Measurement of local blood flow in acute myocardial infarction: loss of 15-^m microspheres during the first hour

Distribution of radiolabeled microspheres is widely utilized for determination of regional blood flow in experimental myocardial infarction studies. The purpose of this investigation was evaluation of the microsphere method during 1 h of regional ischaemia. Special attention was focused upon loss of preocclusion microspheres from ischaemic myocardium; mechanisms for loss and blood flow distribution in non-ischaemic left ventricle. Microspheres (15 μm) were injected into the left atrium in nine pentobarbital anaesthetized cats prior to coronary artery occlusion and again after 1 h of occlusion. Preocclusion blood flow estimates were lower in ischaemic compared with non-ischaemic myocardium (1.36 us. 1.62 cm³min^-1 g^-1, P = 0.002), corresponding to 16%apparent loss. In endocardial ischaemic tissue, development of oedema could account for the loss. In epicardial ischaemic tissue, oedema was not present and loss was therefore due to migration of microspheres. Epicardial loss increased in proportion to restoration of left ventricular contractility. There was no evidence for significant microsphere loss through lymphatic pathways. In non-ischaemic left ventricular tissue, myocardial blood flow was evenly distributed from apex to base, and also between endocardial and epicardial layers. This study quantitates an important limitation to measurements of local blood flow in ischaemic myocardium by radiolabelled microspheres.     

Early changes in collateral blood flow during myocardial infarction in conscious dogs.

We studied the early changes in collateral blood flow (CBF) after acute coronary artery occlusion and the relation of these changes to subsequent necrosis. We measured CBF with 7--9 microns radioactive microspheres before and at various times after circumflex artery occlusion in 42 conscious dogs that were killed 48 h later. CBF increased from 20 s postocclusion to later measurements (5 min, 15 min, 1 h, or 6 h) and did so in both necrotic and nonnecrotic areas of the occluded bed. However, the increase in CBF over time was not gradual, but appeared to occur between 20 s and 5 min, with no further changes for up to 6 h. There was a gradation of CBF in the occluded bed, from periphery to center and subepicardium to subendocardium. Central and subendocardial regions with CBF less than 0.40 ml-min-1-g-1 at 5--15 min postocclusion subsequently showed necrosis whereas epicardial and lateral regions with CBF greater than 0.50 ml/min did not. Thus CBF increases very early throughout the occluded coronary bed, and the level of CBF by 5 min appears to determine whether necrosis ultimately occurs.     

Prostacyclin and regional coronary blood flow in experimental myocardial infarction

Infusion of prostacyclin (PGI2) has been reported to affect infarct size and myocardial blood flow favourably in various animal models of myocardial ischaemia. Recent data suggest that a similar effect of PGI2 may occur also in humans with acute myocardial infarction. We addressed the hypothesis that PGI2 redistributes myocardial blood flow following coronary ligation, and that this effect favours perfusion of myocardium at risk and thereby limits infarct size. Following ligation of a distal branch of the left coronary artery in anaesthetized dogs, PGI2 (2-4 ng/kg/min) was infused for 72 h. Regional myocardial blood flow was assessed immediately after the coronary ligation and at the end of the drug infusion, by injection of 57Co- and 113Sn-labelled microspheres, respectively. Coronary ligation reduced regional coronary blood flow by 40-70%. During the subsequent 72 h the blood flow increased, being at the end of the period 50-70% of the flow in the non-ischaemic myocardium. PGI2 did not affect the spontaneous improvement of regional myocardial blood flow, as assessed at the end of the infusion. PGI2 also failed to affect infarct size, either when expressed in relation to total left ventricular mass, or in relation to area at risk. We conclude that PGI2, when infused immediately after coronary ligation in dogs in a clinically relevant dose, neither affects regional myocardial blood flow in the ischaemic regions, nor the size of the myocardial infarction.     

Papillary muscle rupture as a first event in acute myocardial infarction

Cardiogenic shock caused by papillary muscle rupture in acute myocardial infarction is potentially reversible by surgical treatment. A case of inferior myocardial infarction in a 56-year-old previously healthy man is reported, in which the first event was papillary muscle rupture. The patient was in shock and had a mitral insufficiency murmur. The diagnosis was made by echocardiography and ventriculography. A St. Jude valve was implanted, and the patient was discharged in good health. It is suggested that routine echocardiography be carried out on patients with sudden cardiogenic shock, when a mitral murmur is present.     

Regional myocardial tissue blood flow during beta-adrenergic blockade in cat hearts with acute ischaemia

Selective beta 1- or beta 2-adrenergic blockade was achieved by practolol or IPS 339, respectively, in cats with acute ligation of a coronary artery. During blockade, heart rate was kept constant by atrial pacing and blood pressure reduction was prevented by aortic clamping. Regional myocardial blood flow was measured by the distribution of 15 micron labelled microspheres. Practolol slightly reduced epicardial blood flow in ischaemic myocardium, while blood flow in border and normally perfused myocardium remained unchanged. Following IPS 339, myocardial tissue flow increased in normally perfused myocardium, on average by 37% in the endocardium and 30% in the epicardium. No changes occurred in the other regions. The flow changes brought about by IPS 339 were unrelated to haemodynamic changes, and the coronary vascular resistance was reduced. These results are indicative of coronary vasodilation related to beta 2-adrenergic receptor blockade and was confined to well-oxygenated areas surrounding the acutely ischaemic zone.     

急性心肌梗塞早期心室易损性的电生理实验研究

本文采用Ｓ１－Ｓ２程控电刺激方法同时测定心室易期和室颤阈，并结合其它有关电生理指标，评价了急性心肌梗塞早期心室易损性。结果表明，急性心肌梗塞早期，心室易损期明显延长，室颤阈显著下降，起搏阈值降低，有效不应期缩短，强度间期曲线下移，心室易损期外缘向Ｔ波方向延伸，联律间期与折回间期呈负相关。根据上述指标分析了急性心肌梗塞早期室性心动过速和／或心室颤动产生的电生理机制以及心室易损期在ｒｏｎＴ室性早搏触发     

急性缺氧大鼠的心输出量和局部血流量

以~(99m)Tc标记蟾蜍红细胞(~(99m)Tc-RBC)作为生物微球,用参考血样本方法(RSM)测定急性缺氧大鼠的心输出量(CO)和局部血流量(LBF)。大鼠在麻醉条件下进行人工通气,用10%O~2—90%N_2混合气体通气20分钟造成急性缺氧,左心室内注入~(99m)Tc-RBC 4～6万,从股动脉收集参考血样本(RS)测定CO和LBF,实验结果表明,在人工通气条件下,急性缺氧使大鼠的心率(HR)减慢、CO降低,和以冠状血流和脑血流增加及内脏血流减少为主的血流重新分配。     

Cardiac adrenergic innervation within the first 3 months after acute myocardial infarction.

It is widely accepted that myocardial infarction results in adrenergic denervation of the infarcted and peri-infarcted myocardium. On the contrary, the concept of re-innervation of adrenergic nerve fibres is less well established. Although there is evidence of partial re-innervation occuring several months after myocardial infarction, the extent and time scale of re-innervation are only poorly known. In this study we investigated changes in cardiac adrenergic innervation and myocardial perfusion during the early convalescence period (the first 3 months) after an acute myocardial infarction. Single-photon emission computed tomographic imaging was conducted in 15 men 1 week and 3 months after an acute myocardial infarction with I123-metaiodobentzylguanidine (MIBG) and Tc99m-sestamibi (MIBI) to determine the extent of adrenergic denervation and impaired perfusion, respectively. A MIBG and MIBI defect was determined as regional uptake 相似文献   

Interventricular redistribution of myocardial blood flow during metabolic vasodilation

To determine the effect of metabolic vasodilation on the blood flow distribution within the hypoperfused left anterior descending coronary artery (LAD) of the pig (a perfusion bed containing both left and right ventricular myocardium), 28 anesthetized (isoflurane) pigs were studied during intracoronary dobutamine infusion (2.5±1, SD, g/min) at two levels of reduced, constant coronary inflow. In 8 pigs, coronary inflow was reduced from 59±9 ml/min to 42±10 ml/ min; coronary perfusion pressure fell to 62±2 mm Hg (8260±260 Pa) and then fell further to 54±6 mm Hg (7190±800 Pa) during dobutamine infusion. Subendocardial blood flow in the anterior wall of the left ventricle perfused by the LAD decreased from 0.64±0.12 ml min^–1 g ^–1 with hypoperfusion alone, to 0.40±0.14 ml min^–1 g^–1 (P<0.002) with the addition of dobutamine. Conversely, blood flow to the right ventricular region supplied by the LAD increased significantly from 0.78±0.40 ml min^–1 g^–1 (hypoperfusion alone) to 0.92±0.50 ml min^–1 g^–1 (P<0.008) with dobutamine. In 10 pigs, a more severe reduction of coronary inflow to 26±12 ml/min and subsequent dobutamine infusion resulted in a similar redistribution of blood flow from the left to the right ventricular portion of the perfusion bed. Infusion of dobutamine during hypoperfusion, but with a pressure-constant perfusion system, was associated with increases in blood flow to both the right and left ventricular portions of the perfusion territory. Thus, dobutamine could recruit a significant vasodilator reserve throughout the entire perfusion bed including the left ventricular subendocardium. These data demonstrate that the metabolic vasodilation accompanying inotropic stimulation under flow-limited conditions results in an interventricular redistribution, or steal, of blood flow within the LAD perfusion bed.Supported in part by the American Heart Association California Affiliate grant-in-aid 86-S105 and by the National Institutes of Health Research Grant HL-17682, Ischemic Heart Disease Specialized Center of Research (SCOR) awarded by the National Heart, Lung and Blood Institute, Bethesda, MDMr. Schulz was the recipient of a fellowship from Boehringer Ingelheim Fonds. Dr. Guth is currently a Research Fellow with the Alexander von Humboldt-Stiftung, Jean-Paul-Strasse 12, W-5300 Bonn 2, FRGDr. Thaulow was the recipient of a research fellowship granted by The Fogarty International Center Grant 1 FO5 TWo3753-01 BI-5(12)     

Dynamics of hematologic indicators during acute experimental blood loss

Summary Experiments on female rabbits showed that those of them survive acute blood loss whose blood in the internal organs and cerebral vessels is richer in hemoglobin and erythrocytes than is the blood of the peripheral vessels. Anesthesia diminishes these differences and reduces the number of animals surviving. The reverse effect is produced by benzedrine.Presented by Active Member of the USSR Acad. Med. Sci. Prof. M. D. Tushinsky