Abstract
It is well known that in inflammatory areas the hydrogen ion concentration is frequently increased. 1 According to Abramson, 2 , 5 the chemical changes in tissues incidental to injury would give rise to differences in electric potential sufficient to account for emigration of leucocytes. Migration in such an electric field might be due in part to electrophoresis, in part to amoeboid movement of which the direction was determined by the electric field. 4
The present report is concerned only with the latter manner of progression, amoeboid movement in an electric field, a phenomenon that has been termed, somewhat loosely, galvanotaxis. It seemed of some interest to those of us who are concerned with the general pathology of inflammation and especially with the mechanism of chemotropism to learn whether the amoeboid motion of leucocytes can in fact be directed by an electric current, and, if so, toward which pole the cells move.
Only two papers on galvanotaxis of leucocytes have been found in the literature. Mendelssohn 5 reported that the cells moved toward the cathode, Feringa, 6 that they went toward the anode.∗ The latter of these brief reports does not make it clear whether the author was actually observing the effect of galvanotaxis or electrophoresis. Yet the distinction is important for the present discussion. In electrophoresis the cell is passively transported by electric forces through the liquid or jelly 3 in which it is suspended. In galvanotaxis the cell is actively crawling on a solid support (a glass slide); the electric current merely determines the direction in which it crawls.
Another distinction may be drawn. In electrophoresis the mobility or bodily movement is proportional to the applied electric potential, whereas in galvanotaxis, no effect is evident for small potentials, the effect being easily observed only when the current density exceeds a minimal value.
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