Effects of the β2-Adrenoceptor-Stimulating Agent Terbutaline and Its Antagonist ICI 118.551 on Rat Lung Surfactant (Phospholipid) Metabolism

1988 ◽  
pp. 369-372
Author(s):  
W. Bernhard ◽  
B. Müller ◽  
P. von Wichert
1973 ◽  
Vol 14 (2) ◽  
pp. 145-151
Author(s):  
William J. Longmore ◽  
Carolyn M. Niethe ◽  
Deborah J. Sprinkle ◽  
Rodolfo I. Godinez

1975 ◽  
Vol 229 (5) ◽  
pp. 1316-1320 ◽  
Author(s):  
M Wagner ◽  
HO Heinemann

Prefeeding of alcohol shows the in vivo incorporation of orally administered palmitic acid into phosphatidylcholine of the lung. This impairment is also demonstrable in vitro utilizing lung slices and 14C-labeled palmitate or cytidine 5'-diphosphocholine as precursors. It is concluded that alcohol ingestion affects the utilization of precursors needed for phospholipid formation in the lung.


1997 ◽  
Vol 82 (6) ◽  
pp. 2020-2027 ◽  
Author(s):  
Sergey M. Ksenzenko ◽  
Scott B. Davidson ◽  
Amer A. Saba ◽  
Alexander P. Franko ◽  
Aml M. Raafat ◽  
...  

Ksenzenko, Sergey M., Scott B. Davidson, Amer A. Saba, Alexander P. Franko, Aml M. Raafat, Lawrence N. Diebel, and Scott A. Dulchavsky. Effect of triiodothyronine augmentation on rat lung surfactant phospholipids during sepsis. J. Appl. Physiol. 82(6): 2020–2027, 1997.—Surfactant functional effectiveness is dependent on phospholipid compositional integrity; sepsis decreases this through an undefined mechanism. Sepsis-induced hypothyroidism is commensurate and may be related. This study examines the effect of 3,3′,5-triiodo-l-thyronine (T3) supplementation on surfactant composition and function during sepsis. Male Sprague-Dawley rats underwent sham laparotomy (Sham) or cecal ligation and puncture (CLP) with or without T3supplementation [CLP/T3 (3 ng/h)]. After 6, 12, or 24 h, surfactant was obtained by lavage. Function was assessed by a pulsating bubble surfactometer and in vivo compliance studies. Sepsis produced a decrease in surfactant phosphatidylglycerol and phosphatidic acid, with an increase in lesser surface-active lipids phosphatidylserine and phosphatidylinositol. Phosphatidylcholine content was not significantly changed. Sepsis caused an alteration in the fatty acid composition and an increase in saturation in most phospholipids. Hormonal replacement attenuated these changes. Lung compliance and surfactant adsorption were reduced by sepsis and maintained by T3treatment. Thyroid hormone may have an active role in lung functional preservation through maintenance of surfactant homeostasis during sepsis.


1984 ◽  
Vol 74 (3) ◽  
pp. 677-684 ◽  
Author(s):  
W D Claypool ◽  
D L Wang ◽  
A Chander ◽  
A B Fisher
Keyword(s):  

1981 ◽  
Vol 51 (4) ◽  
pp. 905-910 ◽  
Author(s):  
J. N. Hildebran ◽  
J. Goerke ◽  
J. A. Clements

Because increased ventilation has been associated with an acceleration of lung surfactant turnover, we investigated the effect of fluid and air inflations on the release of surfactant into the air spaces. We found that excised rat lungs, initially lavaged three times at 23 degrees C, release approximately 40–90 micrograms of phospholipid/g wet lung wt into the air spaces in response to a further infusion of fluid into the airway equal to total lung capacity. A single air inflation to the same volume, followed by degassing and lavage, contributes approximately 230 micrograms to the yield of phospholipid. We estimated basal release of phospholipid as 112 micrograms wet lung wt-1 . h-1, which is far less than the 2,050 micrograms -1 . h-1 retrieved during a series of air and fluid inflations. The above findings are consistent with the hypothesis that air inflation to total lung capacity is a major physiological stimulus to release of lung surfactant into the alveolar space. The lung lavage process itself also causes the release of surfactant.


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