MATSUDA Tadashi Hokkaido Univ. Hosp., Med. Staff., 医学部附属病院, 医員
CHO Kazutoshi Hokkaido Univ. Hosp., Lec., 医学部附属病院, 講師 (10312365)
藤本 征一郎 北海道大学, 大学院・医学研究科, 教授 (60001898)
|Budget Amount *help
¥3,700,000 (Direct Cost : ¥3,700,000)
Fiscal Year 2002 : ¥1,900,000 (Direct Cost : ¥1,900,000)
Fiscal Year 2001 : ¥1,800,000 (Direct Cost : ¥1,800,000)
In order to investigate a mechanism for developing chronic lung disease (CLD) of neonate, chronically instrumented dated Suffolk sheep fetuses (n=9) were utilized. At 123 days of gestation catheters were placed in carotid artery and vein of the fetus and amniotic cavity. From 125 days of gestation, lenograstim (50mg/day) was administered through carotid vein of the G arm fetuses for 5 days, saline to control fetuses, and for G+E arm added endotoxin (20mg) to amniotic fluid at the 5th day of lenograstim administration.
On the 7th day after chronic in utero preparation, fetuses were transferred to our neonatal care unit for 10 days. Polymorphic nuclear leukocyte count (PMNc), ventilatory index (VI), ventilatory efficacy index (VEI), and dynamic compliance of the lung (Cdyn) were measured and compared between three groups. After 10 days of neonatal observation, neonates were sacrificed then dissected lungs were pathologically investigated.
Both in G and G+E groups, PMNc values increased significantly at 129 days of gestation. However, only G+E group lung tissues showed diffuse emphysema lesions, focal atelectasis lesions, and multi focal cystic lesions, which were characteristic for Wilson-Mikity Syndrome, the most advanced form of CLD.
Our findings indicated that the activation of increased polymorphic nuclear leukocytes by endotoxin might be an essential step for development of CLD in utero.