1990 Fiscal Year Final Research Report Summary
Inhibitor of Pulmonary Surfactant and Respiratory Distress Syndrome
| Project/Area Number |
01570553
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | Toho University School of Medicine |
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Principal Investigator |
UGA Naoki Toho Univ School Med Medcine Associate Prof., 医学部, 助教授 (90114040)
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| Co-Investigator(Kenkyū-buntansha) |
WAKAE Eriko Toho Univ School Med Medcine Assistant, 医学部, 助手 (20220824)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Respiratory dystress syndrome / Pulmonary surfactant / Lung edema / Dexamethason |
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| Research Abstract |
In 1989 and 1990 we investigated how the artificial surfactant instillation into the damaged lung of rats by the oleic, acid effects on the pulmonary function and blood gases. If it does not improve the pulmonary function any, are there any possibility for the combination treatment with lung lavageor dexamethason and artificial surfactant treatment to improve the pulmonary function of ARDS?
Rat was tracheotomized and ventilated with pressure limited respirator (PIP/PEEP=15/2 cmH20, IMV=50/minutes). The 0.1ml/Kg of oleic acid was injected into the jaguler vein of rats, and arterial pressure and gases were followed. The control group did not have any other treatment. The surfactant group had 120mg/Kg of artificial lung surfactant (surfactant TA ) given into the trachea 150 minutes after the injection of oleic acid. The dexamethasone group had a injection of dexamethasone, 1 mg/Kg intravenously 60 minutes after the oleic acid treatment. The combination group was treated both with the dexam
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ethasone and the artificial surfactant as above. In all groups the static compliance was measured 270 minutes after the oleic acid treatment. The lung was excised carefully, and the ration of wet lung weight/body weight was calculated.
In the the surfactant group blood gases showed worse than the control group significantly after the treatment. The static lung compliance increased in the surfactant group but statistically it was not significant. In the dexamethasone group blood gases showed the tendency of improvement 60 minutes after the injection but the effects were not sustained more than 120 minutes. In the combination group the blood gases showed the improvements significantly if compared to that of the surfactant group, but those were not better than the control group. The lung wet weight ratio was less in the groups which were treated with dexamethasone than in the other groups, but the differences were not statistically significant.
The above results suggest that the artificial surfactant treatment make the pulmonary functions worse in rat lung treated with oleic acid possibly because of excessive lung edema. The dexamethasone treatment may reduce the lung edema and consequently improve the effects of the surfactant treatment. It may worthwhile to make a trial to give dexamethasone in premature infants with the respiratory distress syndrome who were failed to improve by the artificial surfactant treatment. Less
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Research Products
(3 results)
