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心脏停搏诱导温度和氨基酸富集在新生儿心肌保护中的作用。

The role of cardioplegia induction temperature and amino acid enrichment in neonatal myocardial protection.

作者信息

Kronon M T, Allen B S, Bolling K S, Rahman S, Wang T, Maniar H S, Prasad S M, Ilbawi M N

机构信息

Division of Cardiovascular Surgery, The Heart Institute for Children, Hope Children's Hospital, Oak Lawn, Illinois 60453, USA.

出版信息

Ann Thorac Surg. 2000 Sep;70(3):756-64. doi: 10.1016/s0003-4975(00)01713-6.

DOI:10.1016/s0003-4975(00)01713-6
PMID:11016306
Abstract

BACKGROUND

Warm cardioplegic induction improves the ischemically "stressed" adult heart. However, it is rarely used in infants, despite the fact that many newborn hearts are stressed by other factors such as hypoxia. The need for amino acids as well as their mechanism of action has also not been studied.

METHODS

We first assessed the role of cardioplegic induction temperature in 10 nonhypoxic neonatal piglets undergoing 70 minutes of multidose blood cardioplegic arrest. Five piglets (group 1) received a cold (4 degrees C) induction, and 5 (group 2) a warm (37 degrees C) induction. Twenty-six other piglets underwent ventilator hypoxia (fraction of inspired oxygen, 8% to 10%) for 60 minutes before cardiopulmonary bypass (stress). Six piglets (group 3) then underwent 70 minutes of cardiopulmonary bypass without ischemia (hypoxia controls), and 20 underwent 70 minutes of cardioplegic arrest. Five of these (group 4) received cold cardioplegic induction, and 15 received warm induction; in 5 of these (group 5), the warm cardioplegic solution contained amino acids, in 5 others (group 6), it was unsupplemented, and in the remaining 5 (group 7), nitroglycerin was added to determine the role of vasodilation. Myocardial function was assessed by pressure-volume loops (expressed as a percent of control), and coronary vascular resistance was measured with cardioplegic infusions.

RESULTS

In nonhypoxic (normal) piglets, cold (group 1) and warm (group 2) induction completely preserved systolic function (end-systolic elastance, 100% versus 104%) and preload recruitable stroke work (100% versus 102%), with minimal increase in diastolic compliance (162% versus 156%). Hypoxia-reoxygenation alone (group 3) depressed systolic function (end-systolic elastance, 51%+/-2%) and preload recruitable stroke work (54%+/-3%), and raised diastolic stiffness (260%+/-15%). The detrimental effects of reoxygenation persisted (unchanged from reoxygenation alone) with cold induction (group 4) or warm induction without amino acids (groups 6 and 7). In contrast, warm induction with amino acids (group 5) restored systolic function (end-systolic elastance, 105%+/-3%; p < 0.001 versus groups 3, 4, 6, and 7) and preload recruitable stroke work (103%+/-2%; p < 0.001 versus groups 3, 4, 6, and 7), and decreased diastolic stiffness (154%+/-7%; p < 0.001 versus groups 3, 4, 6, and 7). However, there was no difference in myocardial oxygen consumption in hypoxic hearts receiving a warm induction (6.9 versus 6.5 versus 7.3 mL/g per 5 minutes) (groups 5, 6, 7), and coronary vascular resistance was lowest with nitroglycerin (group 7).

CONCLUSIONS

Cardioplegic induction can be given either warm or cold in nonhypoxic neonatal hearts. In contrast, only warm induction with amino acids repairs the hypoxic injury, but the primary mechanism of action is not related to increased metabolic activity or vasodilation.

摘要

背景

温血心脏停搏诱导可改善处于缺血“应激”状态的成年心脏。然而,尽管许多新生儿心脏会受到缺氧等其他因素的影响,但温血心脏停搏诱导在婴儿中很少使用。氨基酸的需求及其作用机制也尚未得到研究。

方法

我们首先评估了心脏停搏诱导温度在10只非缺氧新生仔猪中的作用,这些仔猪接受了70分钟的多剂量血液心脏停搏。5只仔猪(第1组)接受冷(4℃)诱导,5只(第2组)接受温(37℃)诱导。另外26只仔猪在体外循环前(应激)接受60分钟的呼吸机诱导缺氧(吸入氧分数为8%至10%)。然后,6只仔猪(第3组)进行70分钟的体外循环但无缺血(缺氧对照组),20只进行70分钟的心脏停搏。其中5只(第4组)接受冷心脏停搏诱导,15只接受温诱导;在这15只中,5只(第5组)的温血心脏停搏液含有氨基酸,另外5只(第6组)未添加氨基酸,其余5只(第7组)添加硝酸甘油以确定血管舒张的作用。通过压力-容积环评估心肌功能(以对照的百分比表示),并通过心脏停搏液输注测量冠状血管阻力。

结果

在非缺氧(正常)仔猪中,冷(第1组)和温(第2组)诱导完全保留了收缩功能(收缩末期弹性,分别为100%和104%)和可招募前负荷搏出功(分别为100%和102%),舒张顺应性仅有轻微增加(分别为162%和156%)。单独的缺氧-复氧(第3组)降低了收缩功能(收缩末期弹性,51%±2%)和可招募前负荷搏出功(54%±3%),并增加了舒张硬度(260%±15%)。冷诱导(第4组)或无氨基酸的温诱导(第6组和第7组)时,复氧的有害作用持续存在(与单独复氧时相同)。相比之下,添加氨基酸的温诱导(第5组)恢复了收缩功能(收缩末期弹性,105%±3%;与第3、4、6和7组相比,P<0.001)和可招募前负荷搏出功(103%±2%;与第3、4、6和7组相比,P<0.001),并降低了舒张硬度(154%±7%;与第3、4、6和7组相比,P<0.001)。然而,接受温诱导的缺氧心脏的心肌耗氧量没有差异(每5分钟6.9对6.5对7.3 mL/g)(第5、6、7组),并且硝酸甘油组(第7组)的冠状血管阻力最低。

结论

在非缺氧新生心脏中,心脏停搏诱导可以采用温诱导或冷诱导。相比之下,只有添加氨基酸的温诱导才能修复缺氧损伤,但其主要作用机制与代谢活性增加或血管舒张无关。

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