权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Clarification of pathophysiologic machanisms of anaphylactic shock and its treatment

过敏性休克病理生理机制的阐明及其治疗

基本信息

批准号：
05454426
负责人：
MITSUHATA Hiromasa
金额：
$ 4.03万
依托单位：
Jichi Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1995
项目状态：
已结题

项目摘要

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.

1.采用IgE介导的过敏反应模型，观察了犬左室舒张和收缩功能。LV舒张功能，即，为证实过敏反应中一氧化氮（NO）的产生，我们用一氧化氮敏感电极测定了过敏家兔外周组织中NO的含量，该电极置于腹部浅筋膜和腹直肌筋膜之间。在过敏性家兔中可检测到NO的产生。3.我们研究了一氧化氮合酶（NOS）抑制剂是否改善过敏性反应相关的心血管抑制。诱导过敏性循环抑制后，一组接受NOS抑制剂（组I，n=6），另一组接受生理盐水（组II，n=5）。平均动脉压和右心房压力显着高于组I比组II。红细胞压积显着低于组I比组II。心输出量没有组间差异。结论：一氧化氮合酶抑制剂可减轻过敏性休克时犬的低血压，但不能改善心脏抑制。4.与生理盐水对照组相比，L-NAME预处理组动物的存活率较低。在L-NAME预处理的动物中，在过敏反应开始后给予L-精氨酸可增加存活率。与对照组相比，用L-NAME预处理的动物的心输出量显著下降，尽管静脉回流增加。在预先用L-NAME处理的动物中，肺阻力显著增加，并且施用精氨酸减轻了支气管痉挛。总之，这些结果，沿着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。