缺血再灌心肌VFT、钙含量、心律的同步动态变化及SOD对其影响

本实验用雄性Wistar大鼠173只,造成心肌缺血30min,再灌20min。共分19组,分别测定单纯再灌时正常对照,缺血30min、再灌即刻、3min、5min、10min及20min的VFT及钙含量(不含10min测定组),SOD再灌流即刻、3min、5min的VFT及钙含量,串脉冲刺激法测VFT,原子吸收光谱法测心肌钙含量,四导记录仪描记ECG     

家兔心脏短期缺血后再灌流时心功能的变化及SOD的影响

本实验利用家兔急性心肌缺血后早期再灌流动物模型,观察早期再灌流对心功能的影响,并利用自由基清除剂(超氧化物歧化酶,s0D)探索自由基在其中的可能作用。实验过程中测取心功能指标;观察结束后,分别从缺血区与非缺血区心内膜下取心肌电镜标本。实验发现,单纯再灌流组的心功能指标明显低于持续结扎组,SOD再灌流组的心功能比单纯再灌流组恢复得早、恢复程度高;缺血区心肌超微结构的损伤程度,依次为持续结扎组>单纯再灌流组>SOD再灌流组,非缺血区心肌超微结构只是单纯再灌流组变化较明显。结果表明,自由基对短期缺血后再灌流过程中心功能损伤起着一定的作用,其损伤范围随着再灌流的发生扩散到非缺血区。     

弱电流刺激家兔下丘脑乳头体核对缺血心肌再灌流早期心律的影响

对缺血心肌再灌流早期发生的心律失常,人们多从心脏本身研究其机制,而很少考虑与下丘脑的关系。本实验的目的是观察缺血心肌再灌流30秒内弱电流(数拾微安)刺激家兔下丘脑乳头体核对心律的影响,从而探讨缺血心肌再灌流期心律失常的发生与下丘脑的关系。     

模拟缺血及再灌流对绵羊浦肯野细胞的损伤效应

应用细胞内微电极记录方法及电镜观察缺血及再灌流对绵羊浦肯野细胞电活动及超微结构的变化。用缺血溶液(低氧、无糖、高钾及高乳酸)灌流3小时,然后用正常台氏液再灌流2小时。缺血3小时和     

腹蛇抗栓酶对大鼠离体心脏缺血/再灌注损伤的影响

本实验采用20只SD大鼠心脏Langendorff灌流模型,观察了腹蛇抗栓酶对其缺血(15cmH_2O)20min再灌注(70cmH_2O)30min时心率、心律、心肌收缩幅度及心肌组织内MDA、SOD等的影响。结果表明:缺血时,对照组(单纯缺血/再灌和治疗组(灌流液内加入腹蛇抗栓酶2.5U/L)的心率均低于     

镁对缺血心肌的作用

镁对正常心肌及缺血后再灌注心肌的作用已引起广泛重视,本工作拟探讨不同浓度镁对缺血期间心肌功能、代谢及缺血后恢复过程的影响实验采用Wistar大鼠离体等容收缩心脏,行Langendorff灌流。常规K H液预灌30分钟后行低灌流缺血     

心肌挫抑发生机制的实验探讨及高镁的保护作用

心肌挫抑(myocardial stunning)的发生机制迄今尚未阐明。本实验以Langendorff灌流模型,研究了短暂低流缺血(0.2ml/min)15min及再灌10min后心肌形态学、心肌含水量、心肌钙、心肌高能化合物(ATP和磷酸肌酸CP)及心肌血管线密度(Lv)的变化,以及高镁(2.4mM)对心肌挫抑的影响。实验发现:(1)虽然缺血组心肌无任何坏死,但其心率一左室发展压乘积(RPP)仅恢复达缺血前的77％。且与对     

钙离子浓度变化对大鼠缺血心室致颤阈值的影响及其与cAMP、cGMP及ATP的关系

本文目的是观察不同钙离子浓度([Ca~(2 )])对急性局部缺血大鼠心脏室颤阈(VFT)的影响及其与心肌cAMP、cGMP和ATP含量变化的关系。结果表明,[Ca~(2 )]与缺血心脏VFT下降幅度呈正相关(r=0.7998,p<0.05);而[Ca~(2 )]与缺血心肌cAMP/cGMP比值、ATP含量则呈负相关(分别r=-0.887、r=-0.864,均p<0.05);缺血心脏VFT下降幅度与cAMP/cGMP比值亦呈显著负相关(r=-0.992,p<0.01),提示心肌细胞内游离Ca~(2 )水平可能是缺血心室易颤性(VV)的决定因素;cAMP水平或cAMP/cGMP比值则可能是通过影响Ca~(2 )内流而起作用的间接因素;而ATP贮量对缺血心脏VFT下降可能有一定保护作用。     

丹参滴丸对缺血/再灌注损伤心肌高能磷酸化合物的影响

目的 :进一步探讨丹参滴丸对缺血 /再灌注损伤心肌的保护作用及其机制。方法 :采用Ｌａｎｇｅｎｄｏｒｆｆ离体心脏灌流技术 ,制备心肌缺血 /再灌注损伤模型 ,利用高效液相色谱仪 (ＨＰＬＣ)测定离体大鼠心肌组织中的高能磷酸化合物的含量变化。本实验共分 6组 :正常对照组 :大鼠心脏离体后 ,接在灌流装置上持续灌流 75ｍｉｎ。单纯缺血再灌组 :先预灌 1 5ｍｉｎ ,然后停止灌流 ,保持心脏温度恒定在 37℃ ,在无氧 ,无灌流液的条件下旷置 40ｍｉｎ ,再恢复灌流 2 0ｍｉｎ。丹参滴丸前保护组 :预灌时加丹参滴丸 ,后处理同单纯缺血再灌组。丹参…     

绵羊浦肯野纤维在“缺血”溶液灌流时的电生理变化

用缺氧、低pH、高钾、无糖的模拟“缺血”溶液灌流离体绵羊心脏浦肯野纤维,观察了“缺血”对心肌跨膜电位和离子流的影响,变化的先后程序以及可逆性。实验共观察24例。在“缺血”过程中,首先出现动作     

Changes in Passive But Not Active Mechanical Properties Predict Recovery of Function of Stunned Myocardium

The time course of alterations in active and passive mechanical properties of stunned myocardium during ischemia and throughout reperfusion has not been thoroughly quantified. This investigation tested the hypothesis that the amount of injury as well as the rate and extent of recovery of contractile function in postischemic, reperfused myocardium are directly correlated to changes in regional active and passive elastance and viscosity. A modified viscoelastic Voigt model was employed to quantify myocardial mechanical properties. Left ventricular pressure and segment length (in both ischemic and normal regions) were fit to the model consisting of an active elastic spring in parallel with a viscous damper and a passive elastic spring. The mechanical properties of myocardium from dogs which recovered (50%) baseline regional contractile function as determined by percent segment shortening (n=7) were compared to those from dogs that did not recover function (n=7). Both groups displayed decreased active elastance in the ischemic region during coronary artery occlusion, and this decrease was maintained in the nonrecovery group. Increases in viscosity of ischemic myocardium were observed in both groups during coronary occlusion but returned to control only in the recovery group. The nonrecovery group demonstrated increased passive elastance in the ischemic region during coronary occlusion and throughout the reperfusion period whereas the recovery group remained unchanged. We conclude that functional recovery of stunned myocardium is directly related to alterations in mechanical properties caused by ischemia and that changes in passive elastance during occlusion may predict the ability of ischemic myocardium to recover contractile function. © 1999 Biomedical Engineering Society. PAC99: 8719Rr, 8719Uv, 8710+e     

左心室局部心肌缺血时采用压力控制间歇闭塞冠状穴的仿真研究

为了研究左心室局部心肌缺血时采用压力控制间歇闭塞冠状穴（ＰｒｅｓｓｕｒｅＣｏｎｔｒｏｌｅｄＩｎｔｅｒ－ｍｉｔｅｎｔＣｏｒｏｎａｒｙＳｉｎｕｓＯｃｃｌｕｓｉｏｎ，简称ＰＩＣＳＯ）对心血管系统一些重要血液动力学参量的影响以及对缺血心肌的挽救作用，我们建立了一个详细的冠脉循环模型和左心室局部心肌缺血时的组分式模型，并将它们纳入我们原有的心血管循环系统模型中。在计算机仿真实验中，我们考察了缺血心肌的弹性对ＰＩＣＳＯ辅助效果的影响以及ＰＩＣＳＯ的最佳闭塞／释放时间。仿真结果指出：缺血心肌损伤越严重，弹性越小，冠状穴闭塞（ＣＳＯ）期间缺血区域的毛细血管与静脉之间的前、后向血流就越小，ＰＩＣＳＯ的辅助效果也越小；ＣＳＯ不改变心肌的耗氧量，但ＣＳＯ期间的逆向血流能给心肌增加部分供氧量；ＰＩＣＳＯ的最佳闭塞／释放时间是一组使冠状动脉血流以及毛细血管与静脉之间的前、后向血都相对最大时的折中值。     

局部缺血"预处理"诱导家兔相邻非缺血心肌热休克蛋白70基因表达

目的：研究兔心局部缺血“预处理”后,局部缺血和相邻非缺血心肌热休克蛋白７０（ＨＳＰ７０）ｍＲＮＡ的水平变化。方法：提取心肌组织总ＲＮＡ,用ＨＳＰ７０探针进行斑点杂交。结果：缺血预处理组的缺血区和非缺血区ＨＳＰ７０ｍＲＮＡ表达水平均显著高于对照组相应部位（Ｐ＜００５）,而每组内的缺血区及非缺血区间无显著差异（Ｐ＞００５）。结论：局部缺血“预处理”后,缺血和非缺血区两处心肌的内反应呈“一致性”;缺血预处理对心肌的保护作用可能与ＨＳＰ７０的合成增多有关。     

氟伐他汀对兔心肌缺血再灌注损伤的防治效应

目的：观察氟伐他汀对心肌缺血再灌注损伤的防治作用及对心肌ICAM-1 mRNA表达的影响。 方法： 24只日本大耳白兔，随机分3组，假手术组、对照组、处理组（给予氟伐他汀10 mg·kg－1·d－1喂服1周）,所有动物在手术前检测血脂，对照组和处理组复制缺血再灌注模型，假手术组只穿线不结扎。监测血流动力学指标，检测血清乳酸脱氢酶（LDH）和肌酸激酶（CK）的活性。RT-PCR检测缺血区及假手术组对应区域心肌ICAM-1 mRNA的表达。 结果： 各组动物在手术前1 d血脂指标无统计学差异；缺血开始后处理组各时点左室舒张末压（LVEDP）小于对照组（P＜0.05），左室内压变化最大速率（±dp/dtmax）大于对照组（P＜0.05）；他汀组LDH-1、CK、CKMB活性均显著小于对照组（均为P＜0.01)；他汀组心肌组织ICAM-1 mRNA表达显著低于对照组(P<0.01),假手术组表达最少。 结论： 氟伐他汀预处理能减轻心肌缺血再灌注损伤，其机制可能与抑制炎症反应有关。     

Integrative Models for Understanding the Structural Basis of Regional Mechanical Dysfunction in Ischemic Myocardium

Myocardial ischemia and many other cardiac pathologies are associated with regional ventricular dysfunction. Since the distributions of stress and material properties cannot be measured directly in intact myocardium, understanding how regional alterations in myocardial strain or segment function are related to underlying cellular dysfunction must be deduced from theoretical models. Here, we describe how anatomically detailed, three-dimensional computational models can be used in conjunction with experimental or clinical studies to elucidate the structural basis of regional dysfunction in acutely ischemic and ischemic-reperfused (stunned) myocardium in vivo. Integrative experimental and computational analysis shows that: (1) in acutely ischemic myocardium, the transition from abnormal systolic strain in the ischemic region to normal shortening in adjacent, normally perfused tissue is governed primarily by systolic blood pressure and regional fiber orientation rather than the geometry of the perfusion boundary; and (2) in stunned myocardium, the degree of reperfusion injury to the contractile apparatus may be uniform across the wall thickness despite observations that the extent of ischemia and the impairment of regional strain during reperfusion are both significantly greater in the subendocardium. © 2000 Biomedical Engineering Society. PAC00: 8719Hh, 8719Uv, 8719Ff, 8719Rr, 8710+e     

凝集素在大鼠心脏缺血预处理中的应用

目的：实验拟通过刀豆素（ＣＯＮＡ）和麦芽素（ＷＧＡ）检测缺血再灌注损伤大鼠心肌和缺和缺血预处理大鼠心肌细胞膜凝集素受体的变化。方法：采用ＳＤ雄性大鼠１８只分３组：假手术组、缺血再灌注组、缺血预处理线,分别取三组大鼠左心室前壁心肌,常规石蜡包埋切片,分别用刀豆素、麦芽素分子探针进行ＡＢＣ法染色。结果：假手术组ＣＯＮＡ和ＷＧＡ细胞反应强,缺血再灌注组ＣＯＮＡ和ＷＧＡ细胞反应弱。缺血预处理组ＣＯＮＡ和Ｗ     

The effect of verapamil on myocardial ultrastructure during and following release of coronary artery occlusion

Although the calcium channel blocking agent verapamil has been shown to have beneficial effects on ischemic myocardium, its effect on cardiac ultrastructure during regional myocardial ischemia and following coronary reperfusion has not been studied in detail. The purpose of this study was to investigate the effect of verapamil on the ultrastructure of myocardium during the early phase of ischemia and following coronary reperfusion. Open-chest anesthetized dogs were subjected to 1 hr of occlusion of the proximal left anterior descending coronary artery followed by 1 hr of reperfusion. The mean ischemic score, a semiquantitative index of ultrastructural damage, was significantly lower in verapamil-treated (0.9 ± 0.3) than in untreated dogs (1.9 ± 0.2, P < 0.025) during coronary occlusion and especially following reperfusion (1.0 ± 0.3 versus 2.9 ± 0.5, respectively P < 0.025). Verapamil treatment prevented the hastening of ultrastructural damage (explosive cell swelling phenomenon) associated with reperfusion into severely ischemic myocardium. Verapamil resulted in a more profound reduction of the extent of ultrastructural damage of mitochondria compared to other organelles. Thus, this study supports the concepts that verapamil reduces ultrastructural damage both during coronary occlusion and following coronary reperfusion and may reduce ischemic damage by protecting mitochondrial structure.     

大鼠心肌缺血/再灌注损伤及预处理apelin的表达

目的观察大鼠心肌缺血/再灌注损伤及预处理中apelin表达变化,探讨其可能的作用。方法SD大鼠60只随机分成4组:缺血/再灌注组(IR),预处理组(IP),假手术组(SH)和正常对照组(NC)。放免法测定血浆及心肌apelin-36蛋白含量,免疫组化法观察心肌apelin的表达,RT-PCR方法探讨大鼠心肌apelin mRNA表达。结果(1)血浆、心肌组织apelin-36浓度:IR的含量分别比NC低36.1%、45.6%(P<0.01),IP分别比NC低23.8%、24.7%(P<0.01)。SH与NC、IR与IP比无差异(P>0.05)。(2)apelin免疫组化染色吸光度值:IR与IP比NC分别低65.3%和36.8%(P<0.01,P<0.05),IR比IP低45.1%(P<0.05)。SH与NC无差别(P>0.05)。(3)心肌apelin mRNA的水平:IR是NC的40.2%(P<0.01),IP为NC的65.2%(P<0.05),IR是IP组的38.3%(P<0.05),SH与NC无差别(P>0.05)。结论在心肌缺血/再灌注损伤及预处理过程中,大鼠血浆及心肌组织apelin-36蛋白及基因表达下调,提示apelin在该病理生理过程中可能有重要作用。     

Hypoaldosteronism without hyperkalemia

Summary Selective hypoaldosteronism has almost invariably been described with hyperkalemia as principal manifestation. The prevalence of hypoaldosteronism and its relationship to plasma potassium, sodium, renin activity (PRA), body sodium-volume state and renal function was evaluated prospectively in 100 non-azotemic patients with diabetes mellitus and 46 with renal disease and normal to moderately impaired kidney function. Ninety healthy subjects served as controls and provided normal ranges for PRA and aldosterone (PA) relative to age and/or sodium excretion. Six diabetics (6%) and 2 renal patients (4.5%) had hypoaldosteronism; their plasma creatinine was <1.4 mg/100 ml. Nineteen diabetics (19%) and 13 renal patients (26%) had borderline hypoaldosteronism; 10 of the renal group had a plasma creatinine of 1.4 to 3.9 mg/100 ml. Plasma cortisol was consistently normal. Except for the presence of hyperkalemia in one patient with borderline hypoaldosteronism and azotemia, plasma potassium was also normal. Mean age, blood pressure, plasma cortisol and electrolytes, urinary potassium, blood glucose (diabetics only) and blood volume, exchangeable sodium and renal function were comparable between low, borderline-low or normal PA subgroups with diabetes or kidney disease. The body sodium-volume state was normal except for increased (p<0.01) exchangeable sodium in diabetics. PA correlated (p<0,01) with PRA. Mean PRA tended to be lowered in hypoaldosteronism; but some patients of this subgroup and most with borderline hypoaldosteronism had normal PRA. These findings demonstrate that hypoaldosteronism may exist without hyperkalemia or overt sodium wasting and may accompany non-azotemic diabetes mellitus or renal disease. This constellation favors a more facultative role of aldosterone as factor protecting against potassium retention in non-azotemic man. Asymptomatic hypoaldosteronism is probably more common than the symptomatic form and may be caused by angiotensin-deficiency or altered adrenal function.This work was supported by the Swiss National Science Foundation     

脑缺血再灌注后血栓形成与血浆纤维蛋白原水平的变化

目的 :在动物活体模型上 ,连续观察脑缺血 /再灌注时脑软膜微血管内血栓形成的过程并测量缺血 /再灌注不同时期血浆纤维蛋白原的变化。方法 :用夹闭沙土鼠双侧颈总动脉的方法复制脑缺血再灌注模型。颈动脉注入 0 .0 67%异硫氢酸荧光黄 (FITC) 0 .2ml后 ,在荧光显微镜下观察脑软膜微血管内血栓形成的过程 ,并在缺血 15min、30min、再灌注 30min、1h、6h时采血 ,用凝血酶凝固法测量血浆纤维蛋白原。结果 :单纯缺血期血流速度明显减慢 ,细动脉、细静脉管径缩小 ,有部分毛细血管内血流停滞。再灌注后 ,血流速度加快 ,随再灌时间的延长 ,白细胞粘附、贴壁明显增多 ,血管内皮增厚 ,纤维蛋白丝网络血细胞及血小板 ,呈絮状团块附着在血管内壁上 ,逐渐形成壁栓 ,阻碍血细胞的流过。缺血期和再灌注后血浆纤维蛋白原水平均高于正常对照组 ,以缺血 30min和再灌 1h时增高最为明显 (P <0 .0 1)。再灌 6h时又明显降低 ,与单纯缺血 30min组比较有显著性差异 (P <0 .0 1)。结论 :再灌注后快速恢复的血流加重了内皮细胞的损伤 ,白细胞、血小板粘附 ,导致血栓形成 ,并认为血浆纤维蛋白的形成在此病理过程中起着重要的作用