Lindal S, Sørlie D, Jørgensen L
Department of Pathology, University Hospital of Tromsø, Norway.
Scand J Thorac Cardiovasc Surg. 1988;22(3):257-65. doi: 10.3109/14017438809106072.
Ultrastructural changes in endothelial cells of the myocardial microvasculature were studied in 18 patients who underwent aortocoronary bypass surgery under cold ischaemic cardioplegia. Biopsy specimens for electron microscopy were taken from the right atrium before and at the end of aortic cross-clamping and after 20 and 60 min of reperfusion. At the end of the cold ischaemic cardioplegia, the endothelial cells showed reduced numbers of pinocytotic vesicles, moderate intracellular oedema and slight nuclear changes. During reperfusion the endothelial changes became more pronounced and interstitial oedema developed. These changes persisted, or even increased in the first 60 min of reperfusion, in contrast to the myocytic changes, which tended to regress. The endothelial cells of the myocardial microvasculature thus appeared to be more vulnerable than the myocytes to cold ischaemic cardioplegia and reperfusion. Focally reduced blood reperfusion due to endothelial swelling and interstitial oedema did not seem to be the main cause of the focal postischaemic myocytic damage.
对18例在冷缺血性心脏停搏下行主动脉冠状动脉搭桥手术的患者的心肌微血管内皮细胞超微结构变化进行了研究。在主动脉交叉钳夹前、钳夹结束时以及再灌注20分钟和60分钟后，从右心房取电子显微镜检查的活检标本。在冷缺血性心脏停搏结束时，内皮细胞的胞饮小泡数量减少，有中度细胞内水肿和轻微核变化。再灌注期间，内皮变化变得更加明显，间质水肿形成。与趋于消退的心肌细胞变化相反，这些变化在再灌注的最初60分钟持续存在甚至加重。因此，心肌微血管的内皮细胞似乎比心肌细胞更容易受到冷缺血性心脏停搏和再灌注的影响。内皮肿胀和间质水肿导致的局部血流再灌注减少似乎不是缺血后局部心肌细胞损伤的主要原因。
