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Kartagener's syndrome is a rare disease, characterized by situs inversus, sinusitis, dextrocardia and bronchiectasis. This is a report of a rare case of kartagener's syndrome in 20-year-old-male whose chief complaint was purulent sputum, rhinorrhea, & exertional dyspnea. Chest P-A view revealed the dextrocardia and the magenblase in the right subphrenic area, suggesting situs inversus totalis. Multiple small cystic radielu-concies are also seen in lower halves of both thorax, suggesting bronchiectasis. P.N.S view revealed the homogenous increase-d density in all sinuses, tut didn't clear bony destruction. Bronchogram revealed the saccular and tubular dilation of the segmental bronchi in all bronchi, Particularly in the right lower lobe bronchus. EKG finding was alternation of voltage, right atrial hypertrophy and dextrocardia.
Background: The aim of this study was to examine whether PD 123319 (an angiotensin II type 2 [AT2] receptor antagonist) can influence the release of catecholamines (CA) from the perfused model of the rat adrenal medulla. Methods: The adrenal gland was isolated by the modification of Wakade method, and perfused with normal Krebs-bicarbonate solution. The content of CA was measured using the fluorospectrophotometer. Results: During perfusion of PD 123319 (range, 5 to 50 nM) into an adrenal vein for 90 minutes the CA secretory responses evoked by acetylcholine (ACh), high K+, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), and McN-A-343 was dose- and time-dependently inhibited. Furthermore, loading with PD 123319 for 90minutes also markedly inhibited the CA secretory responses evoked by 4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoro-methyl -phenyl)-pyridine-5-carboxylate (Bay-K-8644), cyclopiazonic acid, veratridine, and angiotensin II (Ang II). PD 123319 did not affect basal CA output. Simultaneous perfusion of PD 123319 and CGP 42112 perfused into an adrenal vein for 90 minutes rather more potently inhibited the CA seretory responses evoked by Ach, high K+, DMPP, Bay-K-8644, veratridine, and Ang II compared to the inhibitory effect by PD123319-treated alone. Conclusions: Taken together, these results show that PD 123319inhibits the CA secretion evoked by both cholinergic and Ang II receptor stimulation from the perfused rat adrenal medulla. This inhibitory effect of PD 123319 seems to be exerted by blocking the influx of both Na+ and Ca2+ through their voltage-dependent channels into the rat adrenomedullary chromaffin cells as well as by reducing the Ca2+ release from its cytoplasmic calcium store, which may be relevant to AT2 receptor blockade. Based on these present data, it is thought that PD 123319 has different activity from previously known AT2 antagonist activity in the perfused adrenal medulla, and that AT2receptors may be involved in the rat adrenomedullary CA secretion.
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심각한 교통난 해결을 위해 중앙정부 및 지방자치단체 등에서는 대규모 도로사업 확충에 막대한 투자를 시행하고 있으며 이러한 과정에서 합리적이고 객관적 기준으로 이루어져야 되는 부분 중 하나가 투자우선순위의 평가이다. 제한된 예산 하에서 장기적으로 효율성을 극대화 시킬 수 있는 도로투자계획을 수립하는 것이 궁극적인 목적이다. 그러나 현재 투자우선순위 평가과정은 명쾌한 판단기준과 방법에 대한 지침이 없는 실정이다. 따라서, 본 연구에서는 교통시설 수립계획 및 재정계획의 기본이라 할 수 있는 도로투자 우선순위평가에 대해 기존의 일부 지방자치단체의 투자우선순위평가에서 적용되고 있는 방법을 다양한 평가항목인 도로기능, 지역특성, 정책추진의지, 교통환경을 검토하여 현재의 방법을 보완하면서 객관적인 평가 결과를 제시할 수 있는 방법을 구축하고 경제성 분석을 실시하지 않은 도로에 대하여 실제로 적용해 보는데 있다. 그리고, 평가항목의 가중치변화를 주는 민감도 분석을 통하여 다른 척도의 평가배점으로 인한 도로투자 우선순위 변화를 비교?분석함으로서 AHP분석방법을 통한 도로투자 우선순위 결정결과를 제시하였다.
The present study was designed to investigate whether ethylacetate (EtOAc) fraction extracted from Rubus coreanum affect the contractility of the isolated thoracic aortic strips and blood pressure of normotensive rats. The EtOAc fraction (400 μg/mL) significantly depressed both phenylephrine (PE, 10 μM)- and high K+ (56 mM)-induced contractile responses of the isolated thoracic aortic strips in a concentration-dependent fashion. In the simultaneous presence of L-NAME (an inhibitor of NO synthase, 300 μM) and EtOAc (400 μg/mL), both PE- and high K+-induced contractile responses were recovered to the corresponding control level in comparison with inhibition of EtOAc-treatment alone. Moreover, in the simultaneous presence of EtOAc after pretreatment with 0.4% CHAPS, both PE- and high K+-induced contractile responses were recovered to the corresponding control level compared to the inhibitory response of EtOAc-treatment alone. Also, in anesthetized rats, EtOAc fraction (0.3~3.0 mg/kg) injected into a femoral vein dose-dependently produced depressor responses. This hypotensive action of EtOAc fraction was greatly inhibited after treatment with phentolamine (1 mg/kg), chlorisondamine (1 mg/kg), L-NAME (3 mg/kg/30 min) or sodium nitroprusside (30 μg/kg/30 min). Intravenous infusion of EtOAc fraction (1.0~10.0 mg/kg/30 min) markedly inhibited norepinehrine-induced pressor responses. Taken together, these results demostrate that EtOAc causes vascular relaxation in the isolated rat thoracic aortic strips as well as hypotensive action in anesthetized rats. These vasorelaxation and hypotension of EtOAc seem to be mediated at least by the increased NO production through the activation of NO synthase of vascular endothelium, and the inhibitory adrenergic modulation.
This study was to investigate the effect of lovastatin on the bioavailability or pharmacokinetics of verapamil and its major metabolite, norverapamil, in rats. The pharmacokinetic parameters of verapamil and norverapamil in rats were measured after the oral administration of verapamil (9 mg/kg) in the presence or absence of lovastatin (0.3 or 1.0 mg/kg). The pharmacokinetic parameters of verapamil were significantly altered by the presence of lovastatin compared to the control group (given verapamil alone). The presence of lovastatin significantly (p < 0.05, 0.3 mg/kg; p < 0.01, 1.0 mg/kg) increased the total area under the plasma concentration-time curve (AUC) of verapamil by 26.5-64.8%, and the peak plasma concentration (Cmax) of verapamil by 34.1-65.9%. Consequently, the relative bioavailability (R.B.) of verapamil was increased by 1.27- to 1.65-fold than that of the control group. However, there was not significant change in the time to reach the peak plasma concentration (Tmax) and the terminal half-life (t1/2) of verapamil in the presence of lovastatin. The AUC and Cmax of norverapamil were significantly (p < 0.05) higher than those of presence of 1.0 mg/kg of lovastatin compared with the control group. However, there was no significant change in the metabolite-parent ratio (M.R.) of norverapamil in the presence of lovastatin. The presence of lovastatin significantly enhanced the oral bioavailability of verapamil. The enhanced oral bioavailability of verapamil may be due to inhibition both of the CYP3A-mediated metabolism and the efflux pump P-glycoprotein (P-gp) in the intestine and/or in liver by the presence of lovastatin.