Lohman I C, Halonen M
Respiratory Sciences Center, College of Medicine, University of Arizona Health Science Center, Tucson 85724.
Am Rev Respir Dis. 1993 May;147(5):1223-8. doi: 10.1164/ajrccm/147.5.1223.
Of the mediators released during IgE-induced allergic reactions, it is not known which have the greatest physiologic import in systemic anaphylactic responses. This study describes the effects of histamine and platelet-activating factor (PAF) antagonism (combined) on IgE-induced systemic anaphylaxis in the rabbit. Pretreatment with 30 mumol/kg chlorpheniramine and 30 mumol/kg cimetidine with (Ch/Ci/WEB group) or without (Ch/Ci group) 2.2 mumol/kg of the PAF antagonist WEB 2086 inhibited the anaphylactic alterations in right ventricular pressure, total pulmonary resistance, and decrease in dynamic compliance but not systemic hypotension. Lethality was inhibited only in the Ch/Ci/WEB group. Because previous studies had shown WEB 2086 alone could inhibit the increase in pulmonary resistance, specificity studies were done to determine if WEB 2086 affected histamine activity or release. Responses to intravenously administered histamine (0.54 mumol/kg) were unaffected by WEB 2086 (13.1 mumol/kg). Also, WEB 2086 did not inhibit in vitro antigen-induced basophil degranulation. Thus, the decrease in dynamic compliance and pulmonary hypertension in IgE anaphylaxis appear to be mediated primarily by histamine and the increase in pulmonary resistance by histamine and/or PAF, whereas lethality appears to involve PAF. Some alterations, most notably systemic hypotension, likely involve other allergic mediators.
在IgE诱导的过敏反应中释放的介质中,尚不清楚哪些在全身性过敏反应中具有最大的生理重要性。本研究描述了组胺和血小板活化因子(PAF)拮抗作用(联合)对兔IgE诱导的全身性过敏反应的影响。用30 μmol/kg氯苯那敏和30 μmol/kg西咪替丁预处理,同时(Ch/Ci/WEB组)或不(Ch/Ci组)使用2.2 μmol/kg的PAF拮抗剂WEB 2086,可抑制右心室压力、总肺阻力的过敏改变以及动态顺应性的降低,但不能抑制全身性低血压。仅在Ch/Ci/WEB组中致死率受到抑制。由于先前的研究表明单独使用WEB 2086可抑制肺阻力的增加,因此进行了特异性研究以确定WEB 2086是否影响组胺活性或释放。静脉注射组胺(0.54 μmol/kg)的反应不受WEB 2086(13.1 μmol/kg)的影响。此外,WEB 2086不抑制体外抗原诱导的嗜碱性粒细胞脱颗粒。因此,IgE过敏反应中动态顺应性的降低和肺动脉高压似乎主要由组胺介导,肺阻力的增加由组胺和/或PAF介导,而致死率似乎涉及PAF。一些改变,最明显的是全身性低血压,可能涉及其他过敏介质。