Schnabel P A, Richter J, Schmiedl A, Ramsauer B, Bartels U, Gebhard M M, Mall G, Bretschneider H J
Abteilung Vegetative Physiologie und Pathophysiologie, Universität Göttingen, Federal Republic of Germany.
Virchows Arch A Pathol Anat Histopathol. 1991;418(1):17-25. doi: 10.1007/BF01600240.
During open heart surgery, reperfusion-induced arrhythmias arising after short periods of ischaemia may originate from subendocardial Purkinje fibres. We investigated the ultrastructure of these fibres during 30 min of global ischaemia at 25 degrees C. The effects both with myocardial protection (HTK cardioplegia) and without it (pure ischaemia) were compared qualitatively and morphometrically. After 30 min pure ischaemia overcontraction of sarcomeres, hypercontraction and contraction bands, together with considerable changes in organelles, predominate over cellular oedema. In Purkinje fibres, both cellular and mitochondrial swelling were significantly increased within this 30-min time period from the onset of pure ischaemia. In contrast, following HTK cardioplegia and 30 min ischaemia, cellular and mitochondrial swelling remain moderate and over-contractions are almost entirely lacking. This means that despite remarkable differences between pure ischaemia and HTK cardioplegia in the degree of protection attained it is clear that, compared with the working myocardium, subendocardial Purkinje fibres do not display a higher resistance to early global ischaemia. Further investigations of this sensitivity of Purkinje fibres to global ischaemia and certain drugs may bring about new insights into myocardial protection and pharmacotherapy of arrhythmias.
在心脏直视手术中,短时间缺血后出现的再灌注诱导性心律失常可能源于心内膜下浦肯野纤维。我们研究了在25摄氏度下全局缺血30分钟期间这些纤维的超微结构。对有心肌保护(HTK心脏停搏液)和无心肌保护(单纯缺血)的效果进行了定性和形态计量学比较。单纯缺血30分钟后,肌节过度收缩、超收缩和收缩带,以及细胞器的显著变化,比细胞水肿更为突出。在浦肯野纤维中,从单纯缺血开始的这30分钟内,细胞和线粒体肿胀均显著增加。相比之下,在HTK心脏停搏液处理及30分钟缺血后,细胞和线粒体肿胀保持适度,且几乎完全没有过度收缩。这意味着,尽管单纯缺血和HTK心脏停搏液在获得的保护程度上存在显著差异,但很明显,与工作心肌相比,心内膜下浦肯野纤维对早期全局缺血并未表现出更高的耐受性。对浦肯野纤维对全局缺血及某些药物的这种敏感性进行进一步研究,可能会为心肌保护和心律失常的药物治疗带来新的见解。