Anaphylatoxin-induced shock and two patterns of anaphylactic shock: Hemodynamics and mediators*

Abstract

In the dog, different cardiorespiratory reactions were identified in 2 types of anaphylactic shock and in C5a[fragment a of complement component 5]-AT (anaphylatoxin)-induced shock. All 3 types had in common a portal blood pooling with a consequent decrease in the venous return, cardiac output and arterial pressure. In anaphylaxis (A) of the 1st type, at a low titer of hemagglutinating antibodies, the latent period was 68 s and heart and lung function was unchanged. In the 2nd type, at high titer, the latency was 19 s and pulmonary hypertension and decreased heart contractility occurred. After AT injection pulmonary hypertension appeared with tachypnea and unchanged heart function. Tachyphylaxis, but not cross-over tachyphylaxis against the anaphylactic agent and AT was observed in dogs and isolated guinea pig lungs. AT induced a transient release and A produced a prolonged release of histamine, prostaglandins (PG), and thromboxane A2 and endoperoxides from guinea pig lungs. SRS-A [slow reacting substance of A] was released only in A. Indomethacin inhibited AT-induced release of PG in guinea pig lungs and AT-induced hypotension in the dog, although it did not prevent the drop in cardiac output. These model studies suggest that different patterns of clinical A can occur, depending on the type of antibodies and/or mediators involved.