Varga T, Réffy A, Vándor E
Z Rechtsmed. 1980 Jan;84(2):99-112. doi: 10.1007/BF02114579.
The myocardial alterations were investigated in dogs after hemorrhagic hypotension. Development of metabolic acidosis with increased lactate concentration was observed in all cases. Focal hemorrhages and hypoxic changes developed in the subendocarial region. Typical so-called zonal lesions were demonstrable in the mural myocardium of both ventricles. The hypoxia, increased level of catecholamines, metabolic disturbances, and probably cardiotoxic products may play a role in the pathomechanism. The alterations which are potentially reversible are transformed into irreversible damage only in most severe cases. The necrosis is of hypercontraction type, and is associated with rapid calcification and mononuclear cell infiltration. The morphologic changes may explain the circulatory disturbances of cardiac origin and may represent the basis of development of the low cardiac output syndrome in hemorrhagic shock.
对失血性低血压后的犬心肌改变进行了研究。在所有病例中均观察到代谢性酸中毒伴乳酸浓度升高。心内膜下区域出现局灶性出血和缺氧改变。在两个心室的心肌壁中均可发现典型的所谓带状病变。缺氧、儿茶酚胺水平升高、代谢紊乱以及可能的心脏毒性产物可能在发病机制中起作用。潜在可逆的改变仅在最严重的情况下才会转变为不可逆损伤。坏死为过度收缩型，伴有快速钙化和单核细胞浸润。形态学改变可解释心脏源性循环障碍，并可能是失血性休克中心输出量降低综合征发生的基础。
