Three pulmonary surthctant preparations: from human amniotic fluid, from bronchoalveolar lavage fluid, and from cattle lung tissue homogenate were tested in preclinical studies. The preparations are nontoxic, possess no mutagenic, teratogenic, and allergic activities and do not modify visceral morphology after repeated injections. After a single intratracheal administration the drugs normalize arterial blood oxygenation in 15-30 rain and arrest the respiratory distress syndrome in dogs, which is confirmed roentgenologically and clinically. Key Words: respiratory distress syndrome; surfactant; pharmacological properties; therapeutic activityThe respiratory distress syndrome (RDS) is one of the major causes of neonatal and adult mortality [3,5]. About 30,000 babies with RDS are annually born in Rnssia; in the USA 150,000 RDS cases are recorded annually in adults. In RDS 15-30% newborns and 50-70% adults die [3,5,7]. In preterm newborns RDS is caused by immaturity of type 2 alveolocytes and the resultant primary deficiency of puhnonary surthctant (PS) [2]. In RDS of adults, PS deficiency is secondary, developing as a result of structural and functional disorders in the airblood barrier. It often develops after multiple injury, sepsis, shock lung, radiation injury, etc. Natural and synthetic PS preparations have been widely used all over the world: smwana (USA), surfactant-TA (Japan), curosurf (Italy), alveofact (Germany), exosurf (UK) [8].We developed a technologically inexpensive method for preparing natural PS and chalacterized their physicochemical properties. Three preparations were studied: human PS isolated from parturients' amniotic fluid, PS from bronchoalveolar iavage fluid (PS-BLF), and PS prepared by water-salt extraction of finely dispersed cattle lung (PS-WSE).The pharmacological and therapeutic properties of these PS preparations are studied.
Afterintratracheal administration of "empty" lecithin-cholesterol liposomes to rats it was found out twofold enhancement of the surfactant content with maximum on the 2nd-3rd day and with normalization to the the alveolar macrophages was also increased.It was shown the change of the blast-transformation reaction of bronchoalveolar lavage and blood lymphocytes. Immune complexes content in bronchoalveolar lavage at different period of time after liposomes administration increased 1.5-2-fold. The natural killers (NK) activity of cells obtained from bronhoalveolar lavage and blood was enhanced 10 times and 2 times respectively. It is supposed that enhancement of lung surfactant phospholipid content is caused by substrate stimulation of type I1 alveolocytes activity. The stimulation of immunocompetent cells might be connected with imitation of bacterial attack by liposomes with proteins adsorbed on their surface. control level by the 7th day. Phagocytic index of 203 Copyright 0 1994 by Marcel Dekker, Inc. Journal of Liposome Research Downloaded from informahealthcare.com by McMaster University on 12/08/14 For personal use only. IBb Re1.u. 4.7fO .8 + 4.2-0.3 7. 5+0. + 7.2-0.5 7. lfl. 2 5.4*0.6 Journal of Liposome Research Downloaded from informahealthcare.com by McMaster University on 12/08/14 For personal use only.
Background: Damage to lung surfactant, which is responsible for the lung local immunity, may contribute to the development of bronchial inflammation in patients with bronchial asthma. Different doses of glucocorticoids produce a stimulating or inhibiting effect on the synthesis of the surfactant protein (SP-A) mRNA. Lung surfactant disorders may negatively influence bronchial homeostasis and aggravate the condition of patients with bronchial asthma and COPD. The objective of this study was to evaluate the influence of long-term inhaled corticosteroids (ICS) on the phospholipid levels of the lung surfactant in rats.Methods and Results: Inhalations of prednisolone hemisuccinate (PH) were given to white non-pedigree rats weighing 180-200 g at a dose of 0.3 mg/kg daily for 30 days. Already by the end of the first study period (10 days), lung surfactant phospholipid levels were found to decrease significantly from 1.35±0.060 mg to 1.02±0.045 mg (P<0.001). The decrease was further recorded at Day 20 and Day 30 of the inhalation period: down to 0.94±0.042 mg (P<0.001) and 1.04±0.047 mg (P<0.01), respectively. The phospholipid content continued to decrease after termination of inhalations down to 0.80±0.036 mg (P<0.001) and 0.63±0.028 mg (P<0.001) at Day 40 and 50 of the experiment. By Day 60 of the experiment (30 days after termination of PH), the phospholipid content in the lung surfactant was restored to the baseline level of 1.29±0.058 mg.Conclusion: The content of lung surfactant was found to decrease significantly as a result of long-term ICS treatment, which may have a negative effect for chronic lung diseases. (Int J Biomed. 2016;6(3):167-169.).
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