Introduction: Experimental thrombohemorrhagic phenomena

Abstract

The principal forms of the thrombohemorrhagic phenomenon have been briefly surveyed on the basis of animal experiments. Special emphasis has been laid upon the possibility of producing predictably localized thrombohemorrhagic phenomena by combined treatment with a systemic “conditioning agent” which produces a disease susceptibility and a “challenger” which makes this susceptibility manifest and determines the location of the resulting changes. Through this technic it has been possible to produce fairly selective changes of the thrombohemorrhagic phenomenon in the kidney, heart, vessels, duodenum and jejunum, cecum, spleen, salivary and lacrimal glands, adrenals, uterus, anaphylactoid shock organs or transplantable tumors. The same challengers (epinephrine, 5-HT), which, after proper conditioning, produce disseminated thrombohemorrhagic lesions when injected into dermal connective tissue, can also cause thromboses in large veins if they are injected into their vicinity. These thrombi may lead to embolization of the main pulmonary artery. Apparently, activation of essentially similar pathogenic mechanisms can cause local or general thrombohemorrhagic phenomena, owing to microcirculatory derangements in certain regions, as well as thrombosis of large vessels. A simple technic is described for the production of red or white infarcts of the skin by the application of special clips producing, respectively, partial or complete obstruction of its vessels. This procedure furnished additional data in support of the comparative nonspecificity of the challenger in the causation of pluricausal lesions. Short-time complete obstruction of the circulation in a limited skin area causes only transient edema in otherwise untreated rats but thrombohemorrhagic lesions or calcification in animals sensitized with a THP-conditioner or a calcergic conditioner, respectively.