PULMONARY INTERSTITIAL PRESSURE AND PULMONARY SURFACTANT

1992 Fiscal Year Final Research Report Summary

• Project/Area Number: 03670511
• Research Category: Grant-in-Aid for General Scientific Research (C)
• Allocation Type: Single-year Grants
• Research Field: Pediatrics
• Research Institution: TOHO UNIVERSITY SCHOOL OF MEDICINE
• Principal Investigator: UGA Naoki TOHO UNIVERSITY SCHOOL OF MEDICINE, ASOC Prof, 医学部, 助教授 (90114040)
• Co-Investigator(Kenkyū-buntansha): WAKAE Eriko TOHO UNIVERSITY SCHOOL OF MEDICINE, STAFF., 医学部, 助手 (20220824)
• Project Period (FY): 1991 – 1992
• Keywords: LUNG EDEMA / SURFACTANT / VASOPRESSIN / BRONCHOPULMONARY DYSPLASIA / ステロイドホルモン

Research Abstract

I Using the isolated lung-heart model of rat, the lung compliance is decreased and pulmonary vascular filtration coefficent is increased after the lung lavage with normal saline. We speculated that the deficiency of pulmonary surfactant is more likely to cause the lung edema in same capillary pressure in lung.
II To clarify the effects of vasopressin(AVP) on pulmonary function in premature infants, 25 preterm infants including 14 very low birth weight infants and 6 term infants are prospectively studied. Using the multivariate analysis, gestational week (P<0.02), number of bradycardia in 8 hours of the day (p<0.01), urine sodium concentration (p<0.01) urine osmolality (p<0.001), urinary output volume (p<0.01), total intake volume (p<0.02), and percentile weight change (P<0.05) are associated with the AVP secretion in total infants. Fi02 is also associated if analysis is done in not ventilated infants, and PIP is positively associated in ventilated infants. We conclude that AV P secretio n is higher in less premature infants. and respiratory problems are correlated with AVP secretion. Bradycardia may stimulate the AVP secretion and high level of AVP may deteriolate the pulmonary function through the fluid retention in the lung.
III We hypothesised that dexamethasone treatment may decrease the AVP secretion in the hypopituitary and the increased urine output may improve the pulmonary function in infants with chronic lung desease. So we measured the AVP level in serum and urine, immeadeately before and 4 hours after 0.5 mg/ Kg iv dexamethasone infusion in 8 extremely premature infants with mechanical ventilation. Serum and urine AVP levels were lower after the dexamethasone treatment than before the treatment. One possible explanation of improvement of pulmonary function after the dexamethasone treatment is that dexamethasone suppressed the AVP secretion from the pituitary gland. Lowered AVP secretion increased the urinary fluid secretion and also decreased the pulmonary interstitial fluid and consequently improved the pulmonary gas exchange. Decreased interstitial fluid also suppress the AVP secretion directory if pulmonary edema per se have increased AVP secretion.