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聚(腺苷5'-二磷酸核糖)合成酶抑制剂3-氨基苯甲酰胺并不能改善兔体内与全身性过敏反应相关的心血管抑制、支气管痉挛或生存率。

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.

作者信息

Takeuchi H, Mitsuhata H, Saitoh J, Hasome N, Shimizu R

机构信息

Department of Anesthesiology, Jichi Medical School, Tochigi, Japan.

出版信息

Shock. 1997 Aug;8(2):147-52. doi: 10.1097/00024382-199708000-00016.

Abstract

We investigated whether an inhibitor of poly(adenosine 5'-diphosphoribose) synthetase (PARS) is beneficial in anaphylaxis. Twenty-eight rabbits were randomly allocated to three groups: Group I (control) received .9% NaCl solution 10 min before antigen challenge followed by the infusion 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 before antigen challenge followed by the continuous infusion of 20 mg.kg-1 of 3-aminobenzamide. Group III received 40 mg.kg-1 10 min before antigen challenge followed by the continuous infusion of 20 mg.kg-1 of 3-aminobenzamide. Survival were similar between three groups. Heart rate, mean arterial pressure (MAP), central various pressure, and pulmonary resistance did not differ between three groups. Dynamic pulmonary compliance did not differ in the early phase after the antigen challenge; however, it was significantly lower in Group III than in Groups I and II 15 min after the initiation of anaphylaxis. 3-aminobenzamide per se did not affect heart rate, MAP, central venous pressure, pulmonary resistance, or dynamic pulmonary compliance in animals without systemic anaphylaxis. In conclusion, this PARS inhibitor did not improve cardiovascular depression or bronchospasm in the early phase of systemic aggregated anaphylaxis in rabbits in vivo, implying that the pathophysiological changes associated with systemic anaphylaxis may not be related to activation of an energy-consuming DNA repair cycle triggered by PARS.

摘要

我们研究了聚(腺苷5'-二磷酸核糖)合成酶(PARS)抑制剂在过敏反应中是否有益。28只兔子被随机分为三组:第一组(对照组)在抗原攻击前10分钟接受0.9%氯化钠溶液,随后输注相同溶液。第二组(3-氨基苯甲酰胺20mg·kg-1)在抗原攻击前10分钟接受20mg·kg-1的3-氨基苯甲酰胺(一种PARS抑制剂),随后持续输注20mg·kg-1的3-氨基苯甲酰胺。第三组在抗原攻击前10分钟接受40mg·kg-1,随后持续输注20mg·kg-1的3-氨基苯甲酰胺。三组的存活率相似。三组之间的心率、平均动脉压(MAP)、中心静脉压和肺阻力没有差异。抗原攻击后的早期,动态肺顺应性没有差异;然而,在过敏反应开始15分钟后,第三组的动态肺顺应性显著低于第一组和第二组。在没有全身性过敏反应的动物中,3-氨基苯甲酰胺本身不影响心率、MAP、中心静脉压、肺阻力或动态肺顺应性。总之,这种PARS抑制剂在兔体内全身性聚集性过敏反应的早期并没有改善心血管抑制或支气管痉挛,这意味着与全身性过敏反应相关的病理生理变化可能与PARS触发的耗能DNA修复循环的激活无关。

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