Magnesium에 의한 흰쥐 대동맥 이완

오성숙,이상우,강형섭,김진상,Oh, Sung-suck,Lee, Sang-woo,Kang, Hyung-sub,Kim, Jin-shang 대한수의학회 2003 大韓獸醫學會誌 Vol.43 No.3

Magnesium ion ($Mg^{2+}$) is a vasodilator, but little is known about its mechanism of action on vascular system. In vitro, extracellular magnesium sulfate ($MgSO_4$) produced relaxation in phenylephrine (PE) or high KCl-precontracted isolated rat thorocic aorta with (+E) or without (-E) endothelium in a concentration-dependent manner. The $MgSO_4$-induced relaxations were not affected by removal of the endothelium. Pretreatment of +E or -E aortic rings with nitric oxide synthase (NOS) inhibitors ($20{\mu}M$ L-NNA, $100{\mu}M$ L-NAME, $1{\mu}M$ dexamethasone and $400{\mu}M$ aminoguanidine), cyclooxygenase inhibitor ($10{\mu}M$ indomethacin), guanylate cyclase inhibitors ($10{\mu}M$ ODQ and $30{\mu}M$ methylene blue) and $Ca^{2+}$ transport blocker ($10{\mu}M$ ryanodine) did not affect the relaxant effects of $MgSO_4$. $Ca^{2+}$ channel blockers ($0.3{\mu}M$ nifedipine and $0.5{\mu}M$ veropamil) completely decreased the relaxant effects of $MgSO_4$ in +E and -E aortic rings. However, in $Ca^{2+}$-free medium, $MgSO_4$-induced vasorelaxation was potentiated and this response was inhibited by nifedipine. Protein kinase C (PKC) inhibitors ($1.0{\mu}M$ staurosporine, $0.5{\mu}M$ tamoxifen and $0.1{\mu}M$ H7) or PLC inhibitor ($100{\mu}M$ NCDC) markedly decreased the relaxant effects of $MgSO_4$ in +E and -E aortic rings. In vivo, infusion of $MgSO_4$ elicited significant decreases in arterial blood pressure. After intravenous injection of nifedipine ($150{\mu}g/kg$) and NCDC (3 mg/kg), infusion of $MgSO_4$ inhibited the $MgSO_4$-lowered blood pressure markedly. However, after introvenous injection of saponin (15 mg/kg), L-NNA (3 mg/kg), L-NAME (5 mg/kg), indomethacin (2 mg/kg), methylene blue (15 mg/kg) and aminoguanidine (10 mg/kg) failed to inhibit it. These results suggest that endothelial NQ-cGMP or prostaglandin pathway is not involved in vasorelaxant or hypotensive action of $Mg^{2+}$ and that these effects are due to the inhibitory action of $Mg^{2+}$ on the $Ca^{2+}$ channel or PLC-PKC pathway, and are due to the competitive influx of $Mg^{2+}$ and $Ca^{2+}$ through the $Ca^{2+}$ channel.

멜라토닌이 랫트에서 심박수 및 혈압에 미치는 효과 I. 혈압에 미치는 효과

오성숙,김상진,김진상,Oh, Sung-suck,Kim, Shang-jin,Kim, Jin-shang 대한수의학회 2001 大韓獸醫學會誌 Vol.41 No.3

In recent years, experimental evidence have been suggested that melatonin has either contractive or relaxing effects on the vascular smooth muscle in vitro. But the effect of melatonin on the cardiovascular system in vivo had been emphasized about the hypotensive effect. In this work, we found not only hypotensive effect but also hypertensive effect of melatonin in rats and attempted to determine the mechanism of these effects elicited by melatonin. Regadless of concentration, melatonin(0.002~5 mg/kg) produced increase in mean blood pressure (MBP) in 36% (54/150 cases) and decrease in mean blood pressure in 64%(96/150 cases). As a whole melatonin caused an increase or a decrease in MBP without compensatory decrease or increase in heart rate. The melatonin-induced hypertension was abolished by the pretreatment of phenoxybenzamine, a ${\alpha}$-adrenoceptor antagoninst. The melatonin-induced hypotension was abolished by the pretreatment of propranolol, a ${\beta}$-adrenoceptor antagonist, ODQ, a NO-sensitive guanylate cyclase inhibitor, or nifedipine, a L-type $Ca^{2+}$ channel blocker, but not by bilateral cervical vagotomy. The results indicate that melatonin-induced hypertension may be related to ${\alpha}$-adrenoceptor stimulation and melatonin-indued hypotension may be related to ${\beta}$-adrenoceptor stimulation, inhibition of $Ca^{2+}$ channel and/or activation of guanylate cyclase.

흰쥐에서 ATP 결핍에 의한 혈중 Mg²⁺ 농도조절

김상진,백성수,심소연,오성숙,김진상,Kim, Shang-jin,Baek, Sung-soo,Shim, So-yeon,Oh, Sung-suck,Kim, Jin-shang 대한수의학회 2000 大韓獸醫學會誌 Vol.40 No.2

Since intracellular free $Mg^{2+}$ ($[Mg^{2+}]_i$) appears to be tightly regulated following cellular energy depletion, we hypothesized that the increase in $[Mg^{2+}]_i$ would result in $Mg^{2+}$ extrusion into circulation. Extracellualr $Mg^{2+}$ contents ($[Mg^{2+}]_o$) were measured in rat erythrocytes, the perfused heart and liver, and plasma in the anesthetized rat. Animals were injected intraperitoneally with sodium nitrite ($NaNO_2$) and plasma $Mg^{2+}$ was measured after the injection and then 10 and 20 minutes later. An increase in circulating (plasma) $Mg^{2+}$ ($[Mg^{2+}]_c$) and methemoglobin was observed in animals injected with $NaNO_2$ (30 mg/Kg). The time course of the effects demonstrated that $[Mg^{2+}]_c$ and methemoglobin continued to increase 10 minutes after the $NaNO_2$ injection. Under these conditions, there was a sustained increase in $[Mg^{2+}]_c$, but not in methemoglobin, which was inhibited by pretreatment with potassium cyanide (KCN, 4 mg/Kg), indicating that an increase in $[Mg^{2+}]_c$ was accompanied by ATP depletion. Injection of rotenone (0.9 mg/Kg) or 2,4-dinitrophenol (15 mg/Kg) also induced an increase in $[Mg^{2+}]_c$. Reduced respiration rate from 100/min to 10/min during 30 minutes also caused a time-dependent rise in $[Mg^{2+}]_c$. These increase in $[Mg^{2+}]_c$ were inhibited by pretreatment with KCN. In addition, ATP depletion by $NaNO_2$ or KCN sustainedly increased the $[Mg^{2+}]_o$ in rat erythrocytes. $Mg^{2+}$ efflux was stimulated by KCN in the perfused heart and liver, but not by $NaNO_2$. These results suggest that the activation of $Mg^{2+}$ effluxes into the circulation is directly dependent on the ATP depletion-induced increase in $[Mg^{2+}]_i$ and heart, liver and erythrocytes have a major pool of $Mg^{2+}$ that can be mobilized upon cellular energy state.

인천지역 식중독 환자에서 분리한 병원성 세균의 항생제 내성 및 다제 내성 양상

허명제 ( Myung Je Huh ),오성숙 ( Sung Suck Oh ),장재선 ( Jae Seon Jang ) 한국식품영양학회 2013 韓國食品營養學會誌 Vol.26 No.1

인천지역 식중독 환자에서 분리 배양된 병원성 세균 210주에 대한 항생제 내성시험 결과, tetracycline(43.8%)이 가장 높고, 이어서 ampicillin(34.8%), nalidixic acid(23.8%), sulfamethoxazole/trimethoprim와 chloramphenicol(12.4%), ampicillin/sulbactam(11.4%) 순을 나타냈다. 균주별 항생제 내성결과 살모넬라균은 ampicillin(37.5%)이 가장 높았고, 그 다음 nalidixic acid(30.7%), tetracycline(22.7%), chloramphenicol(20.5%), ampicillin/sulbactam (13.6%) 순을 나타냈다. 병원성 대장균은 tetracycline(59.0%)이 가장 높고, 그 다음 ampicillin(32.8%), nalidixic acid와 sulfamethoxazole/trimethoprim(18.9%), cephalothin(13.1%) 순을 나타냈다. 분리 동정된 병원성 세균의 항생제 다제 내성률은 10개 항생제에 대하여 1제(26.2%, 55/210주), 2제(9.0%, 19/210주), 3제(9.5, 20/210주) 내성 균주의 비율이 높은 반면, 9제 이상에 내성을 나타낸 균주(0.5%, 2/210주)는 적었다. 10개 항생제에 대하여 살모넬라균의 다제 내성율은 1제(10.2%, 9/88주), 2제(13.6%, 12/88주), 3제(11.4%, 10/88주) 내성 균주 비율이 높고, 4제 이상의 내성을 보인 것은 15.9%(14/88주)로 나타났다. 병원성 대장균은 1제(37.7%, 46/122주)가 높고, 2제(5.7%, 7/122주), 3제(8.2%, 10/122주) 4제 이상의 항생제 내성을 보인 것은 22.1%(14/88주)였다. Antimicrobial resistance and multi-drug resistance patterns have been carried out on total of 210 isolated of Salmonella spp. and pathogenic E. coli isolated from food poisoning patients on January through December 2012 in Incheon, Korea. The highest percentage of antibiotics resistance was found to the following antimicrobial agents: tetracycline 43.8%, ampicillin 34.8%, nalidixic acid 23.8%, sulfamethoxazole/trimethoprim and chloramphenicol 12.4%, and ampicillin/sulbactam 11.4%. The highest percentage of resistance was 37.5% to ampicillin for Salmonella spp. and 59.0% to tetracycline for pathogenic E. coli. Overall the multidrug resistance rates of 1 drug was 26.2%, 2 drugs 9.0%, 3 drugs 9.5%, 4 drugs 7.1%, and 5 or more drugs 12.46%. The multi-drug (MDR) strains to four or more antimicrobial agents among the resistant organisms were quite high: 15.9% and 22.1% for Salmonella spp. and pathogenic E. coli, respectively. The study implies that limitation of unnecessary medication use is pertinent in order to maintaining the efficacy of drugs.

Nitrovasodilators에 의한 대동맥 이완 특성

허민,오성숙,강형섭,최은영,김진상 한국수의공중보건학회 2002 예방수의학회지 Vol.26 No.3

The vascular effects of sodium nitroprusside (SNP) and sodium nitrite (SN) were investigated in endothelium-intact (+E) or endothelium-denuded ( E) rat aortic rings precontracted with phenylephrine (PE) or 70 mM KCl. Nitrovasodilators induced a concentration-dependent relaxation in aorta precontracted with either PE or KCl. SNP or SN-induced relaxation was significantly greater in -E and PE-stimulated strips than +E and KCl-stimulated strips. SNP -induced relaxation was significantly augmented by nitric oxide synthase inhibitors, N^(G)-nitro-L-arginine (L-NNA), N^(G)-nitro-L-arginine methyl ester(L-NAME), or aminoguanidine in +E strips, this augmentation was markedly inhibited by 1H-[1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor. SNP or SN-induced relaxation was also augmented by zaprinast, a selective inhibitor of cGMP-phosphodiesterase (PDE), or Ro 20-1724, a selective inhibitor of cAMP-PDE in E strips. This augmentation was markedly inhibited by ODQ. This results suggest that the impairment of endothelium leads to altered responses to nitrovasodilators and that it may be due to a modification in the adenylate and guanylate cyclase-cGMP system.