• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.844-852
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• 1997

Background : Recent studies have documented increased release of endothelin(ET) during acute attack of asthma. The purpose of this study is to observe the link between plasma level and urinary excretion of each and changes during acute exacerbation. Method : Plasma and 24 hour urine were collected from sixteen asthmatics during acute exacerbation, twice ; first day of symptomatic exacerbation and two weeks after treatment. Controls were ten healthy normal subjects. All patients were treated with corticosteroid and beta-2 adrenergic agonist on admission. ET was determined by radioimmmunoassay and had 100% cross reactivity with ET-1, 67% with ET-2, 84% with ET-3, and 8% with Big-ET. Results : Plasma ETs were significantly elevated during acute attack of asthma compared with those in remission and controls.,However, there was no significant changes in urine ET concentrations or total ET amounts in 24 hour urine during exacerbation upto two weeks. Those levels of urine ET in asthmatics were still higher than controls. ET concentrations in plasma or urine were not correlated with pulmonary functional parameters and hypoxemia. Conclusion : The findings suggests that increased plasma ETs are related with exaggerated release during acute asthma. Urinary ET excretion is increased in asthma. However, urine ET changes during exacerbation should be observed in a larger and longer scale.

• Tuberculosis and Respiratory Diseases
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• v.47 no.5
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• pp.629-641
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• 1999

Background: Corticosteroid is most potent and effective anti-inflammatory medication currently available and inhaled form has been used in the long-tenn control of asthma. Fluticasone propionate(Flixotide/Flovent: FP) is highly potent and topically active inhaled corticosteroid and has at least twice the potency of beclomethasone dipropionate(BDP) in the control of asthma. The aim of this study was to compare the efficacy of FP and BDP in several aspects. Method: Fifty patients with asthma were treated in a randomized, parallel group study of 4 weeks duration. During 2-week run-in period $\beta_2$-agonist was administered. After run-in period, FP $500{\mu}g/day$ was administered via Diskhaler or BDP $800{\mu}g/day$ via reservoir dry-power device. During the run-in and treatment period, morning and evening peak expiratory flow rate(PEFR) were measured daily. Daytime and nighttime asthma symptoms, daytime and night-time rescue bronchodilator use were checked daily. $FEV_{1.0}$ and FVC were measured biweekly in both groups. Results: Three patients treated with FP and seven patient treated with BDP were dropped out. Therefore forty patients completed the study. Morning and evening PEFR was increased and diurnal variation of PEFR decreased significantly in both groups. $FEV_{1.0}$ increased significantly in FP treatment group but not in BDP group. There were also improvements in daytime and night-time asthma symptoms, daytime and night-time rescue bronchodilator use in both groups after treatment There were no significant difference between groups in any of the efficacy parameters. Therapeutic effects were demonstrated earlier in patient treated with FP than BDP. Conclusion: In this study, $500{\mu}g/day$ fluticasone propionate was as effective as $800{\mu}g/day$ beclomethasone dipropionate in the control of asthma. Therapeutic effects were demonstrated earlier in patient treated with FP than BDP without adverse effect.

• The Korean Journal of Pharmacology
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• v.25 no.1
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• pp.13-21
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• 1989

The circadian rhythm of spontaneous motor activity was not significantly altered by $T_4$(4mg/kg, i.p. inj. once a day for 5 days: $T_4$) and PTU (fed ad lib in 0.01% drinking water for 5 weeks: PTU). The plasma thyroxine level was markedly increased by $T_4$ but reduced by PTU, and the plasma thyrotropin level was markedly increased by PTU but moderately increased by $T_4$. Clonidine slightly increased the plasma CS level, but the clonidine effect was significantly enhanced by $T_4-pretreatment$. The brain NE and MHPG contents were little affected by $T_4$ but the NE content was significantly decreased by PTU. The SS-induced increase of plasma CS level was moderately decreased by PTU but increased by $T_4$. However, clonidine significantly inhibited the SS-induced increase, and the inhibitory effect of clonidine was not significantly affected by PTU and $T_4$, respectively. The brain MHPG content and MHPG/NE ratio were significantly decreased by clonidine but increased by SS. The clonidine- and SS-induced changes of brain MHPG content and MHPG/NE ratio were not altered by $T_4$. PTU did not affect the SS-induced increase of brain NE turnover but significantly attenuated the clonidine-induced decrease. The SS-induced increases of brain MHPG content and MHPG/NE rtatio were markedly inhibited by clonidine, and the inhibitory effect of clonidine was not affected by $T_4$ and PTU, respectively. These results suggest that the responses to swim-stress is not signigicantly affected by the alteration of thyroid function and that the hypothalamo-adenohypophysis-adrenocortical stimulation in response to swim-stress seems to be mediated via hypothalamic noradrenergic activation, and the stress response may be inhibited by the agonistic activity of clonidine on the presynaptic ${\alpha}_2-adrenoceptor$.