Schnabel P A, Richter J, Schmiedl A, Bach F, Bartels U, Ramsauer B, Gebhard M M, Bretschneider H J
Department of Physiology, Georg-August-University, Göttingen, Germany.
Thorac Cardiovasc Surg. 1991 Aug;39(4):174-82. doi: 10.1055/s-2007-1013958.
Cellular and mitochondrial swelling are regarded as typical intra-ischemic alterations ("IIA"), contraction band lesions (CBL), in contrast, as products of post-ischemic reperfusion. The occurrence of both types of structural deterioration was investigated in Purkinje fibres and subendocardial and intramural working myocardium: initially after St. Thomas- or HTK cardioplegia, then during ensuing global ischemia up to the "practical limit of resuscitability", and following post-ischemic reperfusion. Generally, Purkinje fibres are not better preserved than neighbouring working myocardium. Comparing St. Thomas- and HTK cardioplegia, considerable quantitative, but not qualitative differences in the reaction patterns of different cell types or layers arise. Immediately after cardioplegia, CBL are completely lacking in both cell types. During ischemia, CBL occur occasionally in Purkinje fibres and seldom in subendocardial working myocardium, "IIA" predominate. During post-ischemic reperfusion "IIA" tend to reverse in all layers, whereas CBL are found to remain in the subendocardial cell types. In intramural layers, CBL occur only during reperfusion. Thus, we deduce that cardioplegia only modulates the severity of "IIA" and the frequency of CBL, but cannot abolish the particular sensitivity of subendocardial Purkinje fibres to global ischemia. Prerequisites for the development of irreversible CBL are on the one hand ischemic metabolic alterations and corresponding energy deficits, and, on the other hand, a supply of oxygen. The oxygen may be inadequately supplied via diffusion during ischemia or may be subsequently provided by reperfusion.
细胞肿胀和线粒体肿胀被视为典型的缺血期改变（“IIA”），相比之下，收缩带损伤（CBL）则是缺血后再灌注的产物。在浦肯野纤维以及心内膜下和心肌壁内的工作心肌中研究了这两种结构恶化类型的发生情况：最初在圣托马斯或HTK心脏停搏液灌注后，然后在随后的全心缺血期间直至“复苏的实际极限”，以及缺血后再灌注期间。一般来说，浦肯野纤维并不比相邻的工作心肌保存得更好。比较圣托马斯和HTK心脏停搏液，不同细胞类型或层的反应模式在数量上有相当大的差异，但在质量上没有差异。心脏停搏后立即，两种细胞类型中均完全没有CBL。在缺血期间，CBL偶尔出现在浦肯野纤维中，很少出现在心内膜下工作心肌中，“IIA”占主导。在缺血后再灌注期间，“IIA”在所有层中都倾向于逆转，而CBL则在心内膜下细胞类型中持续存在。在心肌壁内层，CBL仅在再灌注期间出现。因此，我们推断心脏停搏液仅调节“IIA”的严重程度和CBL的频率，但不能消除心内膜下浦肯野纤维对全心缺血的特殊敏感性。不可逆CBL发展的先决条件一方面是缺血性代谢改变和相应的能量缺乏，另一方面是氧气供应。在缺血期间，氧气可能通过扩散供应不足，或者随后可能通过再灌注提供。
