosine;  heart valve replacement
分类号:
R654.2
DOI:
-
文献标识码:
A
摘要:
目的 观察腺苷增强的冷血高钾心肌保护液应用于风湿性心脏病瓣膜置换患者的安全性、耐受性和有效性。方法 随机采集2005年3月10日到2005年5月19日收入我院心脏外科行二尖瓣置换，或者二尖瓣、主动脉瓣联合置换手术的患者共74例。心肌保护液采用冷血高钾保护液，晶体:血液比例为1∶4，K+浓度为16 mmol/L，首次灌注腺苷剂量为0（对照组），0.1，0.5，1.0，2.0 mmol/L。病例数分别为20、12、19、13和10例。首次灌注量为700 ml，速度为300 ml/min，以后每隔25～30 min重复灌注1次，灌注量为 350 ml。只有首次灌注加用腺苷。心脏复跳后3 min采集冠状静脉窦回血，检测心肌酶谱和肌钙蛋白I、T。结果 各剂量组首次心肌保护液灌注前后，患者血压无明显变化。腺苷各组从心肌保护液灌注开始到心脏完全静止所用时间较对照组明显缩短，但是腺苷各组之间没有显著差异［（79±59）s vs （35±25）s，（31±18）s，（34±18）s和（28±20）s］。各组之间自动复跳比例无显著差异。升主动脉开放后到心脏复跳所用时间，虽然大剂量腺苷组（1.0 mmol/L 和2.0 mmol/L）较对照组和小剂量腺苷组明显缩短，但是统计学检验未发现有显著差异。大剂量血管活性药物［多巴胺>5 μg/（kg·min），或者使用肾上腺素］使用的比例在各组之间未发现有显著差异。冠状静脉窦采血进行心肌酶谱分析和肌钙蛋白检测结果显示：多数指标在腺苷组特别是2.0 mmol/L腺苷组较对照组有下降，除AST一项在2.0 mmol/L腺苷组较对照组有显著性降低［（0.5±0.2） μkat vs （0.9±0.5） μkat］，LDH1在0.1 mmol/L腺苷组较对照组有显著性降低［（0.7±0.3）μkat vs （1.1±0.4）μkat）］外，其它数据统计学分析未见明显差异。术后各组患者恢复情况：对照组、0.1、0.5和1.0 mmol/L腺苷组在术后气管插管拔除时间、ICU监护时间、引流量、输血量和术后住院时间等方面均无显著差异，对照组和0.1 mmol/L腺苷组分别住院死亡2例，死亡原因有3例为多脏器衰竭死亡，0.1 mmol/L腺苷组有1例死亡原因为左室破裂。其它组没有住院死亡，统计学分析没有显著性差异。结论 将0.1～2.0 mmol/L的腺苷添加到冷血高钾心肌保护液中应用于瓣膜置换患者的心肌保护是安全的，所有患者都能良好耐受。
Abstract:
AIM To investigate the safety, tolerance and effectiveness of application of adenosine enriched hyperpotassium cold blood cardioplegia in valve replacement patients. METHODS Seventy four patients who had undergone mitral valve replacement or mitral valve and aortic valve replacement procedure between March 10th and May 19th 2005 were recruited in the study. Hyperpotassium cold blood cardioplegia was used in all the patients. The ratio of crystalloid: blood was 1∶4 and the final concentration of potassium was 16 mmol/L. Adenosine was added to the cardioplegia through a separate furcation on the delivery line to avoid degradation. The patients were allocated to 5 groups according to the final concentration of adenosine in the cardioplegia: 0 mmol/L (as control, 20 cases), 0.1 mmol/L (12 cases), 0.5 mmol/L (19 cases), 1.0 mmol/L (13 cases) and 2.0 mmol/L (10 cases). The volume of the first dose of cardioplegia was 700ml and half dose of cardioplegia was delivered every 25-30 minutes during the cardiac arrest period. The velocity of cardioplegia delivery was 300 ml/min. Adenosine was only added in the first dose of cardioplegia. Blood in the coronary sinus was collected 3 min after the ascending aorta was declamped. Myocardium enzyme spectrum and troponin T and I were examined. RESULTS The blood pressure was not significantly altered before and after the first dose of cardioplegia delivery in all the groups. The time used for heart arrest after the first dose of cardioplegia administration was significantly shorter in adenosine enriched groups compared with the control group［（35±25)s,(31±18)s, (34±18)s, (28±20)s vs (79±59) s, P<0.05］, but there was no significant difference among the adenosine enriched groups. After the aorta clamp was removed, the time used for heart beating restoration and the ratio of heart beating restoration free of defibrillation were not significantly different among all the groups. High dose of inotropic drugs used after the weaning of CPB (cardio pulmonary bypass) was not significantly different among all the groups. Examination of the myocardial enzyme spectrum, troponin T and I in blood samples collected from the coronary sinus showed no statistically significant differences among all the groups, though most of the parameters examined in the 2.0 mmol/L adenosine group were a little lower than those in the other groups. The postoperation parameters such as extubation time, ICU (intensive care unit) days, drainage volume, homologous transfusion volume, hospitalization days and inhospital mortality were not statistically different among all the groups. CONCLUSION It is safe and can be well tolerated by all the patients studied when the final concentration of adenosine as 0.1-2.0 mmol/L is supplemented to the hyperpotassium cold blood cardioplegia.

参考文献/References

［1］ Schubert T, Vetter H, Owen P, et al. Adenosine cardioplegia. Adenosine versus potassium cardioplegia:cardiac arrest and postischemic recovery rat heart［J］. J Thorac Cardiovasc Surg, 1989, 98（6）:1057-1065.

［2］de Jong JW, van der Meer P, van Loon H, et al. Adenosine as adjunct to potassium cardioplegia: Effect on function, energy metabolism, and electrophysiology［J］. J Thorac Cardiovasc Surg, 1990, 100(3): 445-454.

［3］ Friehs I, CaoDahn H, Takahashi S, et al. Adenosine prevents protein kinase C activation during hypothermic ischemia［J］. Circulation, 1997, 96(9 suppl):II221-II225.

［4］ Hearse DJ, Stewart DA, Braimbridge MV. Cellular protection during myocardial ischemia. The development and characterization of a procedure for the induction of reversible ischemic arrest［J］. Circulation, 1976, 54(2): 193-202.

［5］ Galinanes M, Hearse DJ. Exogenous adenosine accelerated recovery of cardiac function and improves coronary flow after longterm hypothermic storage and transplantation［J］. J Thorac Cardiovasc Surg, 1992, 104(1): 151-158.

［6］ Fremes SE, Levy SL, Christakis GT, et al. Phase 1 human trial of adenosinepotassium cardioplegia［J］. Circulation, 1996, 94(9 suppl): II370-II375.

［7］ Cohen G, Shirai T, Weisel RD, et al. Optimal myocardial preconditioning in humans［J］. Ann N Y Acad Sci, 1999, 874: 306-319.

［8］ Mentzer RM Jr, Rahko PS, MolinaViamonte V, et al. Safety, tolerance, and efficacy of adenosine as an additive to blood cardioplegia in humans during coronary artery bypass surgery［J］. Am J Cardiol, 1997, 79(12A): 38-43.

［9］ Mentzer RM Jr, Birjiniuk V, Khuri S, et al. Adenosine myocardial protection: preliminary results of a phase II clinical trial［J］. Ann Surg, 1999, 229(5): 643 -649.

［10］Hudspeth DA, Nakanishi K, VintenJohansen J, et al. Adenosine in blood cardioplegia prevents postischemic dysfunction in ischemically injured hearts［J］. Ann Thorac Surg, 1994, 58(6): 1637-1644.

备注/Memo

备注/Memo:
收稿日期：2005-09-20.通讯作者：易定华，教授，主要研究方向为体外循环脏器保护，组织工程生物心脏瓣膜，胸部创伤早期救治和移植免疫机制 Tel：(029)84775307 Email：yidh@fmmu.edu.cn 作者简介：金振晓，主治医师，博士 Tel：(029)84775311 Email：jinzx@fmmu.edu.cn
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