The anaphylactic release of
histamine from perfused, chopped guinea pig lung is very sensitive to changes in the NaCl concentration of the containing medium, and it is ionic strength rather than particle concentration which is critical. Consequently, in studies with inhibitors care must be taken to avoid inadvertently increasing ionic strength and thereby misinterpreting the cause of the inhibition. Since immune
hemolysis exhibits a similar sensitivity to changes in the NaCl concentration of the suspending medium,
salicylaldoxime and
phlorizin, which prevent the participation of the third component of
complement in immune
hemolysis, were investigated for their effect on the
anaphylactic reaction.
Salicylaldoxime is a potent inhibitor of in vitro
anaphylaxis in guinea pig lung, but
phlorizin is only a weak inhibitor.
Potassium cyanide, 1 mM, inhibits the anaphylactic release of
histamine most effectively if the duration of contact between the tissue and the
cyanide prior to
antigen addition is minimal; preincubation of the tissue with
cyanide prior to
antigen addition results in progressive diminution of inhibition even when there is only minimal loss of
cyanide from the containing medium. The anaphylactic release of
histamine from perfused whole lungs or
suspensions of blood-free chopped lung is not prevented by the
cytochrome oxidase inhibitor,
carbon monoxide. In addition, 2-heptyl 4 hydroxyquinoline N
oxide and
malonic acid, which inhibit aerobic metabolism at different sites, do not prevent the reaction. These studies and those with
cyanide indicate that the anaphylactic release of
histamine in guinea pig lung is not dependent on
cytochrome-mediated aerobic metabolism.