超声二维斑点追踪显像技术检测犬顿抑心肌跨壁力学状态的变化

目的 应用超声二维斑点追踪显像技术检测犬顿抑心肌心内、外膜纵向的应变变化,探讨顿抑心肌的跨壁力学变化及其随时间的变化规律。方法 12只犬左冠状动脉前降支结扎20 min,再灌注120 min,分别于结扎前、结扎期间、再灌注后即刻、30、60、90、120 min采集心尖切面图像。应用超声二维斑点追踪显像技术检测缺血及非缺血节段心内膜、心外膜、整体节段应变参数:纵向峰值应变(LS_peak)、峰值应变延迟时间(TPS_LS),并进行比较分析。结果 犬心肌左冠状动脉前降支结扎后、再灌注后即刻缺血节段心内、外膜、整体节段LS_peak明显减低,TPS_LS延长,且LS_peak以心内膜下心肌减低更明显;随再灌注时间延长,二维应变逐渐恢复,心外膜下心肌恢复更快,缺血节段整体心肌恢复正常时,心内膜下心肌仍未恢复正常。非缺血节段在左冠状动脉前降支结扎后、再灌注后即刻心内、外膜下LS_peak明显增加,TPS_LS延长,再灌注30 min恢复正常。结论 超声二维斑点追踪显像技术可检测犬顿抑心肌在缺血及再灌注阶段心内、外膜下心肌二维应变变化。     

Coronary vascular injury due to ischemia-reperfusion is reduced by pentoxifylline.

Myocardial ischemia and reperfusion cause coronary vascular injury involving both the large epicardial arteries and the microcirculation. Although the mechanisms are unclear, leukocytes appear to play an important role. Since the methylxanthine derivative pentoxifylline (PTX) decreases neutrophil activity in vitro, we hypothesized that it might diminish coronary vascular injury due to ischemia and reperfusion. We investigated the effects of PTX on coronary microvascular and epicardial artery injury in open chest, anesthetized dogs undergoing moderate (60 min) or more prolonged (90 min) ischemia due to left anterior descending coronary artery occlusion followed by 60 min of reperfusion. As an index of microvascular injury, we assessed regional permeability with a dual radioisotope protein leak index (PLI) method. Both ischemic periods with reperfusion increased the PLI of severely ischemic (flow less than or equal to 20/ml/min/100 g) myocardium by 2.5- and 3-fold, respectively, compared to nonischemic (flow greater than or equal to 100 ml/min/100 g) myocardium. Treated dogs received PTX (20 mg/kg bolus plus 0.1 mg/kg/min infusion) before ischemia. PTX reduced the increase in the PLI by 40% after 60 min of ischemia (PLI = 5.87 +/- 0.48 vs. 4.10 +/- 0.52 untreated vs. PTX-treated; P less than .05), and by 25% after 90 min of ischemia (6.84 +/- 0.49 vs. 4.84 +/- 0.42; P less than .05). The amount of protein leak was inversely related to ischemic blood flow, and the magnitude of this relationship was significantly reduced in PTX-treated animals. In arterial rings from untreated dogs exposed to 90 min of ischemia followed by reperfusion, there was impaired relaxation to ADP and acetylcholine, but not to sodium nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reperfusion after acute coronary occlusion in dogs impairs endothelium-dependent relaxation to acetylcholine and augments contractile reactivity in vitro.

Endothelial injury may contribute to the augmented coronary vascular tone seen in myocardial ischemia by impairing endothelial production or release of vasodilators. In vitro reactivity of arterial rings was studied after 60 min of coronary occlusion and 60 min of reperfusion in anesthetized dogs. Ischemia without reperfusion blunted contractile reactivity to potassium chloride (KCl), whereas ischemia plus reperfusion augmented contractile responses to both KCl and ergonovine. The response to acetylcholine, an endothelium-dependent vasodilator, was abolished in reperfused arteries, whereas the response to nitroprusside, an endothelium-independent vasodilator, was intact. Verapamil pretreatment restored KCl contractile responses to normal in reperfused coronary rings and partially restored endothelium-dependent relaxation. Electron microscopy revealed a nondenuding epicardial coronary endothelial injury in reperfused arteries. These data support the hypothesis that reperfusion of ischemic myocardium augments reactivity to vasoconstrictor agents by causing endothelial cell damage, excessive calcium influx, and loss of modulating vasodilator function.     

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

The effects of ischemia on the canine myocardial (Na+ + K+)-ATPase complex were examined in terms of alterations in cardiac glycoside binding and enzymatic activity. Ability of the myocardial cell to bind tritiated ouabain in vivo was assessed after 1, 2, and 6 h of coronary occlusion followed by 45 min of reperfusion, and correlated with measurements of in vitro (Na+ + K+)-ATPase activity and in vitro [3H]ouabain binding after similar periods of ischemia. Regional blood flow alterations during occlusion and reperfusion were simultaneously determined utilizing 15 mum radioactive microspheres to determine the degree to which altered binding of ouabain might be flow related. Anterior wall infarction was produced in 34 dogs by snaring of confluent branches of the left coronary system. Epicardial electrograms delineated ischemic and border zone areas. Coronary reperfusion after 2 and 6 h of occlusion was associated with impaired reflow of blood and markedly impaired uptake of [3H]ouabain in ischemic myocardium. In both groups, in vivo [3H]ouabain binding by ischemic tissue was reduced out of proportion to the reduction in flow. Despite near-complete restoration of flow in seven dogs occluded for 1 h and reperfused, [3H]ouabain remained significantly reduced to 58 +/- 9% of nonischemic uptake in subendocardial layers of the central zone of ischemia. Thus, when coronary flow was restored to areas of myocardium rendered acutely ischemia for 1 or more hours, ischemic zones demonstrated progressively diminished ability to bind ouabain. To determine whether ischemia-induced alteration in myocardial (Na+ + K+)-ATPase might underlie these changes, (Na+ + K+)-ATPase activity and [3H]ouabain binding were measured in microsomal fractions from ischemic myocardium after 1, 2, and 6 h of coronary occlusion. In animals occluded for 6 h, (Na+ + K+)-ATPase activity was significantly reduced by 40% in epicardial and by 35% in endocardial layers compared with nonischemic myocardium. Comparable reductions in in vitro [3H]ouabain binding were also demonstrated. Reperfusion for 45 min after occlusion for 6 h resulted in no significant restoration of enzyme activity when compared to the nonreperfused animals. In six animals occluded for 2 h, a time at which myocardial creatine phosphokinase activity remains unchanged, (Na+ + K+)-ATPase activity was reduced by 25% compared with nonischemic enzyme activity. In five dogs occluded for 1 h, (Na+ + K+)-ATPase activity in ischemic myocardium was unchanged from control levels. We conclude that reduced regional myocardial blood flow, local alterations in cellular milieu, and altered glycoside-binding properties of (Na+ + K+)-ATPase all participate in the reduction of cardiac glycoside binding observed after reperfusion of ischemic myocardium. In addition, after 2 or more hours of severe ischemia, myocardial (Na+ + K+)-ATPase catalytic activity is significantly reduced despite incubation in the presence of optimal substrate concentrations.     

Localization of cardiac myosin-specific antibody in myocardial infarction.

Specific localization of purified antibody against cardiac myosin has been demonstrated in areas of altered myocardial membrane permeability after experimental myocardial infarction. Intravenously administered radioiodine-labeled antimyosin was selectively localized in infarcted myocardium of seven dogs 24 h after coronary occlusion. The mean ratio (+/-SE) of antimyosin antibody in infarcted to normal myocardium in the center of the infarct was 4.2+/-0.4 for endocardial and 2.9+/-0.3 for epicardial layers. By utilizing (Fab')2 fragments of antimyosin obtained by pepsin digestion of purified antibody, the ratio of uptake was increased in eight dogs to 6.1+/-0.6 in the endocardial and 3.3+/-0.4 in the epicardial layers at the infarct center 24 h after occlusion. These ratios were further increased in the infarct center to 13.8+/-1.2 in the endocardial and 7.3+/-0.8 in the epicardial layers when eight dogs were sacrificed 72 h after coronary occlusion. The specificity of antimyosin (Fab')2 localization in infarcted myocardium was demonstrated in four dogs by simultaneous intravenous administration of 125I-labeled antimyosin (Fab')2 and 131I-labeled normal rabbit gamma globulin (Fab')2. Nonspecific trapping of normal rabbit IgG (Fab')2 was observed to be about 38% of total antimyosin (Fab')2 uptake in the central zone of infarction. Regional blood flow was related to antimyosin (Fab')2 uptake in infarcted myocardium by utilizing simultaneous administration of 85Sr-labeled microspheres. An inverse exponential relationship between antimyosin (Fab')2 uptake and regional blood flow was observed (r=0.85). The specific localization of antimyosin antibody or its (Fab')2 components in infarcted myocardium suggests a conceptually new approach to myocardial infarct localization and sizing.     

Myocardial layer-specific analysis of ischemic memory using speckle tracking echocardiography

The assessment of post-systolic shortening (PSS) by speckle tracking echocardiography allows myocardial ischemic memory imaging. Because the endocardial layer is more vulnerable to ischemia, the assessment of this layer might be useful for detecting ischemic memory. Serial echocardiographic data were acquired from nine dogs with 2 min of coronary occlusion followed by reperfusion. Regional deformation parameters were measured in the risk and normal areas. Using speckle tracking echocardiography, circumferential strain was analyzed in the endocardial, mid-wall, and epicardial layers; and radial strain was analyzed in the inner half, outer half and entire (transmural) layers. In the risk area, peak systolic and end-systolic strain in the circumferential and radial directions significantly decreased during occlusion, but recovered to the baseline levels immediately after reperfusion in all layers. However, circumferential post-systolic strain index (PSI), a parameter of PSS, significantly increased during occlusion, and the significant increases persisted until 20 min after reperfusion in the endocardial and mid-wall layers. Radial PSI tended to increase after reperfusion in the inner half and entire layers but these increases were not significant compared with baseline. In the normal area, systolic strains and PSI in the radial and circumferential directions hardly changed before and after occlusion/reperfusion in all layers. In layer-specific analysis with speckle tracking echocardiography, circumferential PSS in the endocardial and mid-wall layers may be useful for detecting ischemic memory.     

斑点追踪技术评价犬急性心肌缺血及再灌注心内膜下心肌和心外膜下心肌径向应变

目的应用斑点追踪技术检测犬急性心肌缺血及再灌注不同时间点心内膜下心肌和心外膜下心肌的径向应变。方法选取20只健康成年杂种犬,结扎左冠状动脉第一对角支,分别对结扎前、结扎即刻、60、120和180min及再灌注即刻、60和120min基底水平、乳头肌水平和心尖水平心内膜下和心外膜下心肌的径向应变进行比较。结果在急性缺血过程中,基底水平心肌起代偿作用,其径向应变上升;乳头肌水平和心尖水平心肌下降明显,心尖水平心肌甚至出现反向运动。在急性缺血及再灌注过程中,心内膜下心肌对缺血更加敏感。再灌注后,乳头肌水平和心尖水平心内膜下和心外膜下心肌及跨壁的径向应变仍低于基础状态。结论斑点追踪技术可以评价犬局部及整体心脏功能,并判断急性心肌缺血的透壁程度。     

实时三维斑点追踪显像技术检测犬顿抑心肌左心室舒张功能延迟恢复

目的 应用实时三维斑点追踪显像技术(3D-STI)检测犬顿抑心肌左心室舒张功能的延迟恢复。 方法 结扎12只成年杂种犬左冠状动脉前降支,15 min后行再灌注;分别于缺血前、缺血5 min和15 min、再灌注30 min、60 min、90 min及120 min采集心尖切面三维图像,检测缺血及非缺血心肌峰值纵向应变(LS_peak)、主动脉瓣关闭时的纵向应变、舒张前1/3时点纵向应变,根据公式计算应变显像舒张指数(SI-DI)。 结果 缺血5 min和15 min缺血心肌LS_peak和SI-DI显著降低,随再灌注时间延长而逐渐恢复;LS_peak于再灌注120 min时恢复正常,SI-DI于再灌注120 min时仍低于正常;缺血5 min和15 min非缺血节段心肌LS_peak和SI-DI升高,均于再灌注30 min恢复正常。 结论 应用3D-STI可评价犬顿抑心肌缺血及再灌注阶段左心室局部心肌舒张功能的延迟恢复。     

Myocardial adenine nucleotide depletion within 1 h of acute coronary artery occlusion.

In anaesthetized open-chest casts with occlusion of the left anterior descending coronary artery (LAD), adenine nucleotides and degradation products were studied in small myocardial tissue samples (10-20 mg) with high-pressure liquid chromatography, and tissue blood flow was measured with radioactive microspheres 5, 10, 20, 40, and 60 min after LAD occlusion. There was a rapid and parallel decrease of myocardial ATP and accumulation of adenosine, inosine, hypoxanthine, and xanthine both in epicardial and endocardial half-layers of the ischaemic myocardium within the first 20 min of coronary occlusion. After 40 and 60 min, myocardial ATP content decreased and degradation products accumulated further in the endocardium but stabilized epicardially. Analysis of covariance showed that the slightly higher blood flow in ischaemic epicardial layers, did not explain the transmural difference in ATP content after 40 and 60 min. Adenosine decreased after 40 min of ischaemia in both wall layers reaching negligible amounts after 60 min. It is concluded that breakdown of energy stores is less severe in epicardial than in endocardial wall layers during the first hour after acute coronary occlusion in the cat heart. This transmural difference cannot be explained entirely by less severe epicardial ischaemia. Therefore, transmural heterogeneity in metabolic function during severe ischaemia may also be important.     

应用斑点追踪成像技术对急性心肌缺血及再灌注心内膜下心肌和心外膜下心肌旋转及扭转功能的研究

目的：本研究旨在应用斑点追踪成像（STI）技术通过测定心内、外膜下心肌、跨壁旋转及扭转角度等指标对急性心肌缺血及再灌注期间心脏功能进行评价。方法：对20只健康成年杂种犬结扎左冠状动脉第一对角支下方180 min并再灌注120 min,分别对结扎前、结扎即刻、结扎60 min、结扎120 min和结扎180 min及再灌注即刻、再灌注60 min和再灌注120 min基底水平和心尖水平的旋转及扭转指标进行比较。结果：①基底水平旋转的比较：随着缺血时间延长,跨壁角度逐渐减低。再灌注即刻,跨壁角度一过性增大。再灌注120 min,跨壁角度最低。②心尖水平旋转的比较：跨壁角度从结扎即刻开始下降,至结扎180 min达到最低值。再灌注即刻,跨壁角度快速上升。再灌注60 min、120 min缓慢上升。③扭转的比较：随着缺血时间的延长,跨壁扭转角度明显下降。结扎180 min跨壁扭转角度最低。再灌注即刻跨壁扭转角度快速恢复。结论：STI技术通过定量分析左室心内膜及心外膜下心肌局部和整体的旋转及扭转,可以判断心脏功能的变化。心内外膜下心肌旋转角度及跨壁角度、扭转角度及跨壁角度是评价急性心肌缺血及再灌注后室壁运动及心脏功能的有效手段。     

Regional Myocardial Blood Flow in Awake Dogs

The objectives of this study were to test the hypothesis in awake dogs that during control conditions endocardial vessels are maximally dilated and to determine whether variables introduced by general anesthesia and thoracotomy modify distribution of myocardial blood flow or impair capacity for augmentation of flow in response to a coronary vasodilator stimulus. Myocardial blood flow was measured in relatively small, 2-3 g, left ventricular epicardial and endocardial samples by using 7-10-mum radioisotope-labeled microspheres during control conditions and during infusion of adenosine in dosages which produced maximum increases in coronary blood flow. Measurements were made initially in awake resting animals and were repeated after pentobarbital anesthesia, thoracotomy, and pericardiotomy.Blood flow (mean+/-SEM) in the epicardium and endocardium, respectively, was 0.75+/-0.06 and 0.83+/-0.06 during control conditions and 4.98+/-0.28 and 4.49+/-0.27 cm(3)/min/g during adenosine. These data demonstrate considerable capacity for vasodilation in both myocardial layers and thus refute the hypothesis that endocardial vessels are maximally dilated during control conditions. During control conditions blood flow within epicardial and endocardial layers was essentially homogeneous around the circumference of the left ventricle. In contrast to previous studies in anesthetized animals, however, transmural gradients were present in most regions, i.e., endocardium: epicardium ratio (endo/epi) 1.06-1.16. During adenosine, circumferential epicardial flows were homogeneous; however, circumferential endocardial flows were inhomogeneous and increased less than epicardial flows, endo/epi 0.81-0.99.Anesthesia, thoracotomy, and pericardiotomy increased epicardial and endocardial flow, mean values 1.08+/-0.10 and 1.11+/-0.08 cm(3)/min/g, respectively. Transmural gradients remained in only papillary muscle regions. Adenosine increased epicardial flow comparably before and after anesthesia. Although adenosine increased endocardial flow three- to fourfold after anesthesia, the increase was considerably less than epicardial flow, i.e., endo/epi 0.63-0.78.     

The “No-Reflow” Phenomenon after Temporary Coronary Occlusion in the Dog

The role of microvascular damage in the genesis of the "no-reflow" phenomenon was investigated in the left ventricular myocardium of dogs subjected to temporary occlusions of a major coronary artery for 40 and 90 min. Intravenous carbon black or thioflavin S (a fluorescent vital stain for endothelium) were used to demonstrate the distribution of coronary arterial flow in control and damaged myocardium. These tracers were injected simultaneously with release of the coronary occlusion or after 5 or 20 min of reflow of coronary arterial blood. After 40 min of ischemia plus arterial reperfusion, usually the tracers were evenly distributed throughout the damaged tissue at each time of reperfusion. On the other hand, when reflow was allowed after 90 min of ischemia, portions of the inner half of damaged myocardium were not penetrated by the tracers. Electron microscopic study of this poorly perfused tissue revealed severe capillary damage; endothelial cells with large intraluminal protrusions and decreased pinocytic vesicles were common. Also, occasional intraluminal fibrin thrombi were noted, as well as extravascular fibrin deposits and erythrocytes. Myocardial cells were swollen in both poorly perfused and well-perfused irreversibly injured tissue. Contraction bands and mitochondrial Ca(2+) accumulation were prominent features of irreversible injury with reflow at 40 min but were not noted after 90 min of ischemia in areas with poor perfusion. These results suggest that 40 min of ischemia were tolerated by the capillary bed of the dog heart without serious capillary damage or perfusion defects, but that 90 min of ischemic injury was associated with the "no-reflow" phenomenon, i.e., failure to achieve uniform reperfusion. This failure of reflow was associated with extensive capillary damage and myocardial cell swelling. Death of severely ischemic myocardial cells in this model occurs before the onset of capillary damage and the no-reflow phenomenon.     

Effect of diltiazem on regional oxygenation of reperfused myocardium

Reperfusion after 2 hr of experimental ischemia results in reduced blood flow to the reperfused region, as well as elevated regional O2 extraction in that region. The aim of the present study was to determine whether diltiazem, administered during reperfusion, can improve regional blood flow and lower O2 extraction in the previously occluded region. In open-chest anesthetized dogs, 2-hr occlusion of the left anterior descending coronary artery was followed by a 4-hr period of reperfusion. In 7 of the 15 animals, diltiazem (0.45 micrograms/kg/min) was infused i.v. during the reperfusion period; this was preceded by a loading dose of 0.18 micrograms/kg 10 min before release. Small artery and vein O2 saturations obtained microspectrophotometrically were combined with regional blood flow measurements using radioactive microspheres to determine regional myocardial O2 consumption. In both groups, coronary occlusion lowered regional flow to a similar level. After a 4-hr reperfusion, flow to the subendocardial region of treated hearts was significantly greater than that to the untreated reperfused myocardium (75.6 +/- 46.4 vs. 40.3 +/- 25.8 ml/min/100 g), and did not differ from the preocclusion level. The subendocardium/subepicardium flow ratio was reversed in occluded and untreated reperfused myocardium (subendocardium flow less than subepicardium flow), but was not reversed in treated reperfused regions. Myocardial oxygen extraction was 11.0 +/- 2.4 ml of O2/100 ml of blood in the untreated reperfused subendocardium, and was significantly decreased to 8.5 +/- 0.9 ml of O2/100 ml in the treated subendocardium. The proportion of individual veins having O2 saturations below 25% was significantly reduced by diltiazem treatment from 45.2 to 22.7%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Therapeutic defibrination with ancrod does not protect canine myocardium from reperfusion injury.

The purpose of this study was to determine whether normal fibrinogen contributes to the development of myocardial reperfusion injury by acting as a substrate in vivo for neutrophil adhesion. This was tested in a dog model of acute myocardial infarction that used pentobarbital anesthetized dogs subjected to 90 min regional myocardial ischemia and 5 h reperfusion. Dogs were treated with 1 unit/kg Ancrod (venom from the Malayan pit viper, Agkistrodon rhodostoma) or vehicle i.v. 60 min after left circumflex coronary artery occlusion. Therapeutic defibrination was verified in Ancrod-treated dogs by measurements of clottable fibrinogen, alpha-2 antiplasmin and plasminogen, by the activated partial thromboplastin time and by immunoelectrophoresis. Fibrinogen was depleted to below detectable limits of the assay (less than 0.05 mg/ml) after treatment with Ancrod. The defibrination effect was accomplished by the expected activation of the fibrinolytic system: alpha-2 antiplasmin was decreased by 10% and plasminogen activity was decreased by 30% with Ancrod treatment. There were no measureable differences between the two treatment groups in heart rate, mean arterial blood pressure, rate pressure product or circumflex coronary blood flow throughout the 90 min of regional ischemia or during the 5 h of reperfusion. The relative severity of ischemia between the two treatment groups was similar when assessed with radiolabeled microsphere measurement of myocardial blood flow. The accumulation of neutrophils (measured by myeloperoxidase activity) within the myocardium after reperfusion was not reduced by prior depletion of fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reduction of experimental canine myocardial reperfusion injury by a monoclonal antibody (anti-Mo1, anti-CD11b) that inhibits leukocyte adhesion.

A monoclonal antibody (904) that binds to a leukocyte cell adhesion-promoting glycoprotein, (Mo1; CD11b/CD18) was administered (1 mg/kg, iv.) to open chest anesthetized dogs 45 min after the induction of regional myocardial ischemia. Ischemia was produced by occluding the left circumflex coronary artery (LCX) for 90 min and then reperfusing for 6 h. There was no difference between control and antibody treated groups with respect to arterial blood pressure, heart rate, or LCX blood flow. Administration of antibody produced no observable effect on circulating neutrophil counts, suggesting that antibody-bound neutrophils were not cleared from the circulation. The mean size of myocardial infarct expressed as percentage of the area at risk of infarction that resulted was reduced by 46% with anti-Mo1 treatment (25.8 +/- 4.7%, n = 8) compared to control (47.6 +/- 5.7%, n = 8; P less than 0.01). The area at risk of infarction was similar between groups. Circulating (serum) antibody excess was confirmed in all 8 anti-Mo1 treated dogs by immunofluorescence analysis. Analysis of ST segment elevation on the electrocardiogram as an indicator of the severity of ischemia suggests that the anti-Mo1 reduces infarct size independent of the severity of ischemia. An additional group of dogs (n = 5) was tested with a control monoclonal antibody of the same subtype (murine IgG1) and was found to produce no significant reduction in myocardial infarct size. Accumulation of neutrophils within the myocardium was significantly attenuated with 904 treatment when analyzed by histological methods. These data demonstrate that administration of anti-Mo1 monoclonal antibody after the induction of regional myocardial ischemia results in reduced myocardial reperfusion injury as measured by ultimate infarct size.     

背向散射积分技术评价硝酸甘油对犬顿抑心肌收缩功能延迟保护

目的探讨背向散射积分技术定量评价硝酸甘油对犬顿抑心肌收缩功能的延迟保护.方法20只健康成年杂种犬随机分成缺血再灌注组(A组)和硝酸甘油组(B组),缺血及再灌注阶段检测室壁增厚率(WT)及心动周期变异幅度(CVIB),图像平均强度(AⅡ)的动态变化.实验结束后对心肌组织行病理检查.结果缺血时两组相应区域心肌CVIB和WT明显减低,曲线形态不规则.再灌注后有逐渐恢复趋势.CVIB的动态变化与WT相似,二者具有较好的相关性.再灌注120 min时B组收缩功能抑制分别较对照组减少了34%,30%.应用小剂量多巴酚丁胺后两组相应区域心肌运动增强.AⅡ,标化AⅡ在不同观测时间点之间的差异均无显著性意义.结论背向散射积分技术中的CVIB可用于检测顿抑心肌的收缩功能,多巴酚丁胺负荷试验结合背向散射积分技术可检测顿抑心肌的收缩功能储备,硝酸甘油对犬顿抑心肌收缩功能具有延迟保护作用.     

Origin of acetyl strophanthidin-induced ventricular arrhythmias.

To examine the origin of digitalis-induced ventricular tachycardia (VT), acetyl strophanthidin (AS) (25 mug/min) was perfused into a limited zone of myocardium in intact anesthetized dogs through a catheter placed fluoroscopically in the left anterior descending artery without ischemia. A second catheter in the great cardiac vein sampled venous effluent from this region. His and left bundle branch depolarizations were recorded and bipolar intramural electrograms from endocardial and epicardial sites within the anterior descending region were obtained. No conduction alterations preceded arrhythmia. Cardiac venous K+ rose from 3.3 +/- to 4.4 +/- 0.2 meq/liter (P less than 0.001), indicating egress from the perfused zone. 10 animals (Group 1) were sacrificed 2 min after onset of VT while 11 (Group 2) continued until fibrillation (4-14 min). All showed normal (endocardial leads to epicardial) transmural depolarization during sinus rhythm, but 10/21 demonstrated reversal, usually late during VT, including 8/11 in Group 2. Epicardial activation preceded fascicular activation and QRS. Recordings from the border and circumflex regions in 10 additional dogs (Group 3) demonstrated activation reversal only in the border zone. Myocardial K+ was reduced (mean 63 +/- 1 mueq/g) and Na+ increased (mean 41 +/- 2 mueq/g) in the perfused zone (nonperfused circumflex area K+ 72 +/- 1, Na+ 33 +/- 1 mueq/g, P less than 0.001 for both); changes were similar in inner and outer ventricular wall. In related experiments, subepicardial injections of AS induced activation reversal within the immediate area, similar to recordings during coronary infusion. Reversed transmural activation with early epicardial depolarization suggest VT arises within myocardium; electrolyte gradients between adjacent regions may be causative.     

Effects of propranolol on regional O2 supply and O2 consumption in reperfused dog myocardium

This study was designed to assess whether propranolol would improve the relationship between O2 supply and O2 consumption in the reperfused ischemic dog myocardium. In 14 dogs, the left anterior descending coronary artery was occluded for 2 hr, followed by a 4-hr period of reperfusion. In 7 of the 14 dogs, 1 mg/kg of propranolol was administered 10 min before and again 2 hr after reperfusion. Small artery and vein O2 saturations obtained microspectrophotometrically were combined with regional blood flow measurements using radioactive microspheres to determine regional myocardial O2 consumption. In both groups, 2 hr of occlusion lowered the regional flow to a similar level. In the control group, 4 hr of reperfusion returned the blood flow toward normal levels, from 17 +/- 20 ml/min/100 g (mean +/- S.D.) at the end of occlusion to 60 +/- 42 ml/min/100 g in the affected area compared with 84 +/- 28 ml/min/100 g in the nonischemic area. In the propranolol-treated animals, the flow increase with reperfusion was not significant (25 +/- 30 ml/min/100 g to 45 +/- 26 ml/min/100 g). O2 extraction was greater in the ischemic than in the unaffected area in both groups. However, ischemic region O2 extraction was lower in the propranolol-treated group than in the control group. There were a greater number of arteries and veins with reduced O2 saturations in the control group reperfused area compared with the nonischemic area. Propranolol decreased the number of low O2 saturation vessels in the ischemic area.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial Blood Flow Distribution during Ischemia-Induced Coronary Vasodilation in the Unanesthetized Dog

This study was designed to determine whether coronary vasodilation distal to a flow-limiting coronary artery stenosis could result in redistribution of myocardial blood flow to produce subendocardial underperfusion. Studies were performed in 10 awake dogs chronically prepared with electromagnetic flow-meters and hydraulic occluders on the left circumflex coronary artery. Regional myocardial blood flow was measured using radionuclide-labeled microspheres, 7-10 mum in diameter, injected into the left atrium. A 5(-s) coronary artery occlusion was followed by reactive hyperemia with excess inflow of arterial blood effecting 375+/-20% repayment of the blood flow debt incurred during occlusion. When, after a 5(-s) occlusion, the occluder was only partially released to hold arterial inflow to the preocclusion level for 20 s before complete release, the delayed reactive hyperemia was augmented (mean blood flow repayment = 610+/-45%, P < 0.01). This augmentation of the reactive hyperemia suggested that ischemia was continuing during the interval of coronary vasodilation when coronary inflow was at the preocclusion level. Measurements of regional myocardial blood flow demonstrated that endocardial flow slightly exceeded epicardial flow during control conditions. When arterial inflow was limited to the preocclusion rate during vasodilation after a 5(-s) total coronary artery occlusion, however, flow to the subepicardial myocardium was increased at the expense of underperfusion of the subendocardial myocardium. Thus, in the presence of a flow-limiting proximal coronary artery stenosis, ischemia-induced coronary vasodilation resulted in redistribution of myocardial blood flow with production of subendocardial ischemia in the presence of a net volume of arterial inflow which, if properly distributed, would have been adequate to prevent myocardial ischemia.     

Effect of thromboxane receptor blockade on oxygen supply/consumption variables during reperfusion in the anesthetized dog

The thromboxane A2/PGH2 receptor antagonist SQ 30,741 has been previously shown to reduce infarct size and to improve subendocardial reflow. The purpose of this study was to determine the effect of SQ 30,741 on reperfusion O2 supply/consumption variables. Anesthetized open-chest dogs treated with vehicle or 1 mg/kg + 1 mg/kg/hr SQ 30,741, i.v. (starting 10 min after the onset of ischemia) were subjected to 90 min left circumflex coronary occlusion and 3 hr reperfusion. Regional myocardial blood flow (radioactive microspheres) and arterial and venous O2 saturations (microspectrophotometry) were determined. Animals treated with SQ 30,741 had significantly higher subendocardial reflow at 3 hr (48 +/- 6 ml/min/100 g) compared with vehicle (27 +/- 10 ml/min/100 g). At 3 hr postreperfusion, O2 extraction was significantly higher in the reperfused region compared with the nonischemic region, although extraction was not at maximal values. O2 extraction was similar in vehicle- and SQ 30,741-treated animals despite the near doubling of reflow into the subendocardial region with SQ 30,741. O2 consumption was significantly reduced in the reperfused subendocardial region (1.65 +/- 0.9 ml O2/min/100 g) in vehicle controls compared with the nonischemic subendocardial region (10.2 +/- 2.6 ml O2/min/100 g). SQ 30,741 significantly improved subendocardial reperfused regional O2 consumption (4.03 +/- 0.41 ml O2/min/100 g) compared with vehicle and this increase was proportional to the flow increment (no change in the O2 supply/consumption ratio). SQ 30,741 is thus increasing subendocardial reflow secondary to an increase in O2 consumption and the increased O2 consumption may be due to preservation of myocardial tissue.