Diapedesis

DIAPEDESIS (from Greek dia- through and pēdāo- I jump), the passage of formed elements of blood—red and white corpuscles—through the vessel wall into the surrounding tissue. The term emigration is more commonly used specifically to denote the process of leukocytes passing through the vessel wall, for example during inflammation, in order to emphasize the active nature of the phenomenon—the exit of white corpuscles by means of pseudopodia, as opposed to the passive extrusion of formed elements in diapedesis. The diapedesis of erythrocytes forms the basis of hemorrhages per diapedesin, and therefore has the same etiology and pathogenesis. 1. First of all, purely mechanical factors, such as venous congestion, can cause diapedesis. This phenomenon can be easily observed ad oculos in bilateral ligation of the frog's tongue veins. Under such conditions, it is not difficult to notice after some time what appears to be a button-like protrusion on the outer wall of the vessel—an extruded erythrocyte, the beginning of diapedesis. In these cases, the latter is caused by increased permeability of the vessel wall depending on the divergence of endothelial cells of the wall, as a result of which stomata are formed, or according to some authors, merely greatly dilated pre-existing ones. Abundant diapedesis of congestive origin is observed in the lungs in stenosis of the mitral valve, in the skin and internal organs—in asphyxia, etc. 2. Toxic factors can also make the vessel wall more porous, sometimes apparently by relaxation of the latter, but mainly probably by changing the cementing substance (Kittsubstanz) between endothelial cells. This type of diapedesis can occur in intoxications of both exogenous origin (arsenic, phosphorus, carbon monoxide, Berthollet's salt, putrefactive poison) and endogenous origin on the basis of metabolic disorders (certain forms of jaundice, uremia, Bright's disease). Toxic factors of exogenous nature also include infectious diapedesis of erythrocytes in a number of diseases (smallpox, plague, typhus, septicemia, croupous pneumonia, so-called hemorrhagic septicemias in animals), although in these cases, along with diapedesis, ruptures of small vessels on the basis of bacterial occlusion are also observed. - Inflammatory diapedesis, reaching its highest degree in hemorrhagic inflammation, has a mixed origin—mechanical-toxic. Diapedesis also occurs in hemorrhagic infarct depending on the disturbance of nutrition of vessel walls in the area supplied by the occluded artery. In hemorrhagic diatheses, the matter is mainly about ruptures of vessels, but diapedesis also occurs on the basis of both the thinness of vessel walls, probably congenital, and disturbance of their nutrition. 3. Neurogenic causes of diapedesis include: diapedesis in hysterical patients depending on emotional disturbances or reflex irritations (various sudden hemorrhages: blood spots on the hands, admixture of blood to sweat, etc.). The mechanism of this type of diapedesis has not yet been precisely clarified; it must be assumed that here too it is preceded by sharp vasodilation; in any case, the connection of certain hemorrhages (e.g., into the gastric mucosa, duodenum—with subsequent development of erosions) with damage to the vegetative centers (corpus striatum, thalamus opticus, etc.) has been experimentally established. To non-neurogenic, or hormononeural hemorrhages per diapedesin also belong menstrual, ovarian hemorrhages (into the corpus luteum), as well as many meno- and metrorrhagias, vicarious hemorrhages (e.g., from the nose) in amenorrhea, etc. There are indications that in apoplexies of various organs, particularly the brain, neurogenic diapedesis is of greatest importance. It should be emphasized that modern authors attribute greater importance to the neurogenic factor in diapedesis than was done earlier. - The volume of hemorrhages in diapedesis can reach very large dimensions, just as its rate can be extremely accelerated; both together sometimes give a picture of acute and even fatal hemorrhage per diapedesin. On diapedesis (emigration) of leukocytes in inflammation—see Inflammation.