• Title/Summary/Keyword: 혈관성

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Arginine Vasopressin Therapy of Vasodilatory Shock after Cardiopulmonary Bypass - Two cases- (체외 순환 후 발생한 혈관 확장성 쇼크에 대한 바소프레신 투여요법 -2예 보고-)

  • Ahn Young-Chan;Park Chul-Hyun;Lee Jae-ik;Jeon Yang-Bin;Park Kook-Yang
    • Journal of Chest Surgery
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    • v.39 no.1 s.258
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    • pp.60-63
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    • 2006
  • Vasodilatory shock has been implicated in life-threatening complications after cardiac surgery. This syndrome may result from the vasopressin deficiency following cardiopulmonary bypass (CPB), which do not respond to fluids or usual intravenous inotropes. We used arginine-vasopressin in adults with vasodilatory shock coming on cardiopulmonary bypass. Therefore, we report these cases with a review of articles.

Effects of Cyclooxygenase Inhibitors on Vascular Reactivity and Alterations of Cyclooxygenase Expression (혈관 반응성에 대한 Cyclooxygenase 억제제 효과와 Cyclooxygenase 발현 변화)

  • Lee, Ki-Young;Park, Jin-Woo;Eum, Eun-A;Kang, Young-Jin;Lee, Kwang-Youn;Choi, Hyoung-Chul
    • Journal of Yeungnam Medical Science
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    • v.23 no.1
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    • pp.36-44
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    • 2006
  • Background: There is controversy regarding whether COX-2 specific inhibitors are associated with elevation of blood pressure. We compared the effects of aspirin, indomethacin, and celecoxib for vascular reactivity induced by phenylephrine. We also tested the effects of indomethacin and NO donor on COX-1 and COX-2 protein expression, as well as nitrite production in culture medium of vascular smooth muscle cells. Materials and Methods: In this experiment, we used the isometric tension study for vascular reactivity. After 45 minutes of pretreatment with aspirin, indomethacin, celecoxib, and phenylephrine induced contractions were tested. COX-1 and COX-2 protein expressions were analyzed by Western blot and nitrite production by the Griess reaction. Results: Although celecoxib pretreatment caused enhanced arterial contraction, aspirin pretreatment induced more potent arterial contraction than celecoxib in the isometric tension study of rabbit femoral artery. COX-1 protein expression was unchanged by indomethacin, SNP and NOR-3; COX-2 protein expression was increased by the addition of indomethacin, SNP, and NOR-3. Especially, NOR-3, a NO donor, significantly increased COX-2 protein expression with unstimulated conditions as well as LPS stimulation. Induction of nitrite production was higher with NOR-3 treatment than SNP treatment with LPS stimulation. Conclusion: These results suggest that aspirin caused more potent vascular contraction than celecoxib and indomethacin. COX-2 expression in VSMC depended on the types of NO donor and LPS stimulation.

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Manufacture of Flow Phantom with Stenosis and Imaging Evaluation of Power Doppler (혈관협착팬텀의 제작 및 파워도플러의 영상 평가)

  • Park, Hee-Young;Bae, Jong-Rim;Kim, Jeong-Koo
    • The Journal of the Acoustical Society of Korea
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    • v.28 no.8
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    • pp.732-739
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    • 2009
  • Flow phantom with stenosis was manufactured using an auto-injector to obtain angiostenotic flow information and quality assurance (QA) for ultrasound diagnostic instrumentation. Effectiveness of manufactured flow phantom with stenosis was investigated with power Doppler that was known to have diagnostic efficiency for angiostenosis. The flow phantom with stenosis was manufactured to 70% stenosis with 8 mm and 2.4 mm silicon tube, and silicone tube was covered with gelatin that has acoustic characteristics similar to soft tissue. When the linear transducer was used for measurement, the estimated diameter of normal vessel was measured lower than that of normal value, and the estimated diameter of stenosed vessel was measured higher than that of normal value. The measured parameters were not affected except for the radical conditions such as gain of 60%, PRF of 3000 Hz, use of maximal filter or angle. In addition, when the convex transducer was used for measurement, measurement parameters were affected by gain, PRF, filter, and angle. Therefore it is expected that flow phantom with stenosis manufactured with an auto-injector will be utilized effectively for QA of angiostenotic diagnosis.

특집 - 혈관질환의 주범

  • 사단법인한국당뇨협회
    • The Monthly Diabetes
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    • s.238
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    • pp.26-29
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    • 2009
  • 대혈관질환은 당뇨병환자의 주된 사망원인으로 당뇨병이 없는 사람에 비해 발생할 확률이 2$\sim$5배 높은 중대한 합병증이다. 혈관합병증이 발생하는 원인은 한 가지가 아닌 여러 가지 원인들이 복잡하게 관여하는 것으로 알려져 있다. 최근 많은 연구결과에 따르면 당뇨병성 혈관 합병증의 발생은 일차적으로 동맥경화증에 기인하며 이와 관련된 위험인자로 고혈당, 고혈압, 고지혈증, 흡연, 비만, 운동부족, 가족력 등이 있다.

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Survey of Image Segmentation Algorithms for Extracting Retinal Blood Vessels (망막혈관 검출을 위한 영상분할기법)

  • Kim, Jeong-Hwan;Seo, Seung-Yeon;Song, Chul-Gyu;Kim, Kyeong-Seop
    • Proceedings of the Korean Society of Computer Information Conference
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    • 2019.01a
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    • pp.397-398
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    • 2019
  • 망막혈관 영상에서(retinal image) 혈관의 모양 또는 생성변화를 효과적으로 검진하기 위해서 망막혈관을 자동적으로 분리하는 영상분할 기법의 개발은 매우 중요한 사안이다. 이를 위해서 주로 망막혈관영상의 잡음을 억제하고 또한 혈관의 명암대비도(contrast)를 증가시키는 전처리 과정을 거쳐서 혈관의 국부적인 화소값의 변화, 방향성을 판별하여 혈관을 자동적으로 검출하는 방법들이 제시되어왔으며 최근에는 합성곱 신경망(CNN) 딥러닝 학습모델을 활용한 망막혈관 분리 알고리즘들이 제시되고 있다.

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Intravascular Papillary Endothelial Hyperplasia (Masson's hemangioma) Presenting as a Forearm Mass (전완부에 발생한 내혈관 유두내피 증식증(Masson 혈관종))

  • Chun, Young-Soo;Rhyu, Kee-Hyung;Kim, Sang-Hwan
    • The Journal of the Korean bone and joint tumor society
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    • v.15 no.1
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    • pp.59-64
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    • 2009
  • Intravascular papillary endothelial hyperplasia (IPEH, Masson's hemangioma) is a non neoplastic reactive endothelial proliferation most commonly located in the skin or subcutaneous tissues although it has been reported in multiple locations throughout the body. This lesion may arise from malformed or normal vessels primarily, and may develop with hemangioma, pyogenic granuloma, or lymphangioma. This lesion, though benign, is clinically important since it may present as a mass and be confused histologically with angiosarcoma. The authors report a 27 years old patient with a mass in his forearm which results in intravascular papillary endothelial hyperplasia.

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Effect of pH Change on Vascular Smooth Muscle Contractility in Rat Superior Mesenteric Artery and Its Branches (쥐 상장간막 동맥과 그 분지에서 pH 변화가 혈관평활근 수축성에 미치는 영향)

  • Choi, Soo-Seung
    • Journal of Chest Surgery
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    • v.43 no.4
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    • pp.345-355
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    • 2010
  • Background: Extracellular and intracellular pH ($pH_o$ and $pH_i$), which can be changed in various pathological conditions such as hypoxia, affects vascular contractility. To elucidate the mechanism to alter vascular contractility by pH, the effects of pH on reactivity to vasocontracting agents, intracellular $Ca^{2+}$ influx, and $Ca^{2+}$ sensitivity in vascular smooth muscle were examined. Material and Method: Isometric contractions in rat superior mesenteric arteries (SMA) were observed. Intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) was recorded by microfluorometer using Fura-2/acetoxylmethyl ester in muscle cells. $pH_o$ was increased from 7.4 to 7.8 or decreased to 6.9 or 6.4. $pH_i$ was decreased by applying $NH_4^+$ or propionic acid or modulated by changing $pH_o$ after increasing membrane permeability using $\beta$-escin. Result: Decreases in $pH_o$ from 7.4 to 6.9 or 6.4 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the right and significantly increased half maximal effective concentration (EC50) to NE or SE. Increase in $pH_o$ from 7.4 to 7.8 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the left and significantly reduced EC50 to NE or SE. NE increased $[Ca^{2+}]_i$ in cultured smooth muscle cells from SMA and the increased $[Ca^{2+}]_i$ was reduced by decreases in $pH_o$. NE-induced contraction was inhibited by $NH_4^+$, whereas the resting tension was increased by $NH_4^+$ or propionic acid. When the cell membrane of SMA was permeabilized using ${\beta}$-escin, SMA was contracted by increasing extracellular $Ca^{2+}$ concentration from 0 to $10{\mu}M$ and the magnitude of contraction was decreased by a decrease in $pH_o$ and vice versa. Conclusion: From these results, it can be concluded that a decrease in $pH_o$ might inhibit vascular contraction by reducing the reactivity of vascular smooth muscle to vasoactive agents, $Ca^{2+}$ influx and the sensitivity of vascular smooth muscle to $Ca^{2+}$.