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本研究用14只麻醉开胸犬,分析了阻断冠脉后缺血心肌局部静脉血液中血小板功能变化与体液因素改变的关系。结果表明,心肌缺血时,血小板聚集率(PAgR)明显增大,并伴有TXB_2含量增高、TXB,/6-酮-PGF_(1a)比值增大和血小板计数(PC)减少。此外,随缺血时间延长,全血粘度、红细胞压积(HCT)和红细胞计数(EC)增高,而白细胞计数(NC)、Po_2和pH降低。缺血60min时,将红细胞聚集率与有关参数的百分变化率进行相关分析的结果表明,在PAgR与TXB_2、NC和Po_2之间呈明显正相关(分别为r=0.887,P<0.01;r=0.757,P<0.05;r=0.758,P<0.05),另外在EC和6-酮-PGF_(1a)之间也有正相关关系(r=0.856,P<0.01)。这些结果提示,阻断冠脉后发生的前列腺素、血液粘度、红、白细胞以及缺氧和酸中毒等异常变化,均具有一定的致血小板功能改变的作用。  相似文献   

3.
郭利光  欧阳军 《生物磁学》2009,(16):3188-3190
现已证明了脾脏是人体内最大周围淋巴器官,拥有多种免疫活动性细胞因子,又是储血、滤血、造血、毁血的器官,有着重要的抗感染、抗肿瘤功能,决不能随意切除。所以正确的处理切脾与保脾、保命与保功能的关系至关重要,脾切除后自体脾组织移植进行保留脾脏功能已逐渐被认可。  相似文献   

4.
血道高转移瘤株FC、淋巴合并血道高转移瘤株U14、淋巴道高转移瘤株H22、非转移瘤株P615分别接种于336只纯系近交615小鼠.不同时间取血并处死动物,进行组织学及血液流变学检查.将转移瘤发展过程分为潜伏期、侵袭期、转移早、中、晚期,非转移瘤发展过程分为潜优期、增殖期、囊腔形成期及中心坏死期.本实验结果显示,不同转移能力及途径肿瘤发展的不同时期血液流变学变化规律不同,因而表明肿瘤侵袭、转移与血液流变学变化之间存在互为因果的紧密关系.其临床诊断及治疗意义被讨论.  相似文献   

5.
目的:通过建立脾细胞移植和脾片联合移植动物模型来观察脾片移植早期体液免疫功能恢复状况.方法:Wistar大鼠48只,随机分为4组,其中A组为对照组,行脾切除术,B组为脾片移植组,C组为脾细胞移植组,D组为睥细胞脾片联合移植组,在建立模型前、及模型成功后1周、4周、8周抽血,检测外周血IgM、IgG、IgA水平并进行比较.结果:A组脾切除后IgM逐渐降低(P<0.05);B组移植后8周IgM接近正常(P>0.05);C组移植后IgM到4周逐渐接近正常(P>0.05);而8周逐渐降低(P<0.05);D组术后4周和8周接近正常(P>0.05);在术后1、4周C和D组与A和B组有差异(P<0.05),在术后8周B和D组与A和C组有差异(P<0.05).而IgG、IgA在四组术前术后变化不大(P>0.05).结论:在脾片移植的基础上联合脾细胞移植能弥补脾片移植旱期的部分体液免疫功能.  相似文献   

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肾上腺髓质在急性心肌缺血时血液流变学变化中的作用   总被引:3,自引:0,他引:3  
本实验观察了阻断冠脉血流后血液流变学的变化并分析了肾上腺髓质活动增强在急性心肌缺血早期血液流变学变化中的作用。实验结果表明,对照组阻断冠脉血流40min时全血粘度已显著增加,血细胞压积、血浆纤维蛋白原浓度逐渐升高。阻断冠脉血流前切断双侧内脏大神经可消除心肌缺血早期血液流变学的异常变化,而切断内脏大神经后输注肾上腺素又可使心肌缺血时全血粘度、血细胞压积等各项指标出现明显异常。上述结果提示,阻断冠脉血流后交感-肾上腺系统活动增强可能是急性心肌缺血早期血液流变学变化的重要原因。  相似文献   

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本实验在14只麻醉开胸狗身上观察了急性心肌缺血早期冠脉侧支血流量与血液流变学变化的关系。动物均分为两组:Ⅰ组,在不控制血压的情况下,观察心肌缺血早期单位压力差下冠脉侧支血管流量(CVC)的变化;Ⅱ组,在保持主动脉血压不变的条件下,根据 Wyatt 等公式计算流经缺血区末梢血管的有效侧支血流量(ECF)。实验结果表明,阻断冠脉血流30min时,低切变率下全血比粘度已明显增高,随后继续增加,60min 时Ⅰ、Ⅱ两组分别较对照值增高19.0%和11.4%(均为P<0.01)。血液粘度增高时,CVC 仅轻度降低(p>0.05),但 ECF却随着血液粘度的增高而逐渐明显降低,缺血60min 时较对照值降低12.1±2.6%(P<0.01)。血液粘度变化与 ECF 变化之间呈明显负相关(r=-0.796,p<002)。上述结果提示,心肌缺血早期血液流变学的异常变化虽然对冠脉侧支血管的血流阻力影响较小,但却使流经缺血区末梢血管的有效侧支血流量明显减少而加重心肌缺血。  相似文献   

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急性心肌缺血对血液流变学和心脏收缩功能改变的影响   总被引:1,自引:0,他引:1  
在麻醉开胸狗观察了急性心肌缺血对血液流变学和心脏收缩功能改变的影响。在阻断狗前降支冠脉1h内,血液流变学各参数发生异常变化,表现为高、低切变率下全血粘度(ηbh、ηb1)、血浆粘度、血细胞压积和纤维蛋白原升高,红细胞电泳时间缩短。同步描记心电、心音和颈动脉搏动图而记录的心脏收缩时间间期,表现为射血前期(PEP)延长、左室射血时间(LVET)缩短和PEP/LVET比值增大。此外,动脉舒张压(DAP)升高,心输出量(CO)减少。上述各参数均与对照值有明显差异,P<0.05。缺血40min时,对ηb1和PEP/LVET或DAP进行相关分析,呈明显正相关,P<0.05;ηb1和CO呈明显负相关,P<0.01。结果提示,心肌缺血后发生的血液流变学异常变化,具有增加射血阻力和减少心输出量的作用。  相似文献   

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刘海洲  程琳 《蛇志》1994,6(2):15-17
血液流变学测定在不同人群中价值的研究刘海洲,程琳,黄继田等河南省商丘市人民医院关键词血液流变化;血液粘度;全血粘度;血浆粘度;心脑血管疾病血液流变学测定的研究,是近几年来兴起的新兴边缘学科,被医学界广为重视,纳入了研究的课题。商丘市人民医院从1989...  相似文献   

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褐藻酸钠硫酸酯对血液流变学和血小板聚集的影响   总被引:1,自引:0,他引:1  
褐藻酸钠硫酸酯(Sodium Alginate Sulfates SAS)是以褐藻酸为原料经磺化、酯化而成的硫酸酯多糖的钠盐系列物(Ⅰ、Ⅱ、Ⅲ、Ⅳ)。本文研究了SAS对兔和大鼠血液流变学和血小板聚集的影响,结果发现:SAS静注5mg/kg能够显著降低高切、低切下的全血比粘度,降低血细胞压积,降低红细胞聚集指数,提高红细胞沉降率,从而改善血液的流变特性。实验中还发现,SAS体内外均可缩短大鼠红细胞电泳时间,体内还可以缩短大鼠血小板电泳时间,而体外则可延长血小板电泳时间。SAS体外可诱导兔、大鼠血小板聚集,能够促进ADP诱导的血小板聚集,而对AA诱导的血小板聚集则无促进作用。结果提示:静注SAS能够改善血液的流变特性,增加红细胞和血小板表面电荷,抑制红细胞及血小板间的粘附和聚集,从而使其具有一定的抗血栓作用。同时还提示,SAS在体内循环和代谢的过程中,结构可能发生了变化,从而使其体内、体外的作用特征出现了相对立的结果。  相似文献   

11.
急性心肌缺血时低切变率下全血粘度变化机理研究   总被引:3,自引:0,他引:3  
本实验旨在分析狗急性心肌缺血时低切变率下全血粘度异常升高与红细胞电泳率(EM)和血浆纤维蛋白原浓度变化间的关系。实验结果表明,阻断冠脉血流40min时,低切变率下全血粘度已显著升高,EM明显降低,二者呈高度负相关,此时血浆纤维蛋白原浓度仅轻度增加。缺血时间进一步延长时,EM逐渐恢复,而血浆纤维蛋白原浓度显著升高,此时低切变率下全血粘度升高主要与血浆纤维蛋白原变化有关。  相似文献   

12.
Adenosine and cardioprotection during reperfusion – an overview   总被引:5,自引:0,他引:5  
Ischemic heart disease includes a number of entities that have been grouped in accordance with physiopathology and evolutive criteria. In recent years new ischemic syndromes have been described. Within the new ischemic syndromes, ventricular post-ischemic dysfunction – also known as stunned myocardium – is worth mentioning. In this route, several studies have suggested that reperfusion per se could cause cellular injury (reperfusion injury). In previous years, a protective effect on the injury caused by ischemia and reperfusion in the heart has been attributed to adenosine. These effects have been documented in different experimental in vivo and in vitro models. Thus, the administration of exogenous adenosine, or agonists of adenosine receptors prior to ischemia reduces the size of the infarction, improves the recovery of the ventricular function during reperfusion (attenuating stunning) and prolongs the time period to the ischemic contracture. However, focusing on a potential therapeutic application, it is of the utmost importance to find this protection and learn the mechanisms involved when procedures are applied during early reperfusion.We showed that adenosine, administered from the beginning of reperfusion, attenuated systolic and diastolic (myocardial stiffness) alterations of the stunned myocardium. This protective effect was mediated by the activation of A1 adenosine receptors, and without modification on infarct size. According to some authors, adenosine can decrease the release of endothelin, during early reperfusion, and reduce an overload of Ca2+ that could cause a cellular lesion. Finally, ischemic preconditioning involves a series of intracellular events that are initiated with the activation of the A1 receptor, and end at the sensitive K+ ATP channels of the mitochondria. The phosphorylation and opening of these channels would cause the protective effect. Activation of this specific mechanism during reperfusion has not been studied extensively.  相似文献   

13.
目的:研究动态心电图对无症状性心肌缺血的临床诊断价值。方法:收集我院2014年6月-2015年6月我院接受诊治的冠心病(CAD)患者120例作为研究对象,采用动态心电图仪检测记录24h心电图信息,将动态心电图检测为心肌缺血的患者分为A组(无症状心肌缺血)、B组(有症状心肌缺血),比较两组患者基本信息、心肌缺血发作阵次、ST段下降幅度、ST段下降持续时间、心肌缺血阈变异性、心率及心率失常发生率。结果:120例CAD患者中有95例患者出现心肌缺血,其中A组66例(占69.47%),B组29例(占30.53%),差异显著(P0.05)。A组ST段阵次改变明显高于B组,A组ST段下降幅度、ST段下降持续时间、心肌缺血阈变异性明显低于B组(P0.05)。A、B两组患者心肌缺血发作表现出昼夜节律,在时间段6:00-12:00最高,在时间段0:00-6:00最低(P0.05)。A组患者平均心率显著低于B组患者,心律失常发生率显著高于B组(P0.05)。结论:动态心电图能够准确的诊断出无临床症状心肌缺血,使患者得到及时的治疗,值得临床推广应用。  相似文献   

14.
    
Guanine nucleotide-binding regulatory proteins (G proteins) play a major role in the regulation of a number of physiological processes, such as stimulation or Inhibition of adenylate cyclase activity or gaiting of ionic channels. Myocardial ischemia could induce the changes in receptor-G protein signal transduction system in the heart. Therefore, this article will focus on the role and alterations of G proteins (especially, Gs and Gi) in myocardial ischemia. The Gi protein rapidly loses functional activity during very early myocardial ischemia. In contrast to Gi protein, the function of Gs protein during this phase has not been evaluated. Moreover, the changes in Gs protein after 30 min of ischemia are contradictory. However, the sensitization of the adenylate cyclase activity in the very early phase of acute ischemia is gradually replaced by a decrease in adenylate cyclase activity with prolonged ischemia. The decrease in the function and amount of Gs protein may be one of the factors that induce these changes. The function of Gs protein was also decreased in the canine hearts with ischemia and reperfusion. In contrast to ischemia and reperfusion, there are no significant alterations in G proteins and modulation of adenylate cyclase in the stunned myocardium. It has become increasingly evident that Gi protein may play an important role in the cardioprotective effects of preconditioning. When -adrenoceptor densities are reduced in chronic myocardial ischemia, decreased in the amount and function of Gi protein and increased amount of Gs protein may play the role in preservation of the adenylate cyclase activity. These alterations in G proteins may play the important role in the myocardial function during myocardial ischemia.  相似文献   

15.
炎症是引发心血管疾病的一个重要的危险因子.白细胞数量增多的患者更容易患上急性心肌梗塞、急性冠状动脉等疾病.对临床上白细胞数量高的数据与疾病预测之间的关系,这其中可能有几种机制.测量白细胞的数量和亚群可能是区分急性血管疾病患者危险程度的一种更好的方法.  相似文献   

16.
大鼠心肌整体缺血及离体再灌注致生物膜的损伤作用   总被引:1,自引:0,他引:1  
目的和方法:利用整体大鼠异丙肾上腺素损伤(ISO)和离体大鼠全心停灌/再灌(I/R)两种模型,观察了心肌缺血和缺血/再灌注对心肌生物膜-线粒体膜及肌纤维膜损伤的影响。结果:ISO(5mg/kg,皮下注射)和I/R(20min/20min)可导致大鼠心脏生物膜产生严重损伤,表现为心肌线粒体脂质过氧化产物明显增加,线粒体磷脂酶A2(PLA2)激活,从而导致线粒体膜磷脂(PL)含量减少,磷脂分解产物游离脂肪酸(FFA)增加,膜脂流动性(LFU)降低,线粒体Ca^2 -ATPase及肌纤维膜Na^ ,K^ -ATPase活性降低,线粒体呼吸功能降低、呼吸链氧化磷酸化解偶联,高能磷酸化合物生成减少。结论:整体ISO和离体I/R可导致大鼠心肌线粒体、肌纤维膜结构和功能损伤。  相似文献   

17.
A marked loss of virulence of Babesia bovis for normal cattle was observed during its rapid serial, blood passage in splenectomized calves. In 2 strains studied closely, responses to infection in cattle inoculated with parasites collected from the 11th passages were minimal, although the splenectomized donors were severely affected. The change was reversed by passaging in intact hosts, and in one experiment the parasites had become very virulent at passage 5. The finding has proved useful in the preparation of safe, living vaccines to control babesiosis. Selection either for immunogenic antigens, against immunosuppressive ones, or a combination of these effects may cause the decrease in virulence.  相似文献   

18.
大鼠肝癌诱发过程中血粘度及红细胞变形能力的异常改变   总被引:4,自引:0,他引:4  
为了全面地反映肝癌发生发展整个过程的血液流变性的异常,本实验采用二乙基亚硝胺诱发大鼠肝癌模型,分六个相检测五个切变率下的全血粘度、血浆粘度及红细胞变形能力。结果表明红细胞变形能力随着肿瘤发展逐渐减低,血浆粘度随着诱癌时间延长 渐升高,到肿瘤晚期趋于平缓,而全血粘度先是升高,到诱癌20周以后反而有下降趋势。  相似文献   

19.
    
Hydrogen sulfide (H2S), which has been identified as the third gaseous signaling molecule after nitric oxide (NO) and carbon monoxide (CO), plays an important role in maintaining homeostasis in the cardiovascular system. Endogenous H2S is produced mainly by three endogenous enzymes: cystathionine β-synthase, cystathionine γ-lyase, and 3-mercaptopyruvate sulfur transferase. Numerous studies have shown that H2S has a significant protective role in myocardial ischemia. The mechanisms by which H2S affords cardioprotection include the antifibrotic and antiapoptotic effects, regulation of ion channels, protection of mitochondria, reduction of oxidative stress and inflammatory response, regulation of microRNA expression, and promotion of angiogenesis. Amplification of NO- and CO-mediated signaling through crosstalk between H2S, NO, and CO may also contribute to the cardioprotective effect. Exogenous H2S donors are expected to become effective drugs for the treatment of cardiovascular diseases. This review article focuses on the protective mechanisms and potential therapeutic applications of H2S in myocardial ischemia.  相似文献   

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