• Journal of Yeungnam Medical Science
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• v.1 no.1
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• pp.59-66
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• 1984

Although it is well established that steroid is effective for treatment of neonatal respiratory distress syndrome (NRDS), the action mechanism of steroid on NRDS is not well known. Several authors have insisted that steroid increases secretion of pulmonary surfactant from type II pneumocyte, but others have insisted that steroid does not affect the secretory function of the type II pneumocyte. And some authors have suggested that steroid may ca use compositional change of pulmonary surfactant phospholipid. From these aspects, it is desirable to confirm the effect of steroid on (he secretory function of the type II pneumocyte. In order to know the effect of steroid on pulmonary surfactant activity, phospholipid phosphorus of lung lavage was measured and composition of pulmonary surfactant phospholipid of lung lavage was analyzed by thin layer chromatography (TLC) in control (C), pneumonectomized (PN), and pneumonectomized with betamethasone treated (PNS) rabbits. And lung weight and lung weight-body weight ratio were measured in each experimental group also. In PN group, right lung pneumonectomy was performed under general anesthesia with pentobarbital sodium (30mg/kg). On the fifth day after the surgery, the left lung was excised and measured above parameters. In PNS group, pneumonectomy was performed as PN group, and one day after the surgery, betamethasone was injected for four days intramusculary (4mg/day) and rabbits were sacrificed. The experiment yielded following results. PNS group's lung weight was significantly (p<0.01) heavier than C group's, but in comparison with PN group's it showed no significant change. PNS group's L/B ratio was significantly (p<0.05) higher than C group's, but compared with PN group's it showed no significant change. The value of phospholipid phosphorus content of PNS group was significantly (p<0.01) higher than that of C group. Even if the value of phospholipid phosphorus content in PNS group was not significantly higher than that of PN group, it showed increasing tendency compared with that of PN group. And in an analysis of the thin layer chromatogram, quantity (${\mu}mol/gm$ of wet weight lung) of phosphatidylcholine in PNS group decreased significantly (p<0.05) compared with C and PN group. From these results, it may be suggested that though steroid inhibits cellular hyperplasia in the compensatory growing lung, it auguments the secretory function of type II pneumocyte and causes compositional change of pulmonary surfactant phospholipid.

• Parasites, Hosts and Diseases
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• v.33 no.3
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• pp.187-194
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• 1995

The present study aims to observe changing patterns of serum antibody to hleumuvstis calinii in normal rats of different ages and in immunosuppressed rats. The serum IgG antibody was observed by immunoblotting with crude antigen of f carinii which were purified from the lungs of infected rats. The crude antigens separated in SDS-PAGE resolved more than 20 protein bands from 20 to 200 kDa. Of them,40-45, 50-55, 116 and 200 kDa bands were major antigens of R cori.nii. Most of the normal rats of up to 4 weeks had the antibodies reacting the 4 bands, but none of 8-week-old rats revealed the specific antibody. After the rats grew for 40 weeks, all were found to have the antibody in their serum. Same pattern of serum antibody level by age was found in ELISA. When immunosuppressed rats became heavily infected, the antibody in their serum decreased distinctively. The present results suggest that antibodies in normal newborn rats are transferred from their mother and lowered up to 8 weeks. Thereafter, the levels of the antibodies begin to increase by natural exposure to R cnrinii. It was also confirmed that the intensity of P cnrinii infection is inversely related with levels of serum antibodies.

• 월간산업보건
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• s.295
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• pp.15-19
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• 2012

• Parasites, Hosts and Diseases
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• v.33 no.2
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• pp.101-106
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• 1995

Soluble protein of purified Pneumocvstis cnrinii was prepared from experimentally infected rats. SDS-PAGE of the crude antigen resolved about 20 protein bands from 20 to 200 kDa. Out of thenl, 116 kDa band strongly reacted and 45-55 and 100 kDa bands reacted weakly to the positive reference human serum from U.S.A. Western blot analysis with sera of 130 normal children and 15 newborns in Korea revealed specific IgG antibody reaction to 40-55 and 116 kDa protein bands. Forty percent (40.0%) of the 145 sera were positive with any of the antigenic protein bands of R corinii. The positive rate was 56% in 50 males and 33.3% in 48 females. The protein bands 40-55 and 116 kDa from rat P. carinii were confirmed to cross-react with human sera in Korea.

• Applied Microscopy
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• v.35 no.4
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• pp.84-90
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• 2005

Neutrophils that influx into the alveolar spaces from circulatory bloods play a important role in pathogenesis of acute lung injury. During the acute inflammatory phase, in order to investigate the acceleration of macrophage phagocytosis to the neutrophils is able to reduce the neutrophil-derived acute lung injury, endotoxemia was induced by insufflation of lipopolysaccharide intratracheally and organic germanium was injected intraperitoneally after endotoxin treatment. At 5 h after endotoxin treatment, lung weight and BAL protein concentration are significantly increased (p<0.001) compared to sham, and that was remarkedly decreased (p<0.001, p<0.01) by injection of germanium. In addition germanium treatment resulted to decreased the number of alveolar PMNs and to increase the percentage of engulfed neutrophils by alveolar macrophages. These observations indicate that organic germanium may have a role of reduction to neutrophil-derived acute lung injury in endotoxemia.

• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.418-422
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• 2005

A diffuse alveolar hemorrhage (DAH) is a distinct form of pulmonary hemorrhage that originates from the pulmonary microcirculation. Disseminated intravascular coagulation (DIC) is one cause of DAH. Although HELLP syndrome associated with DIC can cause DAH, there are no published case reports that the authors are aware of. We report the case of a pregnant woman with HELLP syndrome who developed DAH. Because pregnant women with HELLP syndrome can develop DAH as a form of ARDS, a bronchoalveolar lavage may be used to make a differential diagnosis of this lung manifestation.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.513-520
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• 1994

Background: The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2. Methods: In order to investigate the relationship between the activity of alveolar macrophage and the production of $PGE_2$ from activated alveolar macrophage, the authors measured hydrogen peroxide and $PGE_2$ from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica($SiO_2$) suspended in saline(50 mg/ml) in Sprague-Dawley rats. Results: produced by 1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica(Fig. 1). 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05, Fig. 2A) and $PGE_2$(p>0.05, Fig. 2B) release from alveolar macrophages. Alveolar macrophages from rat with silicotic nodules released more hydrogen peroxide and $PGE_2$ than those of control group(p<0.05, Fig. 3). Conclusion: These results suggest that silica particle could activate macrophage directly and enhanced the release of $PGE_2$ and hydrogen peroxide from the alveolar macrophage.

• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.184-205
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• 1995

Background: Pulmonary toxicity by bleomycin has multiple mechanisms including direct tissue toxicity due to oxygen-derived free radicals and indirect toxicity through amplification of pulmonary inflammation. To evaluate the effect of chelators or free radical scavenger to lung damage induced by bleomycin, penicillamine as a copper chelator, deferoxamine as an iron chelator and vitamin E as a free radical scavenger were administered. Methods: Two hundred Wistar rats were divided into five groups: Control, bleomycin treated, bleomycin-penicillamine treated, bleomycin-deferoxamine treated, and bleomycin-vitamin E treated groups. Rats sacrificed on day 1, day 3, day 4, day 7, day 14, and day 28 after treatment. Bronchoalveolar lavage, light microscopic and immunohistologic studies for type I, III, IV collagens, fibronectin, laminin and NBD phallicidin were evaluated. Results: There was a significant increase in the total cell counts of bronchoalveolar lavage on day 1 from all treated animals and vitamin treated group showed an abrupt decrease in total cell counts with decrease of neutrophils on day 3. Bleomycin-vitamin E treated group had the least histologic changes such as pulmonary fibrosis. The alveolar basement membranes were positive for type IV collegen and laminin. Basement membranes of bleomycin, bleomycin-penicillamine, or bleomycin-deferoxamine treated groups were disrupted and fragmented on day 4 or 7. The bleomycin-vitamin E treated group had intact basement membranes until day 28. Conclusion: Bleomycin-induced pulmonary fibrosis was related to the severity of acute injury to oxygen radicals or activation of neutrophils and disruption of basement membrane. Vitamin E seemed to be the most effective antioxidant in the inhibition of bleomycin-induced pulmonary injury and fibrosis.

• The Korean Journal of Physiology
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• v.7 no.2
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• pp.1-8
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• 1973

Though it has been reported by Clements et al. and Avery et al. that the activity of the pulmonary surfactant can be altered by the temperature changes, a conclusive evidence of the effects of temperature on the surfactant system of the lung is yet to come. In the present study, an attempt was made to observe possible effects of a few different degrees of temperature on the activity of the pulmonary surfactant of the rabbit in vivo and in vitro. The rabbit was sacrificed by blood shedding and both lungs were completely removed. The lung washings, obtained by gently lavaging the left lung with saline, was placed at 1) 4C for 1, 5, 10, 15, 30 and 40 days, and 2) 20C for 1, 2, 3, 4, 5 and 7 days for in vitro experiment. For in vivo experiment, the rabbit was placed at 4C for 4, 8, 12 and 24 hours, and the lung lavage was prepared as described above in the in vitro experiment. Tension-area (T-A) diagram of the lung lavage was recorded automatically by a modified. Langmuir-Wilhelmy balance with a synchronized recording system. The surface tensions thus obtained were compared with those of the normal rabbit, and the results are summarized as follows: 1. The maximal surface tension, minimal surface tension and stability index of the normal rabbit lung lavage were $52.5{\pm}2.3\;dynes/cm,\;4.9{\pm}2.3\;dynes/cm$ and 1.65, respectively. 2. In the group where the lung lavage was placed at 4C in vitro, the maximal and minimal surface tensions, and stability index did not show any noticeable changes comparing with the normal values up to 30 days. On the 40th day of the experiment, a tendency of a slight increase in the surface tensions was observed but the change was not significant. 3. When the lung lavage was placed at 20 C in vitro, the maximal surface tension did not show any appreciable change comparing with the normal except on the 7 th day with a slight increase. The minimal surface tension showed an increased value from the 2nd day, and on the 5 th and 7 th experimental day, markedly increased value was observed. The stability index, on the other hand. showed a marked decrease throughout the entire experiment with the value of 0.71 and 0.53 on the 5th and 7 th day, respectively. 4. In the group where the rabbit was placed at 4 C in vivo, the maximal surface tensions and stability index of the lung lavage showed little change from the normal. The minimal surface tension at 12 experimental hour showed a slight increase, but it returned to the normal value at 24 hour.

• Tuberculosis and Respiratory Diseases
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• v.53 no.5
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• pp.519-529
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• 2002

Background : The therapeutic effects of surfactants on acute lung injury derive not only from their recruiting action on collapsed alveoli but also from their anti-inflammatory action in the alveolar sapce. This study evaluated the anti-inflammatory action of a surfactant in an acute lung injury model of rats by neutrophils were recollected from the BAL fluid and the NF-${\kappa}B$ activity of the neutrophilic nuclear protein was evaluated. Methods : Male Sprague-Dawley rats weighing approximately 300 gram were divided into 3 groups, which consisted of 6 rats respectively. In the control group, normal saline(3ml/kg) was instilled into the trachea twice with 30 minute interval. In two other groups, acute lung injury was induced by the intra-tracheal instillation of LPS(5mg/kg). Thirty minutes later, either a surfactant(ST group; 30mg/kg) or normal saline(NT group: 3ml/kg) was instilled via the trachea. Twenty-four hours after the LPS instillation, the BAL fluid was retrieved to measure the WBC count and cytokine(IL-$1{\beta}$ and IL-6) levels. The neutrophils were isolated from the BAL fluid and the nuclear protein was extracted to evaluate the NF-${\kappa}B$ activity using a eletrophoretic mobility shift assay(EMSA). Results : The WBC count of the BAL fluid of the ST group($3,221{\pm}1,914{\times}10^3/{\mu}l$) was higher than that of the control group($356{\pm}275{\times}10^3/{\mu}l$)(p<0.05) and lower than that of the NT group($5,561{\pm}1,757{\times}10^3/{\mu}l$)(p<0.05)). The BAL fluid level of IL-$1{\beta}$ from the NT group($2,064{\pm}1,082pg/ml$) was higher than those of the ST group($360{\pm}234pg/ml$)(p<0.05) and the control group(0pg/ml)p<0.05) and control group($49{\pm}62pg/ml$)(p<0.05). The NF-${\kappa}B$ activity of the neutrophilic nuclear protein in the ST group and NT group was similar. Conclusion : The surfactant, attenuates the alveolar inflammation in the acute lung injury of rats model. However, its anti-inflammatory action does no't appear to be mediated by the inhibition of NF-${\kappa}B$ activity.