| Research Abstract |
1.We assessed LV diastolic and systolic function in IgE-mediated anaphylaxis in dogs. LV diastolic funciton, i.e., isovolumic relaxation, is little impaired in anaphylaxis, and LV systolic function is relatively well preserved during the carly stage following the onset of anaphylaxis.
2.To verify production of nitric oxide (NO) in anaphylaxis, we measured NO in peripheral tissue in anaphylactic rabbits using an NO-sensitive electrode, which was placed between the superficial abdominal fascia and the rectus abdominis fascia. NO production can be detected in anaphylactic rabbits.
3.We investigated whether a No synthase (NOS) inhibitor improves cardiovascular depression associated with anaphylaxis. After induction of anaphylactic circulatory depression, one group received an NOS inhibitor (Group I,n=6), and the other received saline solution (Group II,n=5). Mean arterial pressure and right atrial pressure were significantly higher in Group I than in Group II.Hematocrit was significantly lower in Group I than in Group II.Cardiac output did not differ between the groups. In conclusion, NOS inhibitor attenuates hypotension, but does not improve cardiac depression in anaphylaxis in dogs.
4.Animals pretreated with L-NAME showed lower survival rates than control animals pretreated with normal saline. The survival rate in L-NAME-pretreated animals was increased by the administration of L-arginine after initiation of anaphylaxis. Cardiac output fell significantly in animals pretreated with L-NAME compared with controls, although venous return was increased. In animals pretreated with L-NAME,pulmonary resistance was significantly increased, and administration of arginine attenuated the bronchospasm. In conclusion, these results, along with the low survival rates in the L-NAME-treated animals, suggest that NO production may be beneficial to cardiac depression and bronchospasm in anaphylaxis in vivo.
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