ALPHA-ADRENERGIC HYPER-RESPONSIVENESS IN ASTHMA - ANALYSIS OF VASCULAR AND PUPILLARY RESPONSES

被引:174
作者
HENDERSON, WR
SHELHAMER, JH
REINGOLD, DB
SMITH, LJ
EVANS, R
KALINER, M
机构
[1] NIAID,CLIN INVEST LAB,BLDG 10,ROOM 11N-250,BETHESDA,MD 20014
[2] NEI,EYE MOVEMENT LAB,BETHESDA,MD 20014
[3] WALTER REED ARMY MED CTR,DEPT ALLERGY & IMMUNOL,WASHINGTON,DC 20012
关键词
D O I
10.1056/NEJM197903223001203
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Because alpha-adrenergic stimulation causes bronchoconstriction, the alpha-adrenergic responsiveness of 21 subjects with allergic asthma was compared with that of 16 subjects with allergic rhinitis and 38 normal control subjects. None of the patients had taken medications for at least 30 days before study. Alpha-adrenergic responsiveness was measured by the capacity of phenylephrine to constrict the cutaneous vascular bed and to dilate the pupillary sphincter muscle. Asthmatic subjects required 4.0±0.6 ng to reduce their cutaneous blood flow by 50 per cent, whereas normal controls required 32.0±7.5 ng (P<0.005) and subjects with allergic rhinitis required 23.7±9.4 ng (P<0.02). The pupils of asthmatic subjects dilated by >0.5 mm in response to 1.8±0.14 per cent phenylephrine, patients with allergic rhinitis required 2.4±0.16 (P<0.01), and normal controls needed 2.7±0.07 (P<0.00001). Therefore, the patients with allergic asthma had significantly enhanced alpha-adrenergic responses when compared both to normal subjects and patients with allergic rhinitis; the possibility that increased alpha-adrenergic activity contributes to the asthmatic diathesis warrants further exploration. (N Engl J Med 300:642–647, 1979) BRONCHIAL asthma is a complex of symptoms characterized by paroxysmal wheezing and dyspnea due to bronchial obstruction resulting from bronchospasm, excessive mucoid sputum production and mucosal edema.1 Allergic asthma may be initiated by contact between inhaled antigens and IgE-sensitized pulmonary mast cells, resulting in the non-cytotoxic release of biologically active mediators of anaphylaxis.1,2 It is the interaction of these mediators with various lung cells that causes the airway obstruction. In vitro examination of the immunologic release of mediators from human lung tissue has demonstrated that neurohormones are capable of modulating the secretory reaction: beta-adrenergic agonists suppress mediator release,3 whereas alpha-adrenergic. © 1979, Massachusetts Medical Society. All rights reserved.
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页码:642 / 647
页数:6
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