Clarification of pathophysiologic machanisms of anaphylactic shock and its treatment

1.我们评估了ige介导的狗过敏反应中的左室舒张和收缩功能。在过敏反应中，左室舒张功能，即等容舒张，几乎没有受损，在过敏发生后的早期，左室收缩功能相对保存良好。为了验证过敏反应中一氧化氮（NO）的产生，我们使用一氧化氮敏感电极测量了过敏兔外周组织中的一氧化氮，该电极放置在腹浅筋膜和腹直肌筋膜之间。过敏家兔体内可检测到NO的产生。我们研究了No合成酶（NOS）抑制剂是否能改善与过敏反应相关的心血管抑郁。诱导过敏性循环抑制后，一组给予NOS抑制剂（I组，n=6），另一组给予生理盐水（II组，n=5）。平均动脉压和右心房压均明显高于对照组。I组红细胞压积明显低于II组。两组之间的心输出量没有差异。综上所述，NOS抑制剂可减轻狗过敏反应时的低血压，但不能改善心脏抑制。L-NAME预处理的动物存活率低于生理盐水预处理的对照组动物。l - name预处理动物在过敏反应开始后给予l -精氨酸可提高其存活率。与对照组相比，经L-NAME预处理的动物心输出量显著下降，但静脉回流增加。在经L-NAME预处理的动物中，肺阻力明显增加，精氨酸的使用减轻了支气管痉挛。总之，这些结果，加上l - name治疗动物的低存活率，表明NO的产生可能有利于体内过敏反应中的心脏抑制和支气管痉挛。

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.