Complement depletion and persistent hemodynamic-hematologic responses in protamine-heparin reactions.
Hypotension, bradycardia, pulmonary artery hypertension, neutropenia, and thrombocytopenia have been suspected to be due to complement activation following protamine reversal of heparin. This investigation examined these phenomena in complement-depleted animals. Eight dogs received intraperitoneal naja n. naja cobra venom factor (CVF), 20 U/kg, 48 and 24 hr prior to anticoagulation with sodium heparin, 150 IU/kg, and reversal 30 min later with protamine sulfate, 1.5 mg/kg. Decomplementation was confirmed in all dogs. Systemic blood pressure (BP), pulse (HR), pulmonary artery systolic and diastolic pressures, (PAS, PAD), cardiac output (CO), platelet count (PTC), and white blood count (WBC) with differential were monitored. The maximal mean changes for the entire group were BP, -43 mm Hg; HR, -16; PAS, +6 mm Hg; PAD, +3 mm Hg; CO, -27%; PTC, -49%; and WBC, -48%. These hemodynamic and hematologic responses, occurring in the face of CVF-induced decomplementation, support the conclusion that complement components C3 and C5-C9 are not influential factors contributing to these protamine-heparin-induced events.