• Journal of Chest Surgery
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• 제48권5호
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• pp.371-374
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• 2015

We present a rare case of a patient with aortoiliac occlusive disease on the background of type A crossed renal ectopia, for whom open surgical intervention was required. Aortic exposure in patients with concomitant crossed renal ectopia can present technical challenges to the vascular surgeon. The knowledge of variations in the ectopic renal blood supply is of paramount importance when performing surgery to treat this condition and affects the choice of surgical exposure. We present and discuss the operative details of our patient and outline an approach to this subset of patients.

• Journal of Chest Surgery
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• 제20권2호
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• pp.261-269
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• 1987

From 1976 through 1986, authors have experienced 127 cases of peripheral vascular surgery which had been done in this department. There were 29 cases of atherosclerosis obliterances including 7 Leriche syndrome, 32 Buerger`s diseases, 25 arterial thromboembolisms, 21 vascular injuries, 2 peripheral arterial aneurysms, 2 renovascular hypertensions, 1 congenital A-V malformation, 13 varicose vein of lower extremities, and 2 Jugular venous ectasia. Cases with vena caval disease and aortic disease were excluded. The mean age of ASO and Buerger`s disease was 56.1 yrs, 33.8 yrs respectively. The male to female ratio showed marked male preponderance [27:2, and 30:2], and almost every male patient was smoker. The indication of operation was similar in both disease entities. The method of operation for ASO were bypass procedure [17], thromboendarterectomy [6], and lumbar sympathectomy [5], and for Buerger`s disease were mainly sympathectomy and few bypass procedures and amputations. Seventeen patients with ASO were followed from 3 to 75 month and overall patency rate for bypass or endarterectomy in one and two months and 2 1/2 yr were 93%, 87%, and 31% respectively. Post operatively patient`s symptoms was relieved or alleviated in almost ASO patients, and about 60% of Buerger`s disease. We concluded that in patient with ischemic limb, we must revascularized aggressively for symptomatic relief. And choice of graft for bypass procedure was to be evaluated further.

• 생명과학회지
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• 제32권7호
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• pp.567-577
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• 2022

최근 인구 고령화로 인해 허혈성 심장질환, 허혈성 뇌졸중, 말초 동맥 질환 등의 허혈성 혈관질환의 유병률이 지속적으로 증가하고 있다. 허혈성 질환에 대한 현재 표준화된 치료법은 약물 요법 및 수술을 통한 재관류요법이다. 재관류요법은 손상된 동맥의 기능을 회복시킬 수 있지만 허혈로 인해 손상된 주변 조직의 기능 회복에 있어 효율적이지 않다. 그러므로 허혈 질병을 안전하고 효과적으로 치료하고 주변 조직의 기능을 회복시킬 수 있는 새로운 치료전략의 개발이 필요하다. 이러한 한계를 극복하기 위해 손상된 부위를 재생하는 줄기세포 기반 치료가 허혈성 혈관질환의 유망한 전략으로 연구되어 왔다. 다양한 조직에서 분리할 수 있는 중간엽줄기세포(MSC)는 면역 조절, 혈관 신생 촉진 및 다양한 관련 인자의 분비를 통해 손상된 조직을 재생함으로써 허혈성 질환의 치료에 유망한 것으로 나타났다. 또한, 줄기세포 치료 효과를 높이기 위해 3D 배양법을 이용하거나 세포 프라이밍(Cell Priming)과 같은 MSC 기능을 강화하여 이식 효율을 높이는 새로운 접근법이 연구되고 있다. 이 논문에서는 MSC를 허혈성 질환 치료에 사용하는 다양한 전략을 제공하고 허혈성 부위에서 MSC의 분화(Differentiation), 증식(Proliferation) 및 생착(Engraftment)과 같은 이식의 문제에 대해 논의한다.

• 대한약리학회지
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• 제11권1호
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• pp.33-38
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• 1975

말정혈관확장제(末精血管擴張劑)인 Ethaverine의 임상효과(임상(臨床效果)는 말초동맥질환(末梢動脈疾患)을 갖인 29명(名)의 당뇨질환자(糖尿疾患者)를 대상으로 이중맹검(二重盲檢) 비교차(非交叉) 방법(方法)에 의(依)하여 연구검토(硏究檢討)하였다. 임상적(臨床的)인 개선(改善)은 간헐성파행증(間歇性跛行症)의 발생빈도(發生頻度)를 포함하는 환노(患老)들의 병역(病歷)으로부터 평가(評價)하였다. Ethaverine을 사주(四週) 치료후(治療後)는 임상증상(臨床症狀)을 개선(改善)하는데 있어 위약(僞藥)에 비(比)하여 효과가 없었다. 어째든 간에 Ethaverine은 위약(僞藥)보다는 혈관확장제(血管擴張劑)로서 효력이 있었다. Ethaverine에 의(依)하여 유발(誘發)되는 혈관확장제(血管擴張劑)의 성질(性質)은 alcohol의 그것과 유사하였다. 말초혈관확장제(末梢血管擴張劑)를 연구(硏究)하는 새로운 임상적(臨床的) 방법(方法)을 제시(提示)하였다. 하지(下肢)의 말초혈관(末梢血管) 동맥질환(動脈疾患)의 임상증상(臨床症狀)은 촉맥강도(觸脈强度)의 감소냉감(減少冷感) 및 피부(皮膚)의 변색(變色)등을 들 수 있다. 간헐성파행증(間歇性跛行症)도 수반하는 수가 있다. 혈관조직(血管組織)에 있어서의 병변(病變)이 이같은 증상(症狀)에 선행(先行)하여 일어나며 위중(危重)한 혈관부전(血管不全)의 입증(立證)은 혈관확장제료법(血管擴張劑療法) 또는 외과적(外科的) 처치(處置)를 택하는데 있어서의 결정적(決定的)인 요인(要因)이 된다. 만성 말초동맥질환(末梢動脈疾患)이 있는 술후환자(術後患者)들도 차후혈관확장제(次後血管擴張劑)의 치료(治療)를 받아야한다. 임상보고((臨床報告)에 의(依)하면 말초혈관확장제(末梢血管擴張劑)는 폐새성(閉塞性) 혈관질환(血管疾患)에 대(對)해서 보다는 혈관경련성(血管痙攣性) 말초혈관장해(末梢血管障害)에 대해서 보다 유효하며 비교적 큰 혈관상(血管床)보다는 작은 모세혈관상(毛細血管床) 일때의 혈관(血管)이 가장 잘 감응(感應)한다고 한다. 최근(最近)에 이르러 말초혈관확장제(末梢血管擴張劑)의 임상(臨床)효과는 수많은 임상연구가(臨床硏究家)들 및 임상의(臨床醫)들의 연구대상(硏究對象)이 되고있다. 본연구(本硏究)에서 연구자(硏究者)들은 혈관경련성말초동맥질환(血管痙攣性末梢動脈疾患)을 갖인 환자(患者)들에 대(對)한 말초혈관확장제(末梢血管擴張劑)로써의 Ethaverine HCl의 임상(臨床)효과를 재평가(再評價)하였다. Ethaverine은 각종임상시험결과(各種臨床試驗結果)에 의(依)하면 항경련제(抗痙攣劑)로서는 papaverine 보다도 2배(倍) 내지 4배(倍)정도 그 약효가 강력(强力)하다고 한다.

• The Korean Journal of Pain
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• 제34권4호
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• pp.471-478
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• 2021

Background: The effect of lumbar spinal stenosis (LSS) and peripheral vascular disease (PVD), which occurs with similar degenerative conditions, when seen together, has not been studied. The aim of this study is to examine and compare the relationship between pain, balance, disability, fear of falling, and kinesiophobia in LSS patients with intermittent vascular claudication (IVC). Methods: Seventy-two patients diagnosed with LSS using magnetic resonance imaging participated in this study. Thirty-five patients with IVC symptoms and showing vascular lesions by lower extremity venous and arterial Doppler ultrasonography imaging were included in the IVC-LSS group. The pain, static balance, dynamic balance, disability, fear of falling, and kinesiophobia were evaluated using the numeric rating scale, single leg stance test, Time Up and Go (TUG), the Oswestry Disability Index (ODI), Fall Efficacy Scale-International (FES-I), and Tampa Scale for Kinesiophobia (TSK), respectively. Results: Age and female sex were found to be higher in the IVC-LSS group (P = 0.024; P = 0.012). The IVC-LSS group had a shorter single leg stance time and TUG test duration, pain intensity, ODI, FES-I, and TSK scores were higher than patients with LSS (P = 0.001). Pain, fear of falling, and kinesiophobia were moderately correlated with disability in the IVC-LSS group. No relationship was found between pain and dynamic balance. Also, the pain was not related to kinesiophobia. Conclusions: The findings indicated that IVC causes loss of balance and an increase in pain, disability, fear of falling, and kinesophobia in patients with LSS.

• Tuberculosis and Respiratory Diseases
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• 제62권3호
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• pp.211-216
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• 2007

저자들은 평소 건강하게 지내던62세 남자 환자에게서 발생한 우하지 심부정맥혈전증과 폐색전증의 원인으로 과호모시스테인혈증이 독립적인 위험인자로 작용한 것으로 생각되는 1예를 경험하였기에 문헌고찰과 함께 보고한다.

• Tuberculosis and Respiratory Diseases
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• 제47권2호
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• pp.239-246
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• 1999

저자등은 우하지 동통 및 객혈을 주소로 내원하여 우하지 심부정맥혈전증, 폐색전증 및 뇌정맥혈전증으로 환자에서 과호모시틴혈증이 다발성 혈전증의 원인이었던 1예를 경험 하였기에 문헌고찰과 함께 보고하는 바이다.

• Toxicological Research
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• 제16권1호
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• pp.67-71
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• 2000

It has been demonstrated that the injection of naked DNA expressing vascular endothelial growth factor 165(VEGFl165) to the affected area can provide significant therapeutic effects on peripherol artery occlusive diseases. Success with this type of gene therapy highly depends on the quality of the vector delivering the therapeutic gene, especially in terms of the level and duration of gene expression in the localized area. We have recently developed a vector expressing VEGF165(pCK-VEGF) for the treatment of peripheral artery occulsive diseases and demonstrated high level expression of VEGF165 in mouse skeletal muscle. This study was designed to assess the acute toxicity of intramuscularly injected pCK-VEGF in BALB/c mice and Sprague-Dawely rats. There was no evidence of any changes in clinical signs, body weights, or gross pathological signs. We estimate LD50 values of pCK-VEGF higher than 50mg/kg in mice and 20 mg/kg in rats by intramuscular injection.

• Archives of Pharmacal Research
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• 제28권6호
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• pp.709-715
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• 2005

The purpose of this study was to investigate the effect of atropine on peripheral vasodilation and the mechanisms involved. The isometric tension of rat mesenteric artery rings was recorded in vitro on a myograph. The results showed that atropine, at concentrations greater than 1$\mu$M, relaxed the noradrenalin (NA)-precontracted rat mesenteric artery in a concentration-dependent manner. Atropine-induced vasodilatation was mediated, in part, by an endothelium-dependent mechanism, to which endothelium-derived hyperpolarizing factor may contribute. Atropine was able to shift the NA-induced concentration-response curve to the right, in a non-parallel manner, suggesting the mechanism of atropine was not mediated via the ${\alpha}_1$-adrenoreceptor. The $\beta$-adrenoreceptor and ATP sensitive potassium channel, a voltage dependent calcium channel, were not involved in the vasodilatation. However, atropine inhibited the contraction derived from NA and $CaCl_2$ in $Ca^{2+}$-free medium, in a concentration dependent manner, indicating the vasodilatation was related to the inhibition of extracellular $Ca^{2+}$ influx through the receptor-operated calcium channels and intracellular $Ca^{2+}$ release from the $Ca^{2+}$ store. Atropine had no effect on the caffeine-induced contraction in the artery segments, indicating the inhibition of intracellular $Ca^{2+}$ release as a result of atropine most likely occurs via the IP3 pathway rather than the ryanodine receptors. Our results suggest that atropine-induced vasodilatation is mainly from artery smooth muscle cells due to inhibition of the receptor-mediated $Ca^{2+}$-influx and $Ca^{2+}$-release, and partly from the endothelium mediated by EDHF.

• BMB Reports
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• 제46권7호
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• pp.352-357
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• 2013

Atherosclerosis, which manifests as acute coronary syndrome, stroke, and peripheral arterial diseases, is a chronic inflammatory disease of the arterial wall. Prunella vulgaris, a perennial herb with a worldwide distribution, has been used as a traditional medicine in inflammatory disease. Here, we investigated the effects of P. vulgaris ethanol extract on TNF-${\alpha}$-induced inflammatory responses in human aortic smooth muscle cells (HASMCs). We found that P. vulgaris ethanol extract inhibited adhesion of monocyte/macrophage-like THP-1 cells to activated HASMCs. It also decreased expression of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and ROS, No production in TNF-${\alpha}$-induced HASMCs and reduced NF-${\kappa}B$ activation. Furthermore, P. vulgaris extract suppressed TNF-${\alpha}$-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK). These results demonstrate that P. vulgaris possesses anti-inflammatory properties and can regulate TNF-${\alpha}$-induced expression of adhesion molecules by inhibiting the p38 MAPK/ERK signaling pathway.