Flameng W, Dyszkiewicz W, Minten J
K. U. Leuven, Laboratory of Experimental Cardiac Surgery, Belgium.
Eur J Cardiothorac Surg. 1988;2(4):244-55. doi: 10.1016/1010-7940(88)90079-6.
Long-term preservation of dog hearts was performed over 24 h using Bretschneider-HTK cardioplegia and cold storage. Preservation was assessed in terms of conservation of myocardial tissue levels of high-energy phosphates (HEP) and functional outcome after cardiac transplantation. Serial left ventricular biopsies were taken and analysed for ATP, ADP, AMP, adenosine, inosine, hypoxanthine, xanthine and creatine phosphate. Myocardial structure was studied by electron microscopical examination of a similar biopsy specimen. Cardiac performance was measured before and after cardiac transplantation. Several techniques of cardioplegic arrest were studied: single dose cardioplegia, multidose cardioplegia and continuous perfusion with the cardioplegic solution. In all groups, the hearts were stored at 0.5 degree C for 24 h. In the group of single dose Bretschneider-HTK cardioplegia, myocardial ATP content after 24 h of cold storage was only 25% of control. The total sum of nucleotides at that time interval was however 65% of the control value. Reperfusion of these hearts using a support dog (whole blood reperfusion) did not result in any recovery of ATP. Creatinine phosphate however showed an overshoot. Accumulated nucleosides were washed out. The hearts showed electrical activity but were severely arrhythmic. Contractility was poor. In the group of multidose Bretschneider-HTK cardioplegia, HEP preservation was better than after single dose cardioplegia. ATP content was about 50% of control. The total sum of nucleotides was 85% of control. Ultrastructural assessment of the myocytes revealed only slight ischaemic damage to the mitochondria. Reperfusion on cardiopulmonary bypass after cardiac transplantation did not show any restoration of ATP, but a steady catabolism of HEP. The nucleosides adenosine and inosine were not washed out upon reperfusion. After cardiac transplantation, none of these hearts could be weaned from cardiopulmonary bypass due to irreversible low cardiac output. Histological examination demonstrated irreversible myocardial tissue damage. In the group of continuous cold Bretschneider cardioplegia, HEP content was completely preserved throughout the 24 h of perfusion. Ultrastructure of the myocytes was normal. Reperfusion of the transplanted hearts showed a mild breakdown of ATP to 70% of control values accompanied by a slight accumulation of nucleosides. Haemodynamic recovery however was perfect and none of the hearts needed positive inotropic support. Myocytes after reperfusion had a normal subcellular appearance.(ABSTRACT TRUNCATED AT 400 WORDS)
使用布雷施奈德 - HTK心脏停搏液和冷藏法对犬心脏进行了长达24小时的长期保存。通过评估心肌组织中高能磷酸盐(HEP)水平的保存情况以及心脏移植后的功能结果来评价保存效果。进行了系列左心室活检,并分析了其中的三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)、腺苷、肌苷、次黄嘌呤、黄嘌呤和磷酸肌酸。通过对类似活检标本进行电子显微镜检查来研究心肌结构。在心脏移植前后测量心脏功能。研究了几种心脏停搏技术:单次剂量心脏停搏液、多次剂量心脏停搏液以及心脏停搏液持续灌注。在所有组中,心脏均在0.5摄氏度下保存24小时。在单次剂量布雷施奈德 - HTK心脏停搏液组中,冷藏24小时后心肌ATP含量仅为对照的25%。然而,该时间间隔内核苷酸的总量为对照值的65%。使用供体犬对这些心脏进行再灌注(全血再灌注)未导致ATP的任何恢复。然而,磷酸肌酸出现了超射现象。积累的核苷被冲洗掉。心脏显示出电活动,但严重心律失常。收缩性较差。在多次剂量布雷施奈德 - HTK心脏停搏液组中,HEP的保存情况优于单次剂量心脏停搏液组。ATP含量约为对照的50%。核苷酸的总量为对照的85%。对心肌细胞的超微结构评估显示线粒体仅有轻微的缺血性损伤。心脏移植后在体外循环下进行再灌注未显示ATP的任何恢复,而是HEP持续分解代谢。再灌注时腺苷和肌苷这两种核苷未被冲洗掉。心脏移植后,由于不可逆转的低心输出量,这些心脏无一能够脱离体外循环。组织学检查显示心肌组织存在不可逆转的损伤。在持续冷布雷施奈德心脏停搏液组中,在整个24小时灌注过程中HEP含量完全得以保存。心肌细胞的超微结构正常。移植心脏再灌注显示ATP轻度分解至对照值的70%,同时伴有核苷的轻微积累。然而血流动力学恢复良好,所有心脏均无需正性肌力支持。再灌注后的心肌细胞亚细胞外观正常。(摘要截断于400字)