• 제목/요약/키워드: Arterial smooth muscle

검색결과 105건 처리시간 0.026초

관동맥성형술 후의 혈관 재협착 및 재형성 (Restenosis and Remodeling)

  • 채제건
    • 대한핵의학회:학술대회논문집
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    • 대한핵의학회 1999년도 제38차 춘계학술대회
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    • pp.205-208
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    • 1999
  • 재협착에 관여하는 인자는 매우 다양하다. 평활근 세포의 증식, ECM의 형성, 혈관벽의 초기 혈전형성, 그리고 혈관 재형성 등이 모든 것들이 재협착의 병인에 기여하고 있다. 환자마다 이런 요소들의 기여정도가 다르며 동일 환자에서도 병변에 따른 기여정도가 또한 다르리라 여긴다. 그러나 아직까지 우리는 외막섬유모세포의 역할, 내피세포의 재생, 증식세포의 계획된 죽음 등 재협착의 기전을 불완전하게 이해하고 있고 따라서 보다 완전한 이해를 통해 효과적인 재협착 예방치료가 시행될 수 있을 것이다.

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Tannic acid의 혈압강하작용(血壓降下作用) (Depressor Responses to Intravenously Administered Tannic Acid in Rabbits)

  • 문충배;신홍기;김기순
    • The Korean Journal of Physiology
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    • 제13권1_2호
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    • pp.29-34
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    • 1979
  • The present study was undertaken to investigate depressor action of tannic acid and the mechanism underlies it in the rabbit. The changes in arterial blood pressure were studied after intravenous administration of tannic acid in normal rabbits and the animals pretreated with atropine, propranolol, dibenamine, and hexamethonium. The results obtained were as follows; 1) Following administration of 1.5 mg/kg, 3.0 mg/kg, and 5.0 mg/kg of tannic acid into rabbits the maximum depressor responses observed were $12.0{\pm}0.9\;mmHg$, $23.4{\pm}1.0\;mmHg$, and $34.0{\pm}1.8\;mmHg$ respectively and generally depressor responses increased in proportion to dosage of tannic acid. 2) Since there were no changes in depressor responses to tannic acid in animals pretreated. separately with atropine, propranolol, dibenamine, and hexamethonium, the depressor responses appeared to be resulting from direct vasodilator action of tannic acid on the vascular smooth muscle. Comparing tannic acid and acorn extract in their mechanisms of depressor responses, it is strongly indicated that in acorn there might exist another depressor substance. 3) After administration of large doses of tannic acid, in addition to respiratory changes, the mean arterial blood pressure decreased markedly and was never recovered throughout the experiment. comma Therefore it is also suggested that the lethal action of tannic acid resides in a drastic decline of arterial blood pressure and in respiratory changes as well.

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Haloperidol 이 심혈관계에 미치는 영향 (Experimental Studies on the Cardiovascular Effects of Haloperidol in Cat and Rabbit)

  • 안영수
    • 대한약리학회지
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    • 제11권2호
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    • pp.19-27
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    • 1975
  • Haloperidol, a butyrophenone, was synthetized by Janssen and introduced for the treatment of psychosis. Although structurally different from the phenothiazines, the butyrophenones share many of their pharmacological properties, such as inhibition of conditioned avoidance response, blocking effect of amphetamine reaction, producing catalepsy, antishock effect and protection against the lethal effects of catecholalmines. Chlorpromazine can lower the arterial blood pressure through its adrenergic blocking activity, its direct effect in relaxing vascular smooth muscle, its direct effect in depressing the myocardium and its action in a complex manner on the central nervous system. In the case of haloperidol, however, was not clarified the mechanism of lowering the blood pressure. The present paper describes the effects of haloperidol on cardiovascular system to investigate the mechanisms of its actions on the arterial blood pressure. The results are followings; 1. In anesthetized cats, intravenous administration of haloperidol and chlorpromazine in the dose of 0.1mg/kg produced a slight decrease in the blood pressure, which followed by complete recovery within $30{\sim}60$ minutes. In the dose of 3mg/kg, however, both produced an abrupt and marked decrease of the blood pressure, which followed by delayed recovery. 2. Haloperidol in the dose ranges of 0.1mg to 3.0mg/kg tended to produce the heart rate slowing in the cats, while chlorpromazine has no effect on the rate. 3. Following administration of haloperidol or chlorpromazine, epinephrine reversal in the arterial blood pressure was observed in the cat, however the responses of norepinephrine and acetylcholine were little affected. 4. In the isolated rabbit atrium the contractility was depressed by haloperidol in the doses over 0.5mg per 100ml, but the rate was not affected. In contrast, the epinephrine-induced contractility was not depressed after haloperidol treatment. However, the increased rate of atrium by epinephrine was partially blocked after haloperidol. 5. In the isolated rabbit aortic strip, epinephrine-induced contraction was blocked by haloperidol. With the above results, it may be concluded that the hypotensive effect of haloperidol was largely due to ${\alpha}$-adrenergic blocking properties and the direct effect in depressing the myocardium as well as its action on central nervous system.

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Serotonin에 의한 가토 신동맥 평활근 수축기전 (Contractile Mechanisms of Serotonin in the Renal Arterial smooth muscle of a Rabbit)

  • 이우영;김세훈;장석종
    • The Korean Journal of Physiology
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    • 제24권1호
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    • pp.67-76
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    • 1990
  • The contractile mechanisms of serotonin were investigated in the renal artery of a rabbit. The helical strips of isolated renal artery were immersed in the normal or $Ca^{2+}$-free tris-buffered Tyrode's solution, which was equilibrated with 100% $O_{2}$ at $35^{\circ}C$. The contraction by serotonin or norepinephrine (NE) began at $1{\times}10^{-7}\;M$ and reached the maximal contraction at $1{\times}10^{-5}\;M$. The maximal contraction by serotonin corresponded to $58.1{\pm}4.2%$ of maximal contraction by NE. Cyproheptadine, a serotonin receptor blocker, shifted the concentration-response curve to the right without any reduction in the maximum response but shifted that of NE to the right with reduction in maximum response. And phentolamine, an ${\alpha}-receptor$ blocker, shifted the concentration-response curve of serotonin or NE without any reduction in maximum responses. The $pA_{2}$ values for cyproheptadine against serotonin and NE were $10.35{\pm}0.04$ and $8.45{\pm}0.13$, respectively. The $pA_{2}$ values for phentolamine against serotonin and NE were $6.87{\pm}0.04$ and $8.14{\pm}0.08$, respectively. after the pretreatment with 6-hydroxydopamine, the contraction induced by 100 mM $K^{+}$, tyramine and serotonin reduced to $83.0{\pm}2.0$, $26.8{\pm}6.2$ and $82.0{\pm}3.5%$ of control, respectively. The contraction by serotonin in the $Ca^{2+}$-free Tyrode's solution was increased and sustained with the addition of $Ca^{2+}$ extracellulary. The serotonin-sensitive intracellular $Ca^{2+}$ pool was depleted completely by the pretreatment with NE, but the NE-sensitive intracellular $Ca^{2+}$ pool was depleted partially by the pretreatment with serotonin. From the above results, it is suggested that the contraction induced by serotonin in the renal artery of a rabbit may be due to mechanisms in which serotonin acts directly on specific serotonin receptors and also acts indirectly on ${\alpha}-adrenoceptors$ by displacing NE from neuronal stores.

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황련해독탕(黃連解毒湯)이 가토(家兎)의 혈관긴장성조절(血管緊張性調節)에 미치는 영향(影響) (Effects of HwangRyunHaeDok-Tang and Constituent Herbs on a Contracted Artery of Rabbit)

  • 남창규;김호현;정찬길;성현제;권오율
    • 대한한방내과학회지
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    • 제24권2호
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    • pp.220-232
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    • 2003
  • Objective : The purpose of this study was to analyze the effects of HwangRyunHaeDok-Tang and combinations of constituent herbs on the arterial contraction. Methods : In order to investigate the effects Scutellariae Radix. Coptidis Rhizoma, Phellodendri Cortex and Gardeniae Fructus, in which one of them, two of them, and all of them, were used to exam. Results : The results were summarized as follows; 1. HwangRyunHaeDok-Tang significantly inhibited the contraction of artery induced by Norepinephrine(NE). However the atonic effect was slightly blunted when the vascular endothelial cell was removed. No significant change in the atonic effect of HwangRyunHaeDok-Tang was found when $_L-NNA$ was used as a preliminary treatment. These results indicate that the vascular atonic effect by HwangRyunHaeDok-Tang is slightly dependent on the endothelial cell, and that the HwangRyunHaeDok-Tang works directly to the vascular smooth muscle in creating the vascular atonic effect. 2. The pretreatment of HwangRyunHaeDok-Tang extract significantly inhibited the contractile response to additive application of $Ca^{2+}$ in the strips which were contracted by NE in $Ca^{2+}$-free solution. 3. HwangRyunHaeDok-Tang extract increased the contraction of arterial smooth muscle induced by KCl. Therefore, it can be concluded that HwangRyunHaeDok-Tang may block the NE-receptor or receptor-operated $Ca^{2+}$ channel. 4. It was determined that Scutellariae Radix, Coptidis Rhizoma and Phellodendri Cortex among the ingredients of HwangRyunHaeDok-Tang have a vascular atonic effect. In addition, those ingredients plays a role in strengthening the atonic effect by working with other herbal medicines. Gardeniae Fructus causes the blood vessel to contract. but it does not influence the atonic effects of other herbal medicines. However Gardeniae Fructus tends to inhibit the vascular atonic effect of Phellodendri Cortex. Conclusion : Based on the above results, it can be said that HwangRyunHaeDok-Tang can be applied to cure hypertension considering those three herbs have significant effects of relaxation.

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포도당, 인슐린 및 Angiotensin II가 흰쥐 대동맥평활근세포의 Plasminogen Activator Inhibitor-1 발현 및 성장에 미치는 영향 (The Effects of Glucose, Insulin and Angiotensin II on Plasminogen Activator Inhibitor-1 Expression and Growth of Aortic Vascular Smooth Muscle Cell in Rats)

  • 최세영;이인규;한승세;김재현;박창권;이광숙;유영선;김기식;김윤년
    • Journal of Chest Surgery
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    • 제32권4호
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    • pp.333-340
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    • 1999
  • 배경: PAI-1은 t-PA의 억제인자로서 섬유소융해계에 작용을 하여 혈전형성을 유발한다. PAI-1은 동맥경화된 혈관벽에서 분비가 된다. PAI-1의 증가는 동맥경화증의 위험인자가 되는 당뇨병과 고혈압이 동반된 환자에서 보이며 혈전증유발에 위험인자가 될 수 있다. 본 연구는 고혈당과 인슐린 및 angiotensin II가 PAI-1의 생성 및 평활근세포의 증식에 미치는 영향을 규명하고자 하였다. 대상 및 방법:흰쥐 대동맥평활근세포를 5.5 mM과 22 mM의 포도당 배양액을 사용하여 배양하였다. 배양액에 angiotensin II 및 인슐린을 농도 및 배양시간에 따라 첨가하여 Northern blotting방법으로 PAI-1 유전자발현을 나타내었다. 또한 세포 증식에 대한 포도당, 인슐린 및 angiotensin II의 영향을 규명하기 위하여 MTT assay를 사용하였다. 결과: 5.5 mM과 22 mM의 포도당 배양액에서 angiotensin II(100 nM)를 첨가하여 배양한 결과, 22 mM 포도당 배양액에서 PAI-1 mRNA 발현이 증가되었으며 angiotensin II 투여 4시간에 최고치에 도달하였고 6시간까지 지속되었다. 5.5 mM, 22 mM의 포도당 배양액에 angiotensin II의 농도를 0, 10, 100, 200 nM 투여하여 배양한 결과, PAI-1 mRNA의 발현은 angiotensin II 농도에 따른 증가를 보였으며 22 mM 포도당 배양액시 더욱 뚜렷하게 증가되었다. 배양액에 angiotensin II(100 nM)과 인슐린(100 nM)을 투여하여 배양한 결과, PAI-1 mRNA의 발현은 angiotensin II 단독으로 투여시 증가하였으나 인슐린을 첨가하였을 때는 감소하였다. 5.5 mM과 22 mM의 포도당 배양액에 1, 10, 100 nM의 인슐린과 1, 10, 100 nM의 angiotensin II를 첨가한 후 대동맥평활근세포의 성장속도를 비교한 결과, 5.5 mM보다 22 mM의 포도당이 든 배양액에서 대동맥평활근세포의 성장이 촉진되었으며, 인슐린 및 angiotensin II를 첨가한 경우도 대동맥평활근세포의 성장이 증가되었다. 결론:흰쥐 대동맥평활근세포에서 PAI-1 mRNA의 발현은 포도당 농도가 높을수록 증가되며 angiotensin II의 농도 및 배양시간에 따라 증가되고 인슐린 투여로 감소하였다. 또한 angiotensin II의 투여는 22 mM의 고농도 포도당 투여 후 증가된 PAI-1 mRNA 발현 증가를 더욱 증가시켜 PAI-1 mRNA 발현 증가에 상승작용이 있음을 알 수 있다. 그리고 22 mM의 고농도 포도당, 인슐린 및 angiotensin II는 흰쥐의 대동맥평활근세포의 성장을 촉진시켰다.

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Change of voltage-gated potassium channel 1.7 expressions in monocrotaline-induced pulmonary arterial hypertension rat model

  • Lee, Hyeryon;Kim, Kwan Chang;Hong, Young Mi
    • Clinical and Experimental Pediatrics
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    • 제61권9호
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    • pp.271-278
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    • 2018
  • Purpose: Abnormal potassium channels expression affects vessel function, including vascular tone and proliferation rate. Diverse potassium channels, including voltage-gated potassium (Kv) channels, are involved in pathological changes of pulmonary arterial hypertension (PAH). Since the role of the Kv1.7 channel in PAH has not been previously studied, we investigated whether Kv1.7 channel expression changes in the lung tissue of a monocrotaline (MCT)-induced PAH rat model and whether this change is influenced by the endothelin (ET)-1 and reactive oxygen species (ROS) pathways. Methods: Rats were separated into 2 groups: the control (C) group and the MCT (M) group (60 mg/kg MCT). A hemodynamic study was performed by catheterization into the external jugular vein to estimate the right ventricular pressure (RVP), and pathological changes in the lung tissue were investigated. Changes in protein and mRNA levels were confirmed by western blot and polymerase chain reaction analysis, respectively. Results: MCT caused increased RVP, medial wall thickening of the pulmonary arterioles, and increased expression level of ET-1, ET receptor A, and NADPH oxidase (NOX) 4 proteins. Decreased Kv1.7 channel expression was detected in the lung tissue. Inward-rectifier channel 6.1 expression in the lung tissue also increased. We confirmed that ET-1 increased NOX4 level and decreased glutathione peroxidase-1 level in pulmonary artery smooth muscle cells (PASMCs). ET-1 increased ROS level in PASMCs. Conclusion: Decreased Kv1.7 channel expression might be caused by the ET-1 and ROS pathways and contributes to MCT-induced PAH.

Altered Electrophysiological Properties of Coronary Artery in Iso-prenaline-Induced Cardiac Hypertrophy

  • Kim, Na-Ri;Han, Jin;Kim, Eui-Yong
    • The Korean Journal of Physiology and Pharmacology
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    • 제5권5호
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    • pp.413-421
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    • 2001
  • An impaired smooth muscle cell (SMC) relaxation of coronary artery by alteration of $K^+$ channels would be the most potential explanation for reduced coronary reserve in left ventricular hypertrophy (LVH), however, this possibility has not been investigated. We performed morphometrical analysis of the coronary artery under electron microscopy and measured $Ca^{2+}-activated\;K\;(K_{Ca})$ currents and delayed rectifier K $(K_{dr})$ currents by whole-cell and inside-out patch-clamp technique in single coronary arterial SMCs from rabbits subjected to isoprenaline-induced cardiac hypertrophy. Coronary arterial SMCs underwent significant changes in ultrastructure. The unitary current amplitude and the open-state probability of $K_{Ca}$ channel were significantly reduced in hypertrophy without open-time and closed-time kinetic. The concentration-response curve of $K_{Ca}$ channel to $Ca^{2+}$ is shifted to the right in hypertrophy. The reduction in the mean single channel current and increase in the open channel noise of $K_{Ca}$ channel by TEA were more sensitive in hypertrophy. $K_{dr}$ current density is significantly reduced in hypertrophy without activation and inactivation kinetics. The sensitivity of $K_{dr}$ current on 4-AP is significantly increased in hypertrophy. This is the first study to report evidence for alterations of $K_{Ca}$ channels and $K_{dr}$ channels in coronary SMCs with LVH. The findings may provide some insight into mechanism of the reduced coronary reserve in LVH.

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Effect of Recombinant Human Epidermal Growth Factor Impregnated Chitosan Film on Hemostasis and Healing of Blood Vessels

  • Lee, Sangshin;Jung, Inwook;Yu, Seongcheol;Hong, Joon Pio
    • Archives of Plastic Surgery
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    • 제41권5호
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    • pp.466-471
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    • 2014
  • Background Bleeding can be a problem in wound debridement. In search for an effective hemostatic agent, we experimented with a chitosan film combined with the recombinant human epidermal growth factor (rh-EGF), hypothesizing that it would achieve effective hemostasis and simultaneously enhance arterial healing. Methods Forty-eight Sprague-Dawley rats were used, and 96 puncture wounds were made. The wounds were divided into the following four groups: treated with sterile gauze, treated with gelatin sponge, treated with chitosan, and treated with chitosan combined with rh-EGF. Immediate hemostasis was evaluated, and arterial healing was observed histologically. Results Groups B, C, and D showed a significant rate of immediate hemostasis as compared to group A (P<0.05), but there were no significant differences among groups B, C, and D. Histologically, only group D showed good continuity of the vessel wall after 1 week. It was the only group to show smooth muscle cell nuclei of the vessel wall. Conclusions We observed that chitosan has an effective hemostatic potential and the mix of rh-EGF and chitosan does not interfere with chitosan's hemostatic capabilities. We also identified enhanced healing of vessel walls when rh-EGF was added to chitosan. Further research based on these positive findings is needed to evaluate the potential use of this combination on difficult wounds like chronic diabetic ulcerations.

사궁산(莎芎散)이 실험동물(實驗動物)의 지혈(止血), 뇌압(腦壓), 혈압(血壓) 및 심혈관계(心血管系)에 미치는 영향(影響) (Effects of Sagungsan on the Hemostasis, Intracranial Pressure, Blood Pressure and Cardiovascular System in Expreimental Animals)

  • 안일회;박영순;김세길
    • 대한한방내과학회지
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    • 제15권1호
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    • pp.80-98
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    • 1994
  • According to the original documents, Sagungsan is considered as an effective drug for controlling the hypertensive epistaxis induced by tension of autonomic nerve and it's hyperfunction. The present experiment was designed to understand the effect of Sagungsan extract on the hemostatic action, intracranial pressure, blood pressure and cardiovascular system in experimental animals. And thus the bleeding time, prothrombin time, capillary dilation, blood pressure, Intracranial pressure, and enzymatic analysis of the ATPase activities were studied. The result obtained here were as followings: 1. Sagungsan water extract reduced the bleeding time in mouse, and prolonged the prothrombin time in rabbits. 2. The drug extract increased the tail volume by capillary dilation in rats. 3. The drug extract inhibited the increase of intracranial pressure and arterial blood pressure in rabbits. 4. At the early time, the increase of arterial blood pressure by the drug extract significantly inhibited by pretreated atropin and regitine in rabbits. 5. The drug extract relaxed the smooth muscle by stimulating the Mg2+-Ca2+-ATPase activities of gastric sarcoplasmic reticulum isolated from rabbit stomach. 6. The drug extract stimulated the heart contraction by inhibiting the $Mg^{2+}-Ca^{2+}-ATPase$ activities of cardiac sarcoplasmic reticulum isolated from rabbit heart. The inhibitory mechanism was reversible and noncompatitive. 7. The drug extract increased the hepatic blood volume by stimulating the hepatic total ATPase activities and hepatic metabolism. 8. The drug extract acted as a tranquilizer by inhibiting the neural Na+-K+-ATPase activity. According to the results, Sagungsan water extract dilated the capillaries, stimulated the heart beat, and thus increased the blood flow with decreasing the intracranial pressure and blood pressure. These effects stanches the epistaxis collectively.

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