Animal models have been use to understand various manifestations of anaphylaxis. Circulatory collapse typically occurs in dogs, rabbits may suffer acute pulmonary hypertension, and guinea pigs may experience acute respiratory obstruction. These reactions are classically mediated by the interaction of IgE, the high-affinity IgE receptor found on mast cells and histamine. However, findings from several rodent studies suggest an alternative pathway involving the Ig receptor, macrophages, platelets and platelet-activating factor may be more important in anaphylaxis than previously realized. Strait and colleagues immunized wild-type, IgE-deficient and mast cell-deficient mice using goat antimouse IgD antibody. This technique induced mastocytosis and a large response to goat antigen (IgG) with increased IgE and IgG production. After fourteen days, they challenged the mice with antigen (goat IgG) or rat antimouse IgE monoclonal antibody (mAb). The severity of anaphylaxis was gauged by changes in body temperature, physical activity, and mortality. Findings in this experimental model included similar anaphylactic responses regardless of anti-IgE, mAb-induced, or goat IgG antigen challenge.