Increased airway resistance due to surfactant dysfunction can be alleviated with aerosol surfactant

被引:12
作者
Enhorning, G
Yarussi, A
Rao, P
Vargas, I
机构
[1] SUNY BUFFALO,DEPT OBSTET GYNECOL,BUFFALO,NY 14214
[2] SUNY BUFFALO,DEPT ANESTHESIOL,BUFFALO,NY 14214
关键词
pulmonary surfactant; aerosol surfactant; airway resistance; asthma;
D O I
10.1139/cjpp-74-6-687
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
To investigate the contribution of pulmonary surfactant to a low airflow resistance through narrow conducting airways, a system was developed with which it was possible to determine the resistance meeting a steady flow of air at 0.5 mL/min. The airflow, delivered by an infusion pump, entered the extreme periphery of a conducting airway in an excised rat lung and exited through the trachea. The resistance was determined by measuring the pressure of the air entering the lung. If the airway remained open, the pressure was only slightly above zero; when a blocking liquid column formed in the lumen of the airway, the pressure increased rapidly but dropped abruptly as the liquid was pushed away into a wider airway section. When endogenous pulmonary surfactant was removed with a saline lavage, the airway was blocked almost constantly by an endless re-formation of liquid columns. Consequently, during a 4-min period of pressure recording, free airflow was observed only rarely. However, administration of aerosol surfactant increased the duration of free airflow in relation to the volume administered. After an injection of 80 mL of aerosol surfactant, the airway stayed open 89 +/- 3% of the 4-min recording time compared with only 28 +/- 5% when the same volume of air (80 mL) without surfactant had passed through the airway (p < 0.0001). We conclude that surfactant contributes to a free airflow through conducting airways and may have an important role in the maintenance of low airway resistance.
引用
收藏
页码:687 / 691
页数:5
相关论文
共 23 条
[1]   INDIRECT EVIDENCE OF BRONCHIAL INFLAMMATION ASSESSED BY TITRATION OF INFLAMMATORY MEDIATORS IN BAL FLUID OF PATIENTS WITH ASTHMA [J].
BOUSQUET, J ;
CHANEZ, P ;
LACOSTE, JY ;
ENANDER, I ;
VENGE, P ;
PETERSON, C ;
AHLSTEDT, S ;
MICHEL, FB ;
GODARD, P .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1991, 88 (04) :649-660
[2]   MECHANISMS OF PERSISTENT AIRWAY INFLAMMATION IN ASTHMA - A ROLE FOR T-CELLS AND T-CELL PRODUCTS [J].
BUSSE, WW ;
COFFMAN, RL ;
GELFAND, EW ;
KAY, AB ;
ROSENWASSER, LJ .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1995, 152 (01) :388-393
[3]   ROLE OF INFLAMMATION IN THE HYPERREACTIVITY OF THE AIRWAYS IN ASTHMA [J].
CHUNG, KF .
THORAX, 1986, 41 (09) :657-662
[4]  
CLEMENTS JA, 1957, P SOC EXP BIOL MED, V95, P170
[5]   DEVELOPMENT OF A PROLONGED EOSINOPHIL-RICH INFLAMMATORY LEUKOCYTE INFILTRATION IN THE GUINEA-PIG ASTHMATIC RESPONSE TO OVALBUMIN INHALATION [J].
DUNN, CJ ;
ELLIOTT, GA ;
OOSTVEEN, JA ;
RICHARDS, IM .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1988, 137 (03) :541-547
[6]   PULMONARY SURFACTANT MAINTAINS PATENCY OF CONDUCTING AIRWAYS IN THE RAT [J].
ENHORNING, G ;
DUFFY, LC ;
WELLIVER, RC .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1995, 151 (02) :554-556
[7]   DISRUPTION OF PULMONARY SURFACTANTS ABILITY TO MAINTAIN OPENNESS OF A NARROW TUBE [J].
ENHORNING, G ;
HOLM, BA .
JOURNAL OF APPLIED PHYSIOLOGY, 1993, 74 (06) :2922-2927
[8]   INFLAMMATORY MEDIATORS INVOLVED IN ANTIGEN-INDUCED AIRWAY MICROVASCULAR LEAKAGE IN GUINEA-PIGS [J].
EVANS, TW ;
ROGERS, DF ;
AURSUDKIJ, B ;
CHUNG, KF ;
BARNES, PJ .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1988, 138 (02) :395-399
[9]   ARTIFICIAL PULMONARY SURFACTANT INHIBITED BY PROTEINS [J].
FUCHIMUKAI, T ;
FUJIWARA, T ;
TAKAHASHI, A ;
ENHORNING, G .
JOURNAL OF APPLIED PHYSIOLOGY, 1987, 62 (02) :429-437
[10]   SURFACE-PROPERTY CHANGES FROM INTERACTIONS OF ALBUMIN WITH NATURAL LUNG SURFACTANT AND EXTRACTED LUNG LIPIDS [J].
HOLM, BA ;
NOTTER, RH ;
FINKELSTEIN, JN .
CHEMISTRY AND PHYSICS OF LIPIDS, 1985, 38 (03) :287-298