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기니픽에서 Magnesium의 혈관 이완과 혈압 하강 효과
김정곤,강형섭,김진상 한국수의공중보건학회 2003 예방수의학회지 Vol.27 No.2
The present study evaluated the effects of various agents on magnesium sulfate (Mg^(2+))-induced relaxation in aorta and blood pressure lowering in anesthetized guinea pigs. Mg^(2+) inhibited phenylephrine (PE)- or 40 mM KC1-induced sustained contraction of endothelium-intact (+E) guinea pig aortic rings in concentration-dependent manner. In preparations preconstricted with PE or KC1, Mg^(2+)-induced concentration-dependent relaxations. In preparations preconstricted with PE or KCl, Mg^(2+)-induced relaxations were not affected by the removal of endothelium (-E) and by the pretreatment of aortic rings with NO synthase (NOS) inhibitors (L-NAME and LNNA), guanylate cyclase inhibitors (methylene blue and ODQ, adenylate cyclase inhibitor (MDL), K^(+) channel blockers (glibenclamide and tetrabutylammonium), nifedipine or ryanodine. However, Mg^(2+)-induced relaxations were inhibited by Na^(+)-Mg^(2+) exchange inhibitor (imipramine) or removal (or attenuation) of extracellular Ca^(2+) in +E aortic rings. PE-induced contraction was not inhibited by nifedipine. In addition, Mg^(2+)-induced relaxations were inhibited by phospholipase C inhibitor (NCDC) or inositol monophosphatase inhibitor (lithium), but not by protein kinase C inhibitor (staurosporine). In vi패 infusion of Mg^(2+), directly into the femoral veins of guinea pigs, elicited sustained decrease in arterial blood pressure. The Mg^(2+)-lowered blood pressure was attenuated by intravenous administration of imipramine or lithium, but not by methylene blue, indomethacin, tetrabutylammonium nifedipine, LNNA, L-NAME or saponin (as an endothelium removal agent). These results suggest that endothelium independent vasorelaxant effect of Mg^(2+) on aortic ring appear to play important roles on the antihypertensive action in guinea pig, most likely via the inhibitory action of Mg^(2+) on the intracellular C^(2+) involve in PLC-IP pathway and influx (through the Na^(+)-Mg^(2+) exchanger) into the cell in guinea pig aorta.
관류 심장과 심장 세포에서 Insulin에 의한 Mg^(2+) 유리 조절
정창우,강형섭,김진상 한국수의공중보건학회 2002 예방수의학회지 Vol.26 No.3
It is well known that β-adrenergic stimulation increases the intracelluar cAMP concentration through activation of adenylate cyclase (AC) and evokes marked Mg^(2+) release in the heart, liver, and kidney. The goal of this study was to investigate the effect of insulin on isoproterenol (ISO), norepinephrine (NE), forskolin (FOS), cAMP, or dimaprit (DMP) induced Mg^(2+) efflux from the perfused rat or guinea pig heart and isolated myocytes. We hypothesized that insulin would regulate Mg^(2+) efflux induced by AC activators and cAMP analogues because insulin activates phosphodiesterase (PDE) in the hearts. The Mg^(2+) content in the perfusate was significantly higher in the presence than in the absence of insulin. The addition of ISO, NE, FOS, or cAMP to perfused rat or guinea pig heart and isolated myocytes induced a marked Mg^(2+) efflux. These effluxes were inhibited by insulin. The Mg^(2+) efflux could also be induced by DMP, a histamine H2-receptor agonist, in the perfused guinea pig heart and isolatd myocytes. This effect was also inhibited by insulin. In rat heart and myocytes, the histamine H2-receptor agonist had no effect on Mg^(2+) efflux. In conclusion, these data suggest that insulin regulates Mg^(2+) homeostasis and the inhibitory effect of insulin on adrenoceptor-stimulation or AC activation induced Mg^(2+) efflux may occur through a regulation of cAMP pathway in rat and guinea pig hearts.
Kim, Jin Young,Ghee, Jung Yeon,Lim, Sun Woo,Piao, Shang Guo,Chung, Byung Ha,Yoon, Hye Eun,Hwang, Hyeon Seok,Choi, Bum Soon,Kim, Jin,Yang, Chul Woo The Korean Academy of Medical Sciences 2012 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.27 No.2
<P>Sirolimus (SRL) is a promising drug for replacing calcineurin inhibitors. We performed this study to determine the optimal time of conversion from cyclosporine (CsA) to SRL in an experimental model of chronic CsA nephropathy. Three separate studies were performed. In the first study, SRL was given to rats with or without CsA for 4 weeks. In the second study, rats were treated initially with CsA for 1 week, and then switched to SRL (early conversion). In the third study, CsA was given for 4 weeks and then replaced by SRL for 4 weeks treatment of CsA (late conversion). The influence of SRL on CsA-induced renal injury was evaluated by assessing renal function, histopathology (interstitial inflammation and fibrosis), and apoptotic cell death. Combined CsA and SRL treatment significantly impaired renal function, increased apoptosis, and interstitial fibrosis and inflammation compared with CsA or SRL treatment alone. Early conversion to SRL did not change renal function, histopathology, or apoptosis compared with early CsA withdrawal. By contrast, late conversion to SRL significantly aggravated these parameters compared with late CsA withdrawal. In conclusion, early conversion from CsA to SRL is effective in preventing CsA-induced renal injury in a setting of CsA-induced renal injury.</P>
Improvement of gas Transfer by Hemosome
Kim, Gi-Beum,Hong, Chul-Un,Kim, Jin-Shang,Kim, Min-Ho,Kang, Hyung-Sub SAGE Publications 2010 The International journal of artificial organs Vol.33 No.3
<P>Intravascular oxidation is a respiratory assist method used to treat acute respiratory distress syndrome (ARDS). However, intravascular oxidation through higher gas exchange is needed for successful clinical applications. In this study, an attempt was made to improve the gas exchange of an intravascular lung assist device by decreasing the level of damage to the blood through the microencapsulation of hemoglobin. The results showed that a hemosome 0.8 microm in diameter could be produced by microencapsulating the hemoglobin extracted from fresh bovine blood with the phospholipids extracted from egg yolk. The oxygen saturation curve of hemosome was S-shaped, which is similar to that found in normal blood, and the P50 was 24 mmHg. The oxygen saturation in the mixed solution of hemosome and blood at a 1:4 (v/v%) ratio was similar to that of normal blood. The gas exchange of the blood-hemosome mixed solution was more effective than whole blood. Therefore, the hemosome solution is expected to improve oxygen transfer.</P>
Jin Shang Kim,Antonio Scarpa 대한생리학회-대한약리학회 1999 The Korean Journal of Physiology & Pharmacology Vol.3 No.1
<P> Chemically induced hypoxia has been shown to induce a depletion of ATP. Since intracellular free Mg<SUP>2 </SUP>([Mg<SUP>2</SUP>]<SUB>i</SUB>) appears to be tightly regulated following cellular energy depletion, we hypothesized that the increase in [Mg<SUP>2</SUP>]<SUB>i </SUB>would result in Mg<SUP>2 </SUP>extrusion following hormonal stimulation. To determine the relation between Mg<SUP>2</SUP> efflux and cellular energy state in a hypoxic rat heart and isolated myocytes, [Mg<SUP>2</SUP><SUP></SUP>]<SUB>i</SUB>, ATP and Mg<SUP>2 </SUP>content were measured by using mag-fura-2, luciferin-luciferase and atomic absorbance spectrophotometry. Mg<SUP>2</SUP> effluxes were stimulated by norepinephrine (NE) or cAMP analogues, respectively. Mg<SUP>2</SUP> effluxes induced by NE or cAMP were more stimulated in the presence of metabolic inhibitors (MI). Chemical hypoxia with NaCN (2 mM) caused a rapid decrease of cellular ATP within 1 min. Measurement of [Mg<SUP>2</SUP>]<SUB>i </SUB>confirmed that ATP depletion was accompanied by an increase in [Mg<SUP>2</SUP>]<SUB>i</SUB>. No change in Mg<SUP>2</SUP> efflux was observed when cells were incubated with MI. In the presence of MI, the cAMP-induced Mg<SUP>2</SUP> effluxes were inhibited by quinidine, imipramine, and removal of extracellular Na<SUP></SUP>. In addition, after several min of perfusion with Na<SUP></SUP>-free buffer, a large increase in Mg<SUP>2</SUP> efflux occurred when Na<SUP></SUP>-free buffer was switched to 120 mM Na<SUP> </SUP>containing buffer. A similar Mg<SUP>2</SUP> efflux was observed in myocytes. These effluxes were inhibited by quinidine and imipramine. These results indicate that the activation of Mg<SUP>2</SUP> effluxes by hormonal stimulation is directly dependent on intracellular Mg<SUP>2</SUP> contents and that these Mg<SUP>2</SUP> effluxes appear to occur through the Na<SUP></SUP>-dependent Na<SUP></SUP>/Mg<SUP>2</SUP> exchange system during chemical hypoxia.
Kim, Shang-Jin,Zhang, Haifei,Khaliulin, Igor,Choisy, Sté,phanie C.M.,Bond, Richard,Lin, Hua,El Haou, Said,Milnes, James T.,Hancox, Jules C.,Suleiman, M. Saadeh,James, Andrew F. Ovid Technologies Wolters Kluwer -American Heart A 2012 Circulation. Arrhythmia and electrophysiology Vol.5 No.6
<P>Cardiac ATP-sensitive K(+) channels have been suggested to contribute to the adaptive physiological response to metabolic challenge after β-adrenoceptor stimulation. However, an increased atrial K(+)-conductance might be expected to be proarrhythmic. We investigated the effect of ATP-sensitive K(+) channel blockade on the electrophysiological responses to β-adrenoceptor-induced metabolic challenge in intact atria.</P>