E C Lasser1. 1. University of California, La Jolla, CA 92093-0632, USA. elasser@ucsd.edu
Abstract
BACKGROUND: X-ray contrast media (CM) toxicity resembles IgE-antigen-based anaphylaxis, and CM-related histamine release has been demonstrated in vitro and in vivo. While nobody has succeeded in producing antibodies against injections of neat CM, the ability of CM to compete with a series of antigens against their respective antibodies has recently been demonstrated. However, there is a paradox, since the CM with the strongest antibody binding are nevertheless the least likely to provoke antigen-antibody-related mast cell/basophil release. METHODS: Two strains of rats were subjected to (a) passive cutaneous anaphylaxis (PCA) studies in the presence of various concentrations of CM, (b) blood pressure (BP) tracings following bolus administrations of various prototypical CM and (c) BP tracings in ovalbumin (OVA)-sensitized rats, challenged with OVA plus CM, vs. OVA plus CM-equivalent saline. RESULTS: In the PCA studies, and the OVA challenge studies, the CM appear to act in an antigen excess mode, limiting the potential of the OVA to elicit anaphylactic changes, as demonstrated by permeability studies or by BP levels. The bolus CM studies demonstrate that the more potent CM 'antigens' actually produce an increase in BP and the less potent CM 'antigens', a drop in BP. These changes can be related to the CM acting in an 'antigen' excess mode vs. an 'antigen' equivalent mode. CONCLUSIONS: The CM have the potential to act in an 'antigen' excess or 'antigen'-equivalent mode. The potential to express an 'antigen'-excess mode in vivo, may be unique to CM because of the high concentrations injected. Copyright 2000 S. Karger AG, Basel
BACKGROUND: X-ray contrast media (CM) toxicity resembles IgE-antigen-based anaphylaxis, and CM-related histamine release has been demonstrated in vitro and in vivo. While nobody has succeeded in producing antibodies against injections of neat CM, the ability of CM to compete with a series of antigens against their respective antibodies has recently been demonstrated. However, there is a paradox, since the CM with the strongest antibody binding are nevertheless the least likely to provoke antigen-antibody-related mast cell/basophil release. METHODS: Two strains of rats were subjected to (a) passive cutaneous anaphylaxis (PCA) studies in the presence of various concentrations of CM, (b) blood pressure (BP) tracings following bolus administrations of various prototypical CM and (c) BP tracings in ovalbumin (OVA)-sensitized rats, challenged with OVA plus CM, vs. OVA plus CM-equivalent saline. RESULTS: In the PCA studies, and the OVA challenge studies, the CM appear to act in an antigen excess mode, limiting the potential of the OVA to elicit anaphylactic changes, as demonstrated by permeability studies or by BP levels. The bolus CM studies demonstrate that the more potent CM 'antigens' actually produce an increase in BP and the less potent CM 'antigens', a drop in BP. These changes can be related to the CM acting in an 'antigen' excess mode vs. an 'antigen' equivalent mode. CONCLUSIONS: The CM have the potential to act in an 'antigen' excess or 'antigen'-equivalent mode. The potential to express an 'antigen'-excess mode in vivo, may be unique to CM because of the high concentrations injected. Copyright 2000 S. Karger AG, Basel