血管舒张

Adrenoceptor antagonization did not change the tension of femoral artery, but abolished the ISO induced vasorelaxation of coronary artery.

1受体阻断不影响ISO产生的股动脉血管舒张，但消除了冠状动脉的血管舒张。

RESULTS Endothelium removal, NOS inhibition,β2 adrenoceptor antagonization did not change the vasorelaxation induced by ISO in coronary artery, however, abolished the vasorelaxation in femoral artery.

结果 无论冠状动脉或股动脉ISO均产生浓度依赖的血管舒张。去除内皮， NOS抑制，β2受体阻断不影响ISO产生的冠状动脉血管舒张，而完全消除了股动脉的血管舒张。

The first part consists of three experiments:(1) The rings were incubated in KH, 20, 50 mmol/L 〓 for 1 house, relaxation in response to the EDHF stimuli A23187 in 30nmol/L U46619-induced preconrtaction in the presence of 7 μ mol/L indomethacin, a cyclooxygenase inhibitor, 300μmol/L LNNA, a nitric oxide biosyhnthesis inhibitor, and 1mmol/L tetraethylammonium , a 〓 blocker, or 3 μmol/L glibenclamide , a 〓 blocker, was compared with the control;(2) After the arteries were incubated in KH, UW solution or HTK solution at 4℃ for 4 hours, endothelium-derived relaxation (percentage of 30nmol/L U46619 precontraction) was induced by A23187 in the present of 7 μmol/L indomethacir and 300μmol/L LNNA;(3) After incubation with KH, UW solution and STH (either at 37℃ in oxygenated organ chamber or at 4℃ in a refrigerator for 4 hours), endothelium-derived relaxation (percentage of 30nmol/L U46619 precontraction) was induced by A23187 in the present of 7 μ mol/L indomethacin and 300 μmol/L LNNA.

第一部分研究结果：（1）单纯浸泡于KH的冠状动脉A23187能引发66.67％的血管舒张反应，经TEA及20mmol／L、50mmol／L钾离子作用后，血管舒张反应程度显著降低，但经GBM作用后改变不明显；（2）与保存于KH的冠状动脉相比，A23187引发的血管舒张反应程度，保存于UW液的明显下降，保存于HTK液的无明显变化；（3）在37℃条件下，血管环浸泡于STH出现缓慢轻微的舒张反应，浸泡于UW液初期出现短暂收缩反应，但此后主要以舒张为主：在37℃条件下，血管经UW液保存后，U46619引发的收缩反应程度降低；不论在37℃或4℃条件下，A23187引发的血管舒张反应，经UW液保存后明显下降，但用STH保存后变化不明显。

To conserve blood that will be needed by muscles, skin vessels constrict while vessels of the muscles dilate

为了保存肌肉所需要的血液，皮肤血管收缩，而肌肉血管舒张。

So there are two ways to attack the vascular smooth muscles in terms vascular dilatation.

因此，就血管舒张而言，有两种途径来攻击血管平滑肌。

METHODS: The rabbit hindlimb normothermic tourniquet ischemia model was employed. The tendon on the dorsum of the foot was exposed for observation of microvessels. The responses of arterioles on tendon surface to topical application of 10(-6) mol/L noradrenaline, 10(-6) mol/l acetylcholine (an endothelium-dependent vasodilator) and 10(-4) mol/L nitroglycerin (an endothelium-independent vasodilator) were observed at the period of ischemia and following 30 minutes of reperfusion after 2 hours and 5 hours of ischemia by use of intravital microscopy.

应用兔后肢止血带常温缺血模型及足背肌腱表面微循环观察法，观察肢体缺血 2小时及 5小时再灌注后微动脉对局部滴注血管收缩剂 [去甲肾上腺素(10 - 6 mol/ L ) ]、内皮依赖性血管舒张剂 [乙酰胆碱(10 - 6 mol/ L ) ]及内皮非依赖性血管舒张剂 [硝酸甘油(10 - 4 mol/ L) ]的反应性变化。

Wenxin capsule can promote endolethial cells releasing CO and synthesing 〓, enhance activity of HO, induce angiectasis through activating guanylic cyclase and adenglate cyclate of intracellar of vessel smooth muscle cell to enhance content of intracellar cGMP and AMP. 3. Wenxin capsule can inhibit releasing of platelet activiting factor 〓 which inhibit platelet aggregation and have antithrombosis function. 4. Wenxin capsule can promote activity of t-PA, reduce activity of PAI-1, strengthen fibrinolytic function, therefore inhibit fibrin disposition. 5. Wenxin capsule can inhibit synthesis of smooth muscle cellular DNA. Its function don't kill it directly but prevent transformation from period Go to peried S. 6. Wenxin capsule is an effective prescription of anti-coronary atherosclerosis atherosis. The results of image pattern analysis tastifies that area of lipid plaque in treating group reduce 54% and 58% in contrast with that in control group. The results of light, electro- microscopy show that structure of endolethial cell and smooth muscle cell in treating group is more integral than that in control group.

其作用机制之一是由于该药具有良好的调脂降脂作用，其不仅能明显降低血清LDL-c及升高HDL-c含量，且能有效阻止TC沉积于血管壁，从而保护内皮细胞结构完整；此外，温心胶囊尚具有明显的抗氧化作用，该药不仅能明显降低血浆LPO含量，且能提高SOD活性，同时其对血红素在细胞内代谢的调节作用也参与了抗氧化过程。2 温心胶囊能明显促进内皮细胞释放CO及合成〓，提高HO活性，通过激活血管平滑肌细胞内鸟苷酸环化酶及腺苷酸环化酶引起细胞内cGMP、AMP浓度增加而引起血管舒张。3 温心胶囊能明显抑制血小板激活因子〓的释放，从而抑制血小板聚集，抗血栓形成。4 温心胶囊能明显提高t-PA活性，降低PAI-1活性，增强纤溶功能，从而抑制纤维蛋白沉积。5 温心胶囊能明显抑制平滑肌细胞DNA合成，其抑制作用不是直接杀伤抑制，而是阻止细胞由Go期向S期转化。6 温心胶囊是抗冠状动脉粥样硬化的有效制剂，图象分析结果证实，该药治疗组脂斑面积比对照组缩小了54％和58％，光电镜结果显示内皮细胞及平滑肌细胞结构较为完整。

Objective: To discuss the protective effects of Fuwai modifed solution combined with nicoranil on the endothelium-derived hyperpolarizing factor-mediated relazation relaxation of saphena vessel graft.

目的：探讨常温下阜外改良(Fu Wai Modified， FWM)器官保护液＋尼可地尔对大隐静脉血管桥血管内皮超极化因子介导血管舒张功能的影响。

The activation of endothelial cell caused by TNF-α has detrimental effects on the vasculature. TNF-α can induce the increased apoptosis of gravid trophocyte. TNF-α has been showing up-regulate the vasoconstriction factors such as endothelin and down-regulate the vascular relaxing factors such as NO on the contrary.

肿瘤坏死因子α作为炎性分子，激活血管内皮细胞、间接影响血管舒缩功能，通过各种机制诱导胎盘滋养细胞凋亡增加，增加血管收缩因子并减少血管舒张因子的生成和释放，影响与脂类代谢相关的细胞因子。

Abstract］ Objective To assess the endothelium-dependent relaxation in patients with essential hypertension or hypertension smokers by color Doppler flow imaging.Methods With intermittent ultrasound imaging and power Doppler imaging,we measured endothelium-dependent relaxing function in 72 subjects 24 of whom with essential hypertension,24 of whom with both hypertension and smokingand the others as normal control.We measured the diameter of the superficial femoral and brachial arteries at rest,during reactive hyperaemia,re-test and after sublingual glyceryl trinitrate for evaluating the endothelium-independent dilatation in subjects.The level of plasma NO,ET,PGI2,and TXB2 were determined.

摘要］ 目的探讨原发性高血压及高血压合并吸烟患者血管内皮依赖性舒张功能的改变方法采用彩色普勒高频超声的间歇成像和能量多普勒成像，对24例原发性高血压患者、24例高血压合并吸烟患者及24例正常血压无吸烟史者的血管内皮依赖性舒张功能，包括静息时血管内径、增加流量引起的血管舒张、硝酸甘油引起的血管舒张等，以及对血浆氧化氮、内皮素、血栓素B2（TXB2）和列腺环素（PGI2）等血管活性物质进行检测并比较分析。

Do you know, i need you to come back

你知道吗，我需要你回来

Yang yinshu、Wang xiangsheng、Li decang,The first discovery of haemaphysalis conicinna.

1〕 杨银书，王祥生，李德昌。安徽省首次发现嗜群血蜱。