1994 Fiscal Year Final Research Report Summary
Level of Lung Surfactant Secretion from Type II Alveolar Cells When Inflammation-Associated Substances are Added
Project/Area Number |
05671385
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Obstetrics and gynecology
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Research Institution | Fukushima Medical College |
Principal Investigator |
SUZUKI Rika Fukushima Medical College, Ob.& Gy., Assistant, 医学部, 助手 (10244386)
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Project Period (FY) |
1993 – 1994
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Keywords | lung surfactant / alveolar type II cell / DPPC / HPLC / プロスタグランジン |
Research Abstract |
<DCObjective> DD Evaluate the level of secretion of dipalmitoylphophatidylcholine (DPPC), which is the most prevalent phopholipid in the lung surfactant, in the medium of type II alveolar cell culture, when several substances are added. <DCMethod> DD At 18 and 20 gestational day fetal rat lungs were removed, from which type II alveolar cell suspensions were made (0.5x10^6 cells/dish) and cultured for 8 days (37゚C,5% CO_2). Culture dishes were devided into controlled and experimental groups. Prostaglandin (PG) E_1, dexamethasone (dexa.) and ritodrine (rit.) were added to the experimental groups. DPPC in the culture medium was extracted, purified, and measured by high performance liquid chromatography (HPLC) . <DCResult> DD(1) In both 18 and 20 gestational fetal rats, between control group and dexa.or rit.group, there was no significant difference of DPPC concentration at any stage of the testing period. (2) In the PGE_110^<-8>M added group of 18 gestational day fetal rats, there was a tendency for the DPPC secretion to be promoted through the culture period, and there was a significant difference of DPPC concentration at day 6 of the culture period. (3) In the PGE_110^<-8>M added group of 20 gestational day fetal rats, DPPC secretion did not decline through the culture period. <DCDiscussion> DD Rit.may not stimulate synthesis of lung surfactant in the type II alveolar cell, but may stimulate transient secretion. Although it is said that Dexa.clinically prevents RDS,type II cells could not be directly stimulated to produce surfactant. This showed that glucocorticoids affect other composite systems. PGE_1 has promotive effects to secrete surfactant. It is suggested that this effect does not only depend on intracellular signal transduction, but also direct stimulation of the genes. In the intra-uterine environment PGs are high, so there is the possiblity that surfactant secretion may be promoted.
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