The treatment of cardiovascular collapse and anaphylactic shock is largely empiric. A simple animal model was developed to evaluate the hemodynamic alterations in anaphylaxis. Eight adult New Zealand white rabbits of both sexes were studied. All animals weighed 3.8 kg to 5.3 kg. Sensitization was accomplished w~th a 2-mL subcutaneous dose of horse serum followed in two days with a 2-mL intravenous (IV) dose. At least 14 days elapsed after the IV dose before a 1-mL challenge close of horse serum was given. On the day of the challenge dose, a femoral arterial catheter, arterial temperature probe, and right atrial catheter were placed under methoxyflurane anesthesia. The temperature probe was positioned in the aortic arch. The methoxyflurane was discontinued and the only sedation given during the shock phase was IV diazepam (0.i mg/kg to 0.5 mg/kg). At least 30 minutes after methoxyflurane was discontinued, the challenge dose of horse serum was given through the right atrial catheter. Before and during the shock phase cardiac rhythm, arterial pressure, and intravascuIar temperature were monitored continuously. Cardiac outputs (CO) were performed by a thermodilution technique using 0.8 mL room temperature saline mjectate through the right atrial catheter. Temperature deflection of the aortic probe was recorded and cardiac output was calculated. After giving the challenge dose, CO was measured at three, five, ten, 15, 25, 35, 45, and 60 minutes. All eight animals showed a significant (P < .0005) fall in CO, cardiac index, and blood pressure within three minutes. The fall in cardiac index was 50% or more in all animals. TWo animals died as a result of shock. The other six animals showed spontaneous recovery toward baseline values of CO, cardiac index, and blood pressure by 60 minutes. This model is reproducible and relatively inexpensive, yet it affords good hemodynamic parameters with which one can evaluate new treatment procedures in anaphylactic shock.