• Tuberculosis and Respiratory Diseases
• /
• v.41 no.3
• /
• pp.231-238
• /
• 1994

Backgroud: Since the demonstration of the fact that vascular relaxation by acetylcholine(Ach) results from the release of relaxing factor from the endothelium, the identity and physiology of this endothelium-derived relaxing factor(EDRF) has been the target for many researches. EDRF has been identified as nitric oxide(NO). With the recent evidences that EDRF is an important mediator of vascular tone, there have been increasing interests in defining the role of the EDRF as a potential mediator of hypoxic pulmonary vasoconstriction. But the role of EDRF in modulating the pulmonary circulation is not compeletely clarified. To investigate the endothelium-dependent pulmonary vasodilation and the role of EDRF during hypoxic pulmonary vasoconstriction, we studied the effects of $N^G$-monomethyl-L-arginine(L-NMMA) and L-arginine on the precontracted pulmonary arterial rings of the rat in normoxia and hypoxia. Mothods: The pulmonary arteries of male Sprague Dawley(300~350g) were dissected free of surrounding tissue, and cut into rings. Rings were mounted over fine rigid wires, in organ chambers filled with 20ml of Krebs solution bubbled with 95 percent oxygen and 5 percent carbon dioxide and maintained at $37^{\circ}C$. Changes in isometric tension were recorded with a force transducer(FT.03 Grass, Quincy, USA) Results: 1) Precontraction of rat pulmonry artery with intact endothelium by phenylephrine(PE, $10^{-6}M$) was relaxed completely by acetylcholine(Ach, $10^{-9}-10^{-5}M$) and sodium nitroprusside(SN, $10^{-9}-10^{-5}M$), but relaxing response by Ach in rat pulmonary artery with denuded endothelium was significantly decreased. 2) L-NMMA($10^{-4}M$) pretreatment inhibited Ach($10^{-9}-10^{-5}M$)-induced relaxation, but L-NMMA ($10^{-4}M$) had no effect on relaxation induced by SN($10^{-9}-10^{-5}M$). 3) Pretreatment of the L-arginine($10^{-4}M$) significantly reversed the inhibition of the Ach ($10^{-9}-10^{-5}M$)-induced relaxation caused by L-NMMA($10^{-4}M$) 4) Pulmonary arterial contraction by PE($10^{-6}M$) was stronger in hypoxia than normoxia but relaxing response by Ach($10^{-9}-10^{-5}M$) was decreased, 5) With pretreatment of L-arginine($10^{-4}M$), pulmonary arterial relaxation by Ach($10^{-9}-10^{-5}M$) in hypoxia was reversed to the level of relaxation in normoxia. Conclusion: It is concluded that rat pulmonary arterial relaxation by Ach is dependent on the intact endothelium and is largely mediated by NO. Acute hypoxic pulmonary vasoconstriction is related to the suppression on NO formation in the vascular endothelium.

• Clinical and Experimental Pediatrics
• /
• v.51 no.8
• /
• pp.879-885
• /
• 2008

Purpose : The human lung fibroblast may act as an immunomodulatory cell by providing pro-inflammatory cytokines and chemokines, which are important in airway remodeling. Vascular endothelial growth factor (VEGF) induces mucosal edema and angiogenesis. Thymus and activation regulated chemokine (TARC) induces selective migration of T helper 2 cells. We investigated whether human lung fibroblasts produced VEGF and TARC, and the effects were augmented with the co-culture of fibroblasts and human bronchial smooth muscle cells (HBSMC), and whether dexamethasone can inhibit the proliferation and the release of VEGF in lung fibroblasts. Methods : Human lung fibroblasts were cultured with and without HBSMC, growth-arrested in serum-deprived medium, and pretreated with dexamethasone for 16 hours. After 24-hour stimulation with platelet derived growth factor-BB (PDGF-BB) and/or transforming growth factor-${\beta}$ (TGF-${\beta}$), culture supernatant was harvested for assays of VEGF and TARC. Cell proliferation was assayed using BrdU cell proliferation ELISA kit. Results : 1) The release of VEGF was significantly increased after stimulation with TGF-${\beta}$, and its release was augmented when co-stimulated with PDGF and TGF-${\beta}$. 2) VEGF release induced by PDGF or TGF-${\beta}$ was inhibited by dexamethasone. 3) There was no synergistic effect on the release of VEGF when human lung fibroblasts were co-cultured with HBSMC. 4) Dexamethasone did not suppress human lung fibroblasts proliferations. 5) Neither TGF-${\beta}$ nor PDGF induced TARC release from lung fibroblasts. Conclusion : Human lung fibroblasts may modulate airway remodeling by release of VEGF, but they have no synergistic effects when co-cultured with HBSMC. Dexamethasone suppresses VEGF release, not proliferation of lung fibroblast.

• Journal of Chest Surgery
• /
• v.42 no.4
• /
• pp.540-542
• /
• 2009

Glomus tumor is a distinctive type of perivascular tumor whose cell type is a modified smooth cell that closely resembles the glomus body, and this is where the tumor's name is derived. This kind of neoplasm is a benign and rather uncommon neoplasm that can be found in any part of the body, yet it is most commonly seen in the subungual area. Glomus tumor of the trachea is extremely rare. We present the clinicopathologic findings of a resected glomus tumor of the trachea along with a review of the related literature.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.17 no.2
• /
• pp.461-466
• /
• 2003

The primary mechanism of smooth muscle contraction is phosphorylation of the 20 kDa myosin light chains(LC20) by a myosin light chain kinase(MLCK). Relaxation, then, is generally the result of dephosphorylation of LC20 by myosin phosphatase(MP). Changes in MP activity is one of the important mechanisms in the regulation of Ca2+-sensitivity. Inhibition of MP activity is linked to an increase in phosphorylated myosin light chain(MLC) without an increase in [Ca/sup 2+/]i-levels. It is now generally accepted that Rho-kinase phosphorylates 130 kDa regulatory and myosin binding subunits(M130, MYPT) of MP, which results in an inhibition of MP activity. In addition Rho-kinase can also directly phosphorylate MLC. In the present study, LC20 phosphorylation and MP subunits translocation to the cell membrane were investigated in freshly isolated ferret portal vein smooth muscle single cells treated with PGF2α. We also examined the effect of Y27632(10-5mol/L), Rho-kinase inhibitor, in the MP subunits localization to compare with butanol fraction of Fructus Crataegi in its effect. Butanol fraction of Fructus Crataegi(BFFC; 1㎎/㎖) was more effective in PGF2α induced contraction than those of phenylephrine in its vasodilation effect. It significantly(P<0.05) dephosphorylated the LC20 at time indicated. In addition, the dissociation of subunits are inhibited by BFCF treatment. The results indicate that, in the smooth muscle cells, the relaxation effect of BFFC is associated with increase of MP activity based on inhibition of dissociation of the catalytic and targeting subunits of the phosphatase, and thus decrease the sensitivity of LC20 phosphorylation for Ca/sup 2+/.

• Tuberculosis and Respiratory Diseases
• /
• v.50 no.2
• /
• pp.245-251
• /
• 2001

Recently we have experienced one case of pulmonary lymphangioleiomyomatosis(LAM). A 49 year-old woman visited the outpatient department complaining of longstanding dyspnea, which was aggravated by exercise. Although the chest PA film showed nothing more than a slight increase in interstitial marking, a lung HRCT revealed multiple cystic lesions of a similar size that were scattered through out the whole field in both lungs. An abdominal CT detected an angiomyolipoma located in the midbody of the left kidney. Video-assisted thoracic surgery(VATS) was performed for the pathologic diagnosis. On gross examination of the biopsy lung, a pulmonary LAM was confirmed by a finding of smooth muscle proliferation in the interstitum of the lung. After the final diagnosis, oral medroxyprogesterone was prescribed and she is presently in a stable condition.

• YAKHAK HOEJI
• /
• v.41 no.6
• /
• pp.782-788
• /
• 1997

This study was designed to characterize glucose-enhancing effects on endotoxin-induced prostaglandin production in primary cultured rat vascular smooth muscle cells (VSMC). High glucose treatment significantly augmented prostaglandin (PG) synthesis in lipopolysaccharide (LPS)-stimulated VSMC and this effect was maximal at the concentration of 4mg/ml. It has been reported that increases in glucose metabolism through sorbitol pathway could alter the cytosolic $NADH/NAD^+$ ratio and this change favors de novo synthesis of diacylglycerol (DAG) and, in turn. Results in the activation of protein kinase C (PKC) in vascular tissues. Protein kinase C (PKC) inhibitors, staurosporin and H7, blocked the glucose enhancing effect, and DAG, a PKC activator, significantly increased the PG production stimuated by LPS. Sodium pyruvate, which can reverse the alteration in cytosolic NADH/NAD+ ratio, reduced the high glucose effect on PG production. And also, zopolrestat, a strong aldose reductase inhibitor, almost completely blocked the augmentation effect of glucose on PG synthesis. Arachidonic acid release was significantly increased in high glucose treated group, which implied the increase in $PLA_2$ activity was associated with glucose enhancing effect. Metabloic, labeling study clearly showed that de novo synthesis of prostaglandin H synthase-2 (PGHS-2) is greatly increased in high glucose treated group and this was mitigated by the treatment of zopolrestat. Taken together, the activation of PKC through sorbitol pathway increased the activities of $PLA_2$ and PGHS which resulted in the augmentation in LPS-induced PG production in high glucose treated VSMC.

• Journal of Chest Surgery
• /
• v.32 no.12
• /
• pp.1093-1099
• /
• 1999

배경 : 류마티스성 승모판막 폐쇄부전증과 퇴행성 승모판막 폐쇄부전증에서 승모판막 성형술의 결과와 비교하여 류마티스성 승모판막 폐쇄부전증에서도 승모팍막성형술이 적합한 치료방법이 될 수 있는지를 알아보았다. 대상 및 방법 : 95년 1월부터 98년 12월 까지 승모판막 성형술을 시행받은 184명의 환자중에서 류마티스성 승모판막 폐쇄부전증 49례(1군)의 퇴행성 승모판막 폐쇄부전증 78례(2군)를 대상으로 하였다. 평균연령은 1군이 36.3$\pm$14.6(16-74세) 2군은 52.5$\pm$13.4(14-77)세였다 총 추적 관찰기간은 1군이 72.2인년 2군이77.2인년이었다 두군에서 수술후와 수술후 6개월 1년 및 이후 1년 단위로 주기적인 심초음파를 시행하였고 이를 통계적 검정하였다. 결과 : 두 군간에 수술전 혈류역학적인 차이를 보이지 않았고 수술전 평균 승모판막 폐쇄 부전의 정도는 1군이 3.0$\pm$0.4, 2군이 3.9$\pm$0.3였으나 수술후 추적 관찰에서 각각 0.9$\pm$0.9와 0.8$\pm$0.7정도의 양호한 판막 성형술의 결과를 보였고 승모판막 면적의 변화나 승모판막에서의 평균압력차이 등 혈류역학적인 결과에도 차이를 보이고 있지 않았다 수술조기 사망과 후기 사망은 없었으며 재수술율은 1군이 인년대비 1.4% 2군이 인년대비 2.6%였고 색전발생율은 1군이 인년대비 2.8% 2군이 1.3%였다. 심내막염발생은 1군에서만 1례있었으며 상기 결과들에서 두군간에 의미있는 차이를 보이고 있지는 않았다 결론 : 향후 장기적인 추적 관찰이 필요하나 중기 성적에서 승모판막 성형술이 류마티스성 승모판막 폐쇄 부전증에서도 효과적인 치료방법임을 알수 있었다.다 출생후 폐포막의 FN의 활성은 출생후 5일 및 7일에 최고주에 달했다. 출생직후 1-2일경에 혈관의 조직내 FN의 활성이 양성을 나타내지만 3일이후 활성이감소되었다. 폐포대식세포내 FN의 활성은 출생후 증가되었다. 폐조직내 소기관지의 FN의 활성은 출생후 완만하게 상승되었다. 큰 폐포세포는 출생 1-3일에 일정량의 FN 반응이 세포질과 미세융모내에 관찰되었다. 결론 : 이상과 같은 결과로 흰쥐의 폐포의 분화과정이 계속되는 출생후 폐에서 FN의 분비는 7일이내에 성숙흰쥐의 폐포내 반응과 비슷한 반응으르 보이며 이때 폐의 실질조직은 분화가 거의 완료되었을 것으로 사료되었고 큰 폐포세포에서도 FN이 분비되는 것으로 결론지울수 있다.X>에서 $1,332.75{\mu}g/mL$으로 최 대값을 나타내었으며, 추출시간 4.24시간 및 시료에 대한 용매비 9.71 mL/g에서 가장 높게 나타났다. 추출온도가 높고, 추출시간이 증가할수록 총 polyphenol 함량이 증가하는 경향을 나타내었다. Gallic acid 함량은 $65.84^{\circ}C$에서 $30.51{\mu}g/mL$으로 최대값을 나타내 었으며, 추출시간 1.65시간 및 시료에 대한 용매비 17.17mL/g에서 가장 높은 추출율을 보였다. Gallic acid 함량에 대한 추출조건의 영향은 추출시간과 용매비에 영향을 받는 것으로 나타났으며, 설정된 범위 내에서 온도에 대한 영향은 거의 나타나지 않는 것으로 나타났다. 실험연구가 더 필요하리라 본다. 혈액학적 변화를 유도하고 환자의 연령, 혈소판 수, 대동맥 차단 시간, 체외 순환 시간, 술후 PT 및 aPTT와 같은 다인적 상황들이 술후 출혈에 영향을 미친다는 점들을 시사하고

• The Korean Journal of Physiology and Pharmacology
• /
• v.1 no.6
• /
• pp.759-767
• /
• 1997

In the present study, we characterized the non-vascular smooth muscle relaxant effects of a novel benzoyran derivative ,SKP-450 (2-[2'(1',3'-dioxolone)-2-methyl-4- (2'-oxo-1'-pyrrolidinyl) -6-nitro-2H-1- benzopyran) and its metabolite, SKP-310, in comparison with levcromakalim (LCRK). In the rat stomach fundus, the spontaneous motility stimulated by $10^{-6.5}\;M$ bethanechol was completely eliminated not only by $10^{-7}\;M$ SKP-450 but also by $10^{-6}\;M$ LCRK, which were blocked by $10^{-6}\;M$ glibenclamide. The inhibitory effect of SKP-450 $pD_2,\;3.94{\pm}0.66)$ was much less than LCRK $(pD2,\;5.73{\pm}0.38,\;p<0.05)$. In the bethanechol $(10{-6.5 }\;M)-stimulated$ urinary bladder, the tonus was decreased in association with elimination of spontaneous motility by $10^{-7}\;M$ M SKP-450 and $10^{-6}\;M\;LCRK\;(pD2,\;6.77{\pm}0.06)\;(P<0.05)$, which were inhibitable by $10^{-6}\;M$ glibenclamide. The inhibitory effect of SKP-450 $(pD2,\;7.66{\pm}0.05)$ was significantly more potent than that of LCRK $(pD2,\;6.77{\pm}0.06,\;p<0.05)$. In the rat uterus stimulated by $PGF_{2\alpha}\;(10^{-7}\;M)$, both increased tonus and spontaneous motility were eliminated by $10^{-6}\;M$ LCRK with slight depression of the tonus, but not by SKP-450 $(10^{-5}\;M)$. The stimulated trachea of guinea-pig by $10^{-6.5}\;M$ bethanechol was moderately suppressed by SKP-450 $(10^{-6}{sim}10^{-5}\;M)$ but little by SKP-310. In association with the relaxant effects, SKP-450 $(10^{-6}\;M)$ and LCRK $(10^{-5}\;M)$ caused a significant stimulation of the $^{86}Rb$ efflux from rat urinary bladder and stomach fundus, which were antagonized by $10^{-5}\;M$ glibenclamide, whereas the $K^+$ channel openers could not exert a stimulation of the $^{86}Rb$ efflux from rat uterus. In conclusion, it is suggested that SKP-450 exerts potent relaxant effects on the urinary bladder detrusor muscle and duodenum, whereas it shows much less effect on stomach fundus and uterus as contrasted to LCRK.

• The Korean Journal of Pharmacology
• /
• v.26 no.2
• /
• pp.127-133
• /
• 1990

Dibutyryl-cyclic AMP (db-cAMP) and forskolin were used to investigate vasodilating mechanism of cAMP in rabbit aorta. Db-cAMP and forskolin inhibited the development of contractile tension induced by norepinephrine (NE) concentration-dependently. However, high $K{^+}-induced$ contractile tension was inhibited less effectively by db-cAMP and forskolin. Db-cAMP and forskolin inhibited $^{45}Ca^{2+}$ uptake increased by NE. Forskolin seemed to inhibit $^{45}Ca^{2+}$ uptake increased by high $K{^+}$, but this inhibition was not significant statistically. Db-cAMP inhibited $Ca^{2+}-transient$ contraction by NE in $Ca^{2+}-free$ solution. In conclusion, it seems that cAMP blocks $Ca^{2+}$ influx through receptor operated $Ca^{2+}$ channels (ROCs), but that the effect of cAMP on $Ca^{2+}$ influx through voltage gated $Ca^{2+}$ channels (VGCs) is not clear in this experiment. Furthermore, cAMP is likely to inhibit calcium release from the intracellular stores.

• Journal of Chest Surgery
• /
• v.36 no.12
• /
• pp.970-974
• /
• 2003

There has been an improvement in the prognosis of tumor thrombi invading the inferior vena cava(IVC) and the right atrium(RA) of renal cell carcinoma with radical nephrectomy and tumor thrombectomy with the aid of cardiopulmonary bypass in the last 10 years. A 30 year old woman was diagnosed with right renal tumor with tumor thrombi invading the right renal vein and the IVC above the right renal vein to the RA. She received radical nephrectomy and removal of tumor thrombi in the infrarenal IVC under hypothermic total circulatory arrest using the cardiopulmonary bypass. The tumor recurred 12 months after the initial operation, she received a second operation for tumor removal from the retroperitoneum, suprarenal IVC, and RA. She died 11 months after the second operation due to lung metastases and recurred hepatic vein tumor extended to the RA and right ventricle.