Cuénoud H F, Joris I, Majno G
Am J Pathol. 1978 Aug;92(2):421-58.
The purpose of this study was to find out whether acute massive pulmonary embolism can produce myocardial changes visible by light and electron microscopy. Ww therefore produced pulmonary embolism in rats using plastic microspheres (diameter, 15 +/- 5 mu). Two experimental protocols were used: lethal embolism, with a dose of microspheres known to kill in 3 to 15 hours (these rats were killed after 1 hour), and sublethal embolism, with a dose compatible with 100% survival (these rats were killed after 24 hours). In both groups, the left ventricle was normal. The right ventricle showed two tyes of changes: a) A distinctive lesion of the myocytes, more diffuse after lethal enbolism and different from the "zonal lesion" of shock. It consisted primarily in a localized shredding of the myofibrillar system; hence, the name shredding is proposed. Earlier stages of this lesion were represented by focal dissolution of the Z line (Z lysis). The pathogenesis of these lesions appeared to be primarily mechanical. b) Necrosis was already apparent at 1 hour and was more extensive after 24 hours. The pathogensis of the necrotic lesions is best explained by a temporary ischemia followed by delayed reflow; a possible potentiating role of endogenous catecholamines cannot be excluded. Most capilaries in the necrotic foci remained functional; this explains the rapid rate of the healing process of such lesions. A comparison is drawn between the observed foci of necrosis and the human myocardial lesions knowns as "miliary infarcts" and "myocytolysis." It is proposed that a factor common to all three is the preservation of the microcirculatory vessels and that our experimental model helps illuminate the pathogenesis of the human lesions. It is concluded that the right ventricle of acute cor pulmonale may develop cellular changes with a complex pathologenesis (mechanical, ischemic, and possibly hormonal). The nature of the changes found in our model could represent the morphologic substrate of right-sided failure; it can be correlated with the electrocardiographic abnormalities found in the comparable human condition.
本研究的目的是确定急性大面积肺栓塞是否会产生光镜和电镜下可见的心肌变化。因此，我们用塑料微球（直径15±5微米）在大鼠中制造肺栓塞。采用了两种实验方案：致死性栓塞，使用已知在3至15小时内可致死的微球剂量（这些大鼠在1小时后处死），以及亚致死性栓塞，使用与100%存活相容的剂量（这些大鼠在24小时后处死）。在两组中，左心室均正常。右心室呈现出两种变化：a）心肌细胞的一种独特病变，在致死性栓塞后更弥漫，且与休克的“带状病变”不同。它主要表现为肌原纤维系统的局部撕裂；因此，提出了“撕裂”这一名称。该病变的早期阶段表现为Z线的局灶性溶解（Z溶解）。这些病变的发病机制似乎主要是机械性的。b）坏死在1小时时已很明显，24小时后更广泛。坏死性病变的发病机制最好用暂时缺血后延迟再灌注来解释；内源性儿茶酚胺的可能增强作用不能排除。坏死灶中的大多数毛细血管仍保持功能；这解释了此类病变愈合过程的快速性。将观察到的坏死灶与已知的人类心肌病变“粟粒性梗死”和“心肌溶解”进行了比较。提出三者共有的一个因素是微循环血管的保留，且我们的实验模型有助于阐明人类病变的发病机制。得出的结论是，急性肺心病的右心室可能会发生具有复杂发病机制（机械性、缺血性以及可能的激素性）的细胞变化。我们模型中发现的变化性质可能代表右侧心力衰竭的形态学基础；它可与在类似人类情况下发现的心电图异常相关。
