Summary
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.
Zusammenfassung
Die Verfasser untersuchen myokardiale Läsionen, die bei Hunden im Falle hämorrhagischer Hypotonie entstanden sind. Bei allen Tieren wurde eine mit steigender Lactatkonzentration verbundene metabolische Acidosis registriert. In den subendokardialen Herzgebieten sind fokale Hämorrhagien und hypoxische Läsionen entstanden. In der wunden Muskulatur wurden typische sogenannte zonale Läsionen festgestellt. An ihrer Entstehung können die Hypoxie, die steigende Konzentration der Katecholamine, metabolische Schädigungen und vielleicht noch verschiedene kardiotoxische Materialien eine Rolle spielen. Die Läsion ist potentiell reversibel und geht nur in schweren Fällen in einen irreversiblen Prozeß über. In solchen Fällen bildet sich eine Zellnekrose vom hyperkontraktilen Typ aus, die mit schneller Verkalkung und mononuklearer Zellinfiltrierung verbunden ist. Die beobachteten mophologischen Veränderungen können die Entstehung des „low cardiac output“-Syndroms im hämorrhagischen Schock begründen.
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Varga, T., Réffy, A. & Vándor, E. Myocardial lesions in hemorrhagic hypotension. Z Rechtsmed 84, 99–112 (1980). https://doi.org/10.1007/BF02114579
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DOI: https://doi.org/10.1007/BF02114579