AN INHIBITOR OF POLY(ADENOSINE 5'-DIPHOSPHORIBOSE) SYNTHETASE, 3-AMINOBENZAMIDE, DOES NOT IMPROVE CARDIOVASCULAR DEPRESSION, BRONCHOSPASM, OR SURVIVAL ASSOCIATED WITH SYSTEMIC-ANAPHYLAXIS IN RABBITS IN-VIVO

We investigated whether an inhibitor of poly(adenosine 5'-diphosphorib ose) synthetase (PARS) is beneficial in anaphylaxis. Twenty-eight rabb its were randomly allocated to three groups: Group I (control) receive d .9% NaCl solution 10 min before antigen challenge followed by the in fusion of the same solution. Group II (3-aminobenzamide 20 mg.kg(-1)) received 20 mg.kg(-1) of 3-aminobenzamide (a PARS inhibitor) 10 min be fore antigen challenge followed by the continuous infusion of 20 mg.kg (-1) of 3-amino-benzamide. Group III received 40 mg.kg(-1) 10 min befo re antigen challenge followed by the continuous infusion of 20 mg.kg(- 1) of 3-aminobenzamide. Survival were similar between three groups. He art rate, mean arterial pressure (MAP), central venous pressure, and p ulmonary resistance did not differ between three groups. Dynamic pulmo nary compliance did not differ in the early phase after the antigen ch allenge; however, it was significantly lower in Group III than in Grou ps I and II 15 min after the initiation of anaphylaxis. 3-aminobenzami de per se did not affect heart rate, MAP, central venous pressure, pul monary resistance, or dynamic pulmonary compliance in animals without systemic anaphylaxis. In conclusion, this PARS inhibitor did not impro ve cardiovascular depression or bronchospasm in the early phase of sys temic aggregated anaphylaxis in rabbits in vivo, implying that the pat hophysiological changes associated with systemic anaphylaxis may not b e related to activation of an energy-consuming DNA repair cycle trigge d by PARS.