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异丙肾上腺素预防犬类过敏反应

Prevention of canine anaphylaxis with isoproterenol.

作者信息

Silverman H J, Taylor W R, Smith P L, Kagey-Sobotka A, Lichtenstein L M, Bleecker E R

出版信息

Am Rev Respir Dis. 1986 Aug;134(2):243-7. doi: 10.1164/arrd.1986.134.2.243.

DOI:10.1164/arrd.1986.134.2.243
PMID:3017167
Abstract

Sympathomimetic agents are used to reverse the cardiovascular and respiratory abnormalities that are associated with anaphylactic shock. In addition, in vitro studies have demonstrated that beta-adrenergic stimulation modulates IgE-mediated release of chemical mediators. To separately evaluate the ability of isoproterenol, a beta-adrenergic agonist, to prevent mediator release and anaphylactic shock, as well as to reverse the cardiopulmonary manifestations of systemic anaphylaxis, we administered a continuous infusion of isoproterenol before and during canine anaphylactic shock. An intravenous injection of Ascaris suum antigen was used to produce shock, which was characterized by a 50 +/- 15% (mean +/- SEM) decrease in mean arterial blood pressure, a 30 +/- 8% decrease in cardiac output, and a 122 +/- 95% increase in total pulmonary resistance. These changes were associated with significant increases in plasma histamine concentrations from 1.1 +/- 0.1 to 158.4 +/- 137 ng/ml. Administration of a continuous infusion of isoproterenol during anaphylactic shock did not significantly improve any of these physiologic abnormalities. However, when isoproterenol was administered prior to the injection of antigen, these physiologic changes were prevented and histamine release was inhibited in a significant proportion of animals. In contrast, beta-adrenergic stimulation did not prevent nonimmunologic shock and mediator release induced with compound 48/80. We conclude that the administration of a beta-adrenergic agonist prevented the cardiopulmonary manifestations of anaphylactic shock by inhibiting mediator release and that the physiologic effects of isoproterenol administered during systemic anaphylaxis were minimal.

摘要

拟交感神经药用于逆转与过敏性休克相关的心血管和呼吸异常。此外,体外研究表明,β-肾上腺素能刺激可调节IgE介导的化学介质释放。为了分别评估β-肾上腺素能激动剂异丙肾上腺素预防介质释放和过敏性休克的能力,以及逆转全身性过敏反应的心肺表现,我们在犬过敏性休克之前和期间持续输注异丙肾上腺素。静脉注射猪蛔虫抗原以引发休克,其特征为平均动脉血压下降50±15%(平均值±标准误),心输出量下降30±8%,总肺阻力增加122±95%。这些变化与血浆组胺浓度从1.1±0.1显著增加至158.4±137 ng/ml相关。在过敏性休克期间持续输注异丙肾上腺素并未显著改善这些生理异常中的任何一项。然而,当在注射抗原之前给予异丙肾上腺素时,这些生理变化得到预防,并且在相当比例的动物中组胺释放受到抑制。相比之下,β-肾上腺素能刺激并不能预防由化合物48/80诱导的非免疫性休克和介质释放。我们得出结论,给予β-肾上腺素能激动剂通过抑制介质释放预防了过敏性休克的心肺表现,并且在全身性过敏反应期间给予异丙肾上腺素的生理效应极小。

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