• Korean Journal of Veterinary Research
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• v.43 no.4
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• pp.587-595
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• 2003

The aim of this study was to investigate trazodone's effect on vasorelaxation and blood pressure lowering and to examine its underlying mechanism of action in isolated thoracic aorta and anesthesized rats. Precontracted aortic rings with high KCl were relaxed with trazodone, at concentrations of $50{\mu}M$ or greater. However, precontracted rings with phenylephrine (PE) were relaxed with trazodone, at concentrations of $0.03{\mu}M$ or greater, in a concentration-dependent manner. These relaxant effects of trazodone on endothelium intact rat aortic rings were significantly greater than those on denuded rings. The trazodone-induced relaxations were suppressed by nitric oxide synthase (NOS) inhibitors, N(G)-nitro-L-arginine (L-NNA) and N(omega)-nitro-L-arginine methyl ester (L-NAME), guanylate cyclase inhibitors, methylene blue and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a $Ca^{2+}$-activated $K^+$ channel blocker, tetrabutylammonium (TBA), a $Ca^{2+}$ channel blocker, nifedipine, $Na^+$ channel blockers, lidocaine and procaine, and removal of extracellular $Na^+$, but not by aminoguanidine, 2-nitro-4-carboxyphenyl-n, n-diphenylcarbamate (NCDC), indomethacin, glibenclamide and clotrimazole. In vivo, infusion of trazodone elicited significant decrease in arterial blood pressure. Trazodone-induced decrease in blood pressure was markedly inhibited by pretreatment of intravenous injection of saponin, L-NNA, methylene blue, TBA, lidocaine or nifedipine. These findings suggest that the endothelium-dependent relaxation and decrease in blood pressure induced by trazodone is mediated by release of NO from the endothelium, activation of TBA-sensitive $Ca^{2+}$-activated $K^+$ channels or inhibition of $Ca^{2+}$ entry through voltage-gated channel.

• Journal of the Korean Applied Science and Technology
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• v.35 no.3
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• pp.643-653
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• 2018

This study was investigated the mechanism of action of n-6/n-3 fatty acid ratio on the metabolic partitioning of blood glycerolipids by in vivo monitoring technique in hyperlipidemic animal model rats. The ratio of cholesteryl 14C-oleate metabolized in the liver of total glycerolipids was lower in the order of n-6/n-3 ratios of 4:1, 15:1, 30:1 and control group (p<0.05). The secretion amount of phospholipid was higher in the order of n-6/n-3 ratio 4:1, 15:1, 30:1 than the control (p<0.05). The secretion amount of triglyceride was lower in especially 4:1, in order of n-6/n-3 4:1, 15:1 and 30:1 compared with the control. The ratio of phospholipid partitioning to total glycerolipid was high in orfer of n-6/n-3 ratio 4:1, 15:1, 30:1 and control (p<0.05). The triacylglycerol partitioning (%) via liver was higher 72.97, 75.93, 78.12% in n-6/n-3 4;1, 15:1, 30:1, respectively than the control of 82.25%, according to increased n-6/n-3 (p<0.05). The phospholipid partitioning (%) was lower 25.15, 18.87, 18.15% in n-6/n-3 4;1, 15:1, 30:1, respectively, compared to control 11.04%, according to increased n-6/n-3 (p<0.05).

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.5
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• pp.401-408
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• 2009

$K^+$-$Cl^-$-cotransport (KCC) has been reported to have various cellular functions, including proliferation and apoptosis of human cancer cells. However, the signal transduction pathways that control the activity of KCC are currently not well understood. In this study we investigated the possible role of phospholipase $A_2$ ($PLA_2$)-arachidonic acid (AA) signal in the regulatory mechanism of KCC activity. Exogenous application of AA significantly induced $K^+$ efflux in a dose-dependent manner, which was completely blocked by R-(+)-[2-n-butyl-6,7 -dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1Hinden-5-yl]oxy]acetic acid (DIOA), a specific KCC inhibitor. N-Ethylmaleimide (NEM), a KCC activatorinduced $K^+$ efflux was significantly suppressed by bromoenol lactone (BEL), an inhibitor of the calciumindependent $PLA_2$ ($iPLA_2$), whereas it was not significantly altered by arachidonyl trifluoromethylketone ($AACOCF_3$) and p-bromophenacyl bromide (BPB), inhibitors of the calcium-dependent cytosolic $PLA_2$ ($cPLA_2$) and the secretory $PLA_2$ ($sPLA_2$), respectively. NEM increased AA liberation in a doseand time-dependent manner, which was markedly prevented only by BEL. In addition, the NEM-induced ROS generation was significantly reduced by DPI and BEL, whereas $AACOCF_3$ and BPB did not have an influence. The NEM-induced KCC activation and ROS production was not significantly affected by treatment with indomethacin (Indo) and nordihydroguaiaretic acid (NDGA), selective inhibitors of cyclooxygenase (COX) and lipoxygenase (LOX), respectively. Treatment with 5,8,11,14-eicosatetraynoic acid (ETYA), a non-metabolizable analogue of AA, markedly produced ROS and activated the KCC. Collectively, these results suggest that $iPLA_2$-AA signal may be essentially involved in the mechanism of ROS-mediated KCC activation in HepG2 cells.

• Journal of the Korean Chemical Society
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• v.24 no.2
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• pp.150-154
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• 1980

Kinetic studies of the reaction of benzyl benzenesulfonate with pyridine in acetone were carried out by the electric conductivity method under 1 to 2000 bars and at 20 to $40^{\circ}C$. The rate increases with increasing pressure and temperature. The activation enthalpy $({\Delta}H^{\neq}),\;entropy\;({\Delta}S^{\neq})$ and activation volume $({\Delta}V^{\neq})$ of the reaction are obtained by the above experiment. The isokinetic relationship between $({\Delta}H^{\neq})\;and\;({\Delta}S^{\neq})$ for pressure change in the reaction was shown, and its isokinetic temperature was $342^{\circ}K$. From all of the above results it was found that this reaction precedes on the $S_N2$ reaction mechanism in which the rate of the reaction was determined by $C{\cdots}N$ bond formation at transition state.

• Applied Microscopy
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• v.33 no.1
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• pp.1-16
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• 2003

As is well known that N-nitroso-N-methylurethane (NNNMU) causes acute lung injury (ALI) in experimental animals. And ALI caused by NNNMU is very similar to ARDS in human being in its pathology and progress. In its context, we investigated the pathogenetic mechanism of ARDS associated with oxidative stress by neutrophils in Sprague-Dawley rat model of NNNMU-induced ALI. NNNMU had increased lung weight/body weight ratio (L/B ratio), lung myeloperoxidase (MPO) activity, protein content and number of neutrophils in bronchoalveolar fluid (BALF) compared with those of control rat (p<0.001, respectively). In contrast, the amount of pulmonary surfactant in BALF was decreased by NNNMU (p<0.001). Morphologically, light microscopic examination denoted pathological findings such as formation of hyaline membrane, infiltration of neutrophils and perivascular cuffing in the lungs of NNNMU-treated rats. In addition, ultrastructural changes such as the necrosis of endothelial cells, swelling and vacuolization of lamellar bodies of alveolar type II cells, and the degeneration of pulmonary surfactant were identified after treatment of NNNMU. Very interestingly, cerium chloride electron microscopic cytochemistry showed that NNNMU had increased the production of cerrous-peroxide granules in the lung, which signified the increased production of hydrogen peroxide in the lung. Collectively, we conclude that NNNMU causes acute lung leak by the mechanism of neutrophilic oxidative stress of the lung.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.4
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• pp.149-154
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• 2007

Kainic acid (KA) causes neurodegeneration, but no consensus has been reached concerning its mechanism. Nitric oxide may be a regulator of the mechanism. We identified differentially expressed genes in the hippocampus of mice treated with kainic acid, together with or without L-NAME, a nonselective nitric oxide synthase inhibitor, using a new differential display PCR method based on annealing control primers. Eight genes were identified, including clathrin light polypeptide, TATA element modulatory factor 1, neurexin III, ND4, ATPase, $H^+$ transporting, V1 subunit E isoform 1, and N-myc downstream regulated gene 2. Although the functions of these genes and their products remain to be determined, their identification provides insight into the molecular mechanism(s) involved in KA-induced neuronal cell death in the hippocampal CA3 area.

• Journal of the Korean Chemical Society
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• v.27 no.2
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• pp.95-101
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• 1983

The pseudo-first order rate constants have been obtained for the solvolysis of benzoyl cyanide in various aqueous solvent mixtures and ethanol-trifluoroethanol mixtures at 1, 5, 10, 15 and $20^{\circ}C$. Values of n in the Kivinen polt, m values of Grunwald-Winstein polt, $\beta$ values of Leffler relationship and values of m and l in the extended Grunwald-Winstein polt have been calculated and studied the transition state variation caused by solvent changes using the More O'Ferrall polt and quantum mechanical approach. It has been shown that the reaction proceed via the associative $S_N2$ mechanism, using the transition state parameters and quantum mechanical model approach.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2003.07b
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• pp.934-937
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• 2003

Glasses in the system $CuO-P_2O_5-V_2O_5$ were prepared by a press-quenching method on the copper plate. The glass-ceramics from these glasses were obtained by post-heat treatment, and the crystallization behavior and DC conductivities were determined. The conductivities of the glasses were range from $10^{-6}s.Cm^{-1}$ at room temperature, but the conductivities of the glass-ceramics were $10^{-3}s.Cm^{-1}$ increased by $10^3$ order. The crystalline product in the glass-ceramics was $CuV_2O_6$. Heat-treatment conditions influenced the crystal growth of $CuV_2O_6$ and conductivity. The linear relationship between in (${\sigma}T$) and $T^{-1}$ suggested that the electrical conduction in the present glass-ceramics would be due to a small polaron hopping(SPH) mechanism.

• International Journal of Concrete Structures and Materials
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• v.8 no.1
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• pp.1-14
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• 2014

In the present paper, a behavioral model is proposed for study of the individual contributions to shear capacity in shear-critical reinforced concrete members. On the basis of the relationship between shear and bending moment (V = dM/dx) in beams subjected to combined shear and moment loads, the shear resistant mechanism is explicitly decoupled into the base components-beam action and arch action. Then the overall behavior of a beam is explained in terms of the combination of these two base components. The gross compatibility condition between the deformations associated with the two actions is formulated utilizing the truss idealization together with some approximations. From this compatibility condition, the ratio of the shear contribution by the tied arch action is determined. The performance of the model is examined by a comparison with the experimental data in literatures. The results show that the proposed model can explain beam shear behavior in consistent way with clear physical significance.

• Journal of applied mathematics & informatics
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• v.6 no.3
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• pp.697-726
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• 1999

In this paper we develop a now procedure to control stepsize for linear multistep methods applied to semi-explicit index 1 differential-algebraic equations. in contrast to the standard approach the error control mechanism presented here is based on monitoring and contolling both the local and global errors of multistep formulas. As a result such methods with the local-global stepsize control solve differential-algebraic equation with any prescribed accuracy (up to round-off errors). For implicit multistep methods we give the minimum number of both full and modified Newton iterations allowing the iterative approxima-tions to be correctly used in the procedure of the local-global stepsize control. We also discuss validity of simple iterations for high accuracy solving differential-algebraic equations. Numerical tests support the the-oretical results of the paper.