ラット胎存肺サファクタント産生に関する実験的研究

Abstract

Perinatal anoxia was experimentally produced in fetal rats to examine the effect of anoxia on pulmonary lecithin levels. The right uterus of adult Sprague-Dawley rats was exposed by laparatomy on the 19th day of pregnancy, and the right uterine artery was compressed for 2 minutes and then released for 1 minute. This procedure was repeated five times. Thus the rat fetuses in the right uterine horn experienced anoxia for a total of 10 minutes, while the littermates in the left horn were free from anoxia. The fetuses were delivered by cesarean section 24 hours after these treatments, and the lecithin content of the lungs was measured.Pulmonary lecithin levels of the anoxic group were found to be significantly lower than those of the control group. Furthermore, it was found that body weight was significantly less and lung wet weight was significantly greater in the anoxic group. The lungs of the anoxic group showed partial atelectasis, interstitial edema, congestion and the presence of red cells and desquamated epithelial cells in the alveolar lumen.A second experiment was conducted to examine the effects of CDP-ch oline and prednisolone upon the pulmonary lecithin levels of the anoxic fetuses. The fetuses in both uterine horns were exposed to anoxia by the same method used in the first experiment. The rats were divided into three groups. The fetuses in the right horn of the first group were injected intraperitoneally with CDP-choline (200mg/kg), the fetuses in the right horn of the second group with CDP-choline (200 mg/kg) and prednisolone (60mg/kg), and the fetuses in the right horn of the third group with prednisolone (30 mg/kg). The fetuses in the left horn of each group were injected with an amount of saline solution equivalent to the amount of medication received by the fetuses of the right horn, and served as the control group.It was found that when CDP-ch oline was administered in this way (group one), there was no acceleration in the production of lecithin. But the newborn rats which had been injected with prednisolone (group three) showed a significantly higher titer of pulmonary lecithin than did the control group. As for group two, injection with a large dose of prednisolone did not result in an increase of lecithin production, but there was a significant weight loss.It can be conc luded from these results that an anoxic episode during the perinatal period inhibits production of pulmonary surfactant, and is one of the causes of intrauterine growth retardation. The effects of anoxia cannot be corrected by a single administration of CDP-choline. An adequate prednisolone injection can accelerate pulmonary lecithin production, as already reported by other investigators. An overdose of prednisolone reduces the pulmonary lecithin levels, and retards weight gains of rat fetuses significantly.