[Ultrastructural bases of pulmonary edema in myocardial infarct].
A total of 347 patients with myocardial infarction were investigated. Of those, 115 had uncomplicated course of the disease, while pulmonary edema developed in 80, cardiac asthma in 37, pulmonary edema and cardiogenic shock in 35, and various other complications in 80; the outcome was lethal in 80 cases. The pathogenetic contribution of increased permeability to the development of myocardial infarction and its complications is demonstrated. Transendothelial pinocytosis is a trigger mechanism of pulmonary edema. Its pathomorphism is achieved in five steps, each corresponding to a certain degree of ultrastructural transformation of endothelial and alveolar cells. Pulmonary surfactant damage adds to the effect of tissue factors of increased aerohematic barrier permeability.
D000328:Adult; D000368:Aged; D002199:Capillary Permeability; D006801:Humans; D008168:Lung / Q000098:blood supply / Q000648:ultrastructure; D008833:Microcirculation / Q000648:ultrastructure; D008854:Microscopy, Electron; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications* / Q000473:pathology; D011650:Pulmonary Alveoli / Q000648:ultrastructure; D011654:Pulmonary Edema / Q000209:etiology* / Q000473:pathology; D011663:Pulmonary Surfactants / Q000032:analysis; D012770:Shock, Cardiogenic / Q000209:etiology / Q000473:pathology; D013997:Time Factors
D011663:Pulmonary Surfactants
Ul'trastrukturnye osnovy oteka legkikh u bol'nykh infarktom miokarda.