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本文观察山莨菪碱(654-2)对大鼠缺血心肌的保护作用。发现大鼠左冠状动脉主干结扎后早期腹腔注射654-2,可使结扎后6小时及21天时的梗塞范围显著缩小,并使21天时的左室心肌收缩性恢复得更好,而结扎后3小时缺血区心肌的超微结构改变得到显著改善。654-2对冠脉结扎与非冠脉结扎大鼠的直接血液动力学作用表现为平均动脉压、心输出量和左室心肌收缩性显著降低,提示654-2可以减少心肌氧耗量,从而对缺血心肌发生有利影响。  相似文献   

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目的研究冠状动脉在不同后负荷条件下,冠脉搭桥手术后竞争流对左乳内动脉(left internal mammary artery,LIMA)血流动力学影响。方法模拟LIMA到前降支(left anterior descending,LAD)搭桥手术三维模型(three-dimensional,3D),建立与冠脉模型相对应的集中参数模型(lumped parameter model,LPM,0D),为其提供1倍和1.2倍两种不同后负荷的边界条件,同时在LAD主干处设置了25%、40%、50%、60%、75%5种不同直径狭窄程度,使用计算流体力学(computational fluid dynamics,CFD)耦合计算冠脉3D模型和0D模型,从血流动力学角度分析不同后负荷时竞争流对LIMA的影响。结果 1倍后负荷时,LAD总流量约为80 m L/min,随狭窄率增加,RC/G从2.025减小到0.280,LIMA平均血流量从26.598 m L/min增加到62.310 m L/min,震荡剪切指数(oscillatory shear index,OSI)从0.1557减小到0.0020,狭窄率小于50%时,时间平均壁面切应力(time-average wall shear stress,TAWSS)低于1 Pa;1.2倍后负荷模型中,LAD总流量为71 m L/min,随狭窄率增加,RC/G从2.222减小到0.289,LIMA平均血流量从22.188 m L/min增加到54.810 m L/min,OSI从0.1790降低到0.0024,狭窄率小于60%时TAWSS低于1 Pa。后负荷改变时,相同狭窄程度下桥血管在收缩期血流量变化很小,但舒张期流量随后负荷增大而减小。结论当冠脉后负荷较大时,竞争流强度偏大。当血管管径和狭窄程度都相同时,后负荷大的患者LIMA桥血管会因偏低的WSS和较高的OSI更容易引起"线性征",降低桥血管远期通透性。  相似文献   

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运动对冠心病患者血浆纤溶活性的影响及其临床意义   总被引:3,自引:0,他引:3  
为探讨冠心病患者血浆纤溶活性变化及其与冠脉病变程度的关系。本文比较了冠心病组和正常对照组在桨极量运动前后血浆组织型纤溶酶的激活物(tPA),纤溶酶原么物抑制剂-1(PAI-1)活性的变化。及其与心肌缺血面积的相关性。结果显示:(1)运动前冠心组tPA及PAI-1活必闹于正常对照组(P〈0.05),运动后冠心病组PAI0-1活性明显升高(P〈0.05),而tPA活性水平明显下降(P〈0.05);(2  相似文献   

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目的:探讨锁骨下动脉、颈总动脉和椎动脉分叉处的血流动力学特性,分析该处发生血管狭窄引起大脑供血不足的 血流动力学原因。方法:采用内蒙古民族大学附属医院神经内科提供的CT数据,应用医学建模软件MIMICS20.0将患者 二维CT数据进行三维血管重建,经过网格划分及边界条件设置后导入计算流体力学软件FLUENT14.5中。计算和分析 不同血液入口速度的锁骨下动脉、颈总动脉和椎动脉分叉处的血流动力学特性。结果:在血液入口速度不同的情况下,锁 骨下动脉、颈总动脉和椎动脉分叉处的血液流场分布、血液压力分布和血管壁面切应力分布有显著变化。在血液入口速 度增大时,锁骨下动脉分叉处和颈总动脉分叉处的血液流速快、血管壁压力大,颈总动脉内侧血管壁面切应力大,但锁骨 下动脉分叉处和颈总动脉分叉处血管壁面切应力数值和变化幅度小,属于低切应力区。结论:通过血流动力学数值模拟 研究,分析锁骨下动脉、颈总动脉和椎动脉分叉处易发生粥样斑块病变导致大脑供血不足的血流动力学原因。  相似文献   

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Institute of Theoretical and Experimental Biophysics, Academy of Sciences of Russia, Pushchino. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 113, No. 6, pp. 593–595, June, 1992.  相似文献   

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Changes in the general hemodynamics were studied in healthy unanesthetized dogs after injection of angiotensin II for 60 min into the superior vena cava and portal vein at the rate of 27 ng/kg/min. Portal administration of the peptide was found to induce a weaker pressor effect. After systemic injection of angiotensin II the arterial pressure rose as the result of an increase in peripheral vascular resistance, and the minute volume of the circulation was reduced. After portal injection of angiotensin the increase in arterial pressure was due chiefly to an increase in the minute volume of the circulation. The differences in the hemodynamic responses cannot be explained entirely by metabolism of the peptide in the liver. After portal injection of angiotensin II it is possible that depressor substances from the liver enter the blood stream.Laboratory of Clinical and Experimental Surgery, Institute of Cytology and Genetics, Academy of Sciences of the USSR, Siberian Division. Laboratory of Endocrinology, Institute of Clinical and Experimental Medicine, Academy of Medical Sciences of the USSR, Siberian Branch, Novosibirsk. (Presented by Academician of the Academy of Medical Sciences of the USSR V. P. Kaznacheev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 81, No. 5, pp. 520–522, May, 1976.  相似文献   

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Delayed consequences of acute hypoxia were studied in 60-day-old rat pups. The animals were exposed to acute hypobaric hypoxia on day 10 of embryogenesis. The offspring of intact females served as the control. Reactivity of mesenteric lymphatic vessels to norepinephrine was studied by vital microscopy. The frequency and duration of lymphatic vessel contractions in males significantly increased compared to the control. In females the duration of norepinephrine-induced lymphatic vessel contractions increased, while the frequency and amplitude of contractions and basal vascular tone did not differ from the control. Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 138, No. 7, pp. 16–18, July, 2004  相似文献   

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Myocardial bridging is recognized as an anatomical variation of the human coronary circulation in which an epicardial artery lies in the myocardium for part of its course. Thus, the vessel is 'bridged' by myocardium. The anterior interventricular branch of the left coronary artery has been reported as the most common site of myocardial bridges but other locations have been reported. The purpose of this study was to provide more definitive information on the vessels with myocardial bridges, the length and depth of the bridged segment, and the relationship between the presence of bridges and coronary dominance. Two hundred formalin-fixed human hearts were examined. Myocardial bridges were found in 69 (34.5%) of the hearts with a total of 81 bridges. One bridge was found in 59 of these hearts and multiple bridges were observed in ten (eight with double bridges and two with triple bridges). Bridges were most often found over the anterior interventricular artery (35 hearts). Bridges were also found over the diagonal branch of the left coronary artery (14), over the left marginal branch (five) and over the inferior interventricular branch of the left coronary artery (six). Bridges were also found over the right coronary artery (15 hearts), over the right marginal branch (four) and over the inferior interventricular branch of the right coronary artery (two). The presence of bridges appeared to be related to coronary dominance, especially in the left coronary circulation. Forty-six (66.6%) of the hearts with bridges were left dominant. Forty-two of these had bridges over the left coronary circulation and four over the right coronary circulation. Seventeen hearts (24.6%) were right dominant. Eleven of these had bridges over the right coronary circulation and six over the left coronary circulation. The remaining six hearts were co-dominant with four having bridges over the left coronary circulation and two over the right coronary circulation. The mean length of the bridges was 31 mm and the mean depth was 12 mm. The possible clinical implications of myocardial bridging may vary from protection against atherosclerosis to systolic vessel compression and resultant myocardial ischaemia.  相似文献   

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