瓣膜病和冠心病患者不同时间心肌毛细血管对结晶性停搏液的反应

V. P. Zakharova, Oleksii A. Krykunov, P. M. Semeniv, A. Balabai, Andrii A. Hulich
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引用次数: 0

摘要

目标。研究瓣膜缺损和冠心病患者心肌毛细血管对停搏液反应的形态学表现。材料和方法。对手术材料和切片材料进行了形态学研究。用于显微镜研究的心肌碎片来自心脏直视手术不同阶段的患者和在未经手术干预的保守治疗阶段死亡的患者。一名健康青年死于与生命不相容的损伤,其心肌的类似样本被研究作为对照。对于电子显微镜研究,在灌注第185分钟从患者身上采集心肌样本。后果心肌的组织学制剂显示心肌细胞(CMC)明显弥漫性肥大,有时处于失代偿期(核周水肿、肌原纤维丢失、细胞凋亡)。CMC的这种转变显然与二尖瓣和主动脉瓣联合缺陷引起的功能超负荷有关。肌肉纤维的变化伴有间质纤维化和核周纤维化。在受动脉粥样硬化影响的冠状动脉池中,3名患者可见小范围局灶性冠状动脉纤维化的迹象,以及梗死后粗糙的疤痕。所有患者都有心肌急性缺氧损伤的迹象,表现为CMC缩短和间质水肿。结论。在患有冠状动脉疾病的心脏主动脉瓣和二尖瓣合并缺陷的患者中,心肌纤维化现象占主导地位。心脏瓣膜病合并冠心病会导致微循环床血管中交替和代偿适应过程的发展。心脏停搏液给药后185分钟,小血管中重要细胞器损失最大,灌注后3小时出现不可逆变化。
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The Reaction of Myocardial Capillaries to Crystalloid Cardioplegia of Different Durations in Patients with Valvular Pathology and Coronary Heart Disease
The aim. To study the morphological manifestations of the response of the myocardial capillaries to cardioplegia in patients with valvular defects and coronary heart disease. Materials and methods. Morphological research of operative and sectional material was carried out. Myocardium fragments for microscopical study were obtained from patients at different stages of an open-heart surgery and patients who died at the stage of conservative treatment without surgical intervention. Similar samples of the myocardium of a healthy young man who died from injuries incompatible with life were studied as a control. For electron microscopy study, samples of myocardium were taken from patients at the 185th minute of perfusion. Results. Histological preparations of the myocardium showed pronounced diffuse hypertrophy of cardiomyocytes (CMCs), sometimes at the stage of decompensation (perinuclear edema, loss of myofibrils, apoptosis). This transformation of CMCs was obviously related to their functional overload caused by combined defects of the mitral and aortic valves. Changes in muscle fibers were accompanied by interstitial and perinuclear fibrosis. In the pool of coronary arteries affected by atherosclerosis, signs of small focal coronary fibrosis were visible, as well as rough post-infarction scars in 3 patients. All the patients had signs of acute hypoxic damage to the myocardium in the form of CMCs shortening and interstitial edema. Conclusions. In patients with combined defects of the aortic and mitral valves of the heart with coronary artery disease, the phenomena of myocardial fibrosis prevail. Heart valve disease combined with coronary heart disease lead to the development of both alterative and compensatory-adaptiveprocesses in the vessels of the microcirculatory bed. The greatest loss of vital organelles in small vessels is observed at 185 min after administration of cardioplegic solution, irreversible changes develop 3 h after perfusion.
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42
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