Schnabel P A, Schmiedl A, Ramsauer B, Bartels U, Gebhard M M, Richter J, Bretschneider H J
Abteilung Vegetative Physiologie und Pathophysiologie, Zentrum Physiologie und Pathophysiologie, Göttingen, Federal Republic of Germany.
Virchows Arch A Pathol Anat Histopathol. 1990;417(6):463-71. doi: 10.1007/BF01625725.
Contraction bands usually occur in the intramural working myocardium following post-ischaemic reperfusion. In the subendocardium, however, they are found during ischaemia. Thus, we ascertained the contraction states of Purkinje fibres, transitional cells, subendocardial and intramural parts of the working myocardium during 30 min global ischaemia at 25 degrees C. The effects with and without myocardial protection were compared. At the onset of pure ischaemia contraction bands are completely lacking in all cell types. During pure ischaemia contraction bands are found in all subendocardial cell types but not in the intramural working myocardium. A peak of pathological contraction states is found in the intramural working myocardium at the onset (0 min), in the subendocardial working myocardium at 10 min, in the transitional cells and Purkinje fibres at 30 min of pure ischaemia. Histidine-, tryptophan-, ketoglutarate-enriched (HTK) cardioplegia prevents contraction bands completely at the onset of ischaemia and prevents both contraction bands and pathological contraction states during ischaemia almost completely. Striking differences in the physiological contraction states are seen only in the working myocardium: HTK cardioplegia brings about dominance of relaxation during ischaemia. These findings may be due mainly to the effects of global ischaemia on the one hand and to catecholamines, calcium and oxygen on the other.
收缩带通常在缺血后再灌注时出现在壁内工作心肌中。然而，在缺血期间可在心内膜下发现收缩带。因此，我们确定了在25℃下30分钟全心缺血期间浦肯野纤维、移行细胞、工作心肌的心内膜下部分和壁内部分的收缩状态。比较了有和没有心肌保护的效果。在单纯缺血开始时，所有细胞类型均完全没有收缩带。在单纯缺血期间，所有心内膜下细胞类型中均可发现收缩带，但壁内工作心肌中未发现。在单纯缺血开始时（0分钟），壁内工作心肌出现病理性收缩状态高峰，在心内膜下工作心肌中在10分钟时出现高峰，在移行细胞和浦肯野纤维中在30分钟时出现高峰。富含组氨酸、色氨酸、酮戊二酸（HTK）的心脏停搏液在缺血开始时可完全防止收缩带出现，并在缺血期间几乎完全防止收缩带和病理性收缩状态出现。仅在工作心肌中观察到生理收缩状态的显著差异：HTK心脏停搏液在缺血期间导致舒张占优势。这些发现可能主要一方面归因于全心缺血的影响，另一方面归因于儿茶酚胺、钙和氧的影响。
