Anderson M W, deShazo R D
Department of Medicine, Tulane University School of Medicine, New Orleans, La.
J Allergy Clin Immunol. 1990 May;85(5):856-8. doi: 10.1016/0091-6749(90)90068-f.
To understand better the mechanism of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema, we studied the effects of ACE-inhibitor treatment on wheal-and-flare responses to histamine, codeine, and bradykinin in 10 normal subjects. No change in the size of wheal-and-flare reactions to histamine occurred, but the size of wheal reactions to codeine and bradykinin increased in all study subjects after ingesting the ACE inhibitor, captopril. Five of 10 study subjects developed flushing reactions after ACE-inhibitor treatment. We conclude that inhibition of bradykinin metabolism by ACE inhibitors is the probable cause of ACE inhibitor-related angioedema and that substance P is not the predominant mediator in this process.
为了更好地理解血管紧张素转换酶（ACE）抑制剂相关性血管性水肿的机制，我们研究了ACE抑制剂治疗对10名正常受试者的风团和潮红反应（针对组胺、可待因和缓激肽）的影响。对组胺的风团和潮红反应大小没有变化，但在摄入ACE抑制剂卡托普利后，所有研究对象对可待因和缓激肽的风团反应大小均增加。10名研究对象中有5名在ACE抑制剂治疗后出现了潮红反应。我们得出结论，ACE抑制剂对缓激肽代谢的抑制作用可能是ACE抑制剂相关性血管性水肿的原因，且P物质不是该过程中的主要介质。
