Role of Histamine in Producing the Eosinophilia of Magnesium Deficiency.

The acute phase of the magnesium deficient syndrome is characterized by a dermal hyperemia(6) in rats and dermal mast cells degranulate in this phase(3). The blood eosinophilia which occurs in the acute phase of magnesium deficiency (Table I, Group 8) is highly significant (P = < .01) and may be caused by the endogenous release of mast cell secretory products. However, administration of commercial histamine, (Table I, Groups 1, 2, 3) in a variety of doses, routes and time intervals (some not reported here) failed to duplicate the eosinophilia produced by magnesium deficiency. Administration of 48/80 in gradually increasing doses for 3 days produced a significant (P = < .01) eosinophilia (Table I, Group 11) of comparable magnitude to that produced by dietary magnesium deficiency. One large dose of 48/80 (Table I, Group 10) proved fatal to 50% of the animals. Since 48/80 is supposed to be a fairly specific mast cell degranulating agent (7), one would assume that a mast cell product or products were responsible for the blood eosinophilia. Administration of heparin in combination with histamine also failed to significantly elevate the number of circulating eosinophils (Table I, Groups 4, 5). Curiously, the large dose of heparin administered with histamine (Table I, Group 4) killed 50% of the rats. Massive subcutaneous edema was observed and tail vein blood appeared watery and pale pink. This reaction was less apparent when the smaller dose of heparin was administered. Serotonin administered with histamine was without effect on circulating eosinophils. An antihistamine, pyribenzamine, when administered daily to rats while on the magnesium deficient regimen (Table I, Group 9) prevented the eosinophilia which should have occurred at this time (P = < .01 when compared with Group 8).