Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the effects of chronic exercise on the coronary collateral circulation of dogs with normal coronary arteries, 1-yr-old purebred beagles were divided into sedentary control and exercising groups. The latter were trained to run on a treadmill. A lower maximal heart rate during a standardized exercise test protocol after a 10- to 12-week training period and a higher gastrocnemius cytochrome oxidase activity in the runners attested to the presence of cardiovascular and skeletal muscle training effects. However, left ventricular weights, left ventricle/body weight ratios, myocardial myofibrillar and myosin ATPases, and hemodynamics were similar in sedentary and exercising dogs except for a significantly higher resting cardiac output in the runners. After occlusion of the left anterior descending coronary artery, both collateral conductance (retrograde flow/aortic pressure) and collateral flow measured with microspheres tended to be lower in the trained dogs, but differences were not significant. The endocardial/epicardial flow ratio in the ischemic area after coronary occlusion did not distinguish between exercisers and controls. Thus treadmill running in the dog with normal coronary arteries produced a training effect, but had no effect on coronary collateral vessels.
 ...
PMID:Effect of exercise on collateral development in dogs with normal coronary arteries. 21 85

We examined the feasibility of early imaging of myocardial infarcts by intracoronary injection of 131I-labelled cardiac myosin-specific antibody (Fab')2. The left anterior descending coronary artery was occluded for 5 hours by a balloon catheter introduced through the carotid artery in 12 dogs. The catheter was withdrawn and 1 mCi 201Tl was injected intravenously and 500 muCi of 131I antibody were injected into the main left coronary artery. Six of these animals demonstrated evidence of myocardial infarction by ECG and subsequent triphenyl-tetrazolium chloride staining, while the others did not. In each of the infarcted animals, in vivo scintograms one-half hour after injection of isotope showed uptake of 131I in the anteroapical region of the heart corresponding to the region of absent 201Tl uptake. This relationship was confirmed in the excised hearts and in heart slices. In slices, 131I uptake corresponded to regions that did not stain with triphenyltetrazolium chloride. In the six animals that did not show evidence for infarction after coronary occlusion, uptake of 131I was not demonstrated, either in vivo or in excised specimens. In four additional dogs subjected to the same procedure, 125I-labelled (Fab')2 from nonimmune IgG was injected simultaneously into the left main coronary artery with 131I-labelled canine myosin-specific antibody (Fab')2. The ratio of uptake between infarct center and normal tissue was 34.3 +/- 1.5 (mean+/-SEM) for the specific antibody fragment as contrasted to 6.6+/-0.4 for the nonimmune IgG fragment, indicating that intracoronary injection does not favor nonspecific sequestration of protein in regions of infarction. Thus, the intracoronary administration of myosin-specific antibody fragments leads to early and specific one-half hour imaging of myocardial infarcts.
 ...
PMID:Early imaging of experimental myocardial infarction by intracoronary administraion of 131I-labelled anticardiac myosin (Fab')2 fragments. 70 69

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.
 ...
PMID:Localization of cardiac myosin-specific antibody in myocardial infarction. 95 77

In a recent overview on stunning, Bolli listed the three pillars on which theories on stunning rest: its causation by oxygen radicals, the amplification of damage by Ca2+ overload, and the resulting excitation contraction uncoupling. Our own experiments with SOD and catalase do not convince us that stunning is caused by free radicals, because we and others were unable to show improvement. An important pathway of radical generation, i.e., xanthine oxidase, does not exist in the hearts of several families of mammals, but stunning can of course be produced in these species. We agree with Bolli that stunning represents a disturbance of electromechanical coupling, but we acknowledge the controversy that exists with regard to the subcellular seat of the defect. Our results would support hypotheses that pinpoint the defect to the sarcoplasmic reticulum. However, the possibility of multiple defects should also be considered: Our finding of altered Ca2+ ATPase expression and Kusuoka's finding of altered myofibrillar Ca2+ sensitivity are not necessarily mutually exclusive but may be complementary, or may represent different stages of ischemic damage. Our finding of decreased myosin expression may help to explain the long persistence of the contractile defect. From the available evidence, the hypothetial possibility evolves that stunning is not just an injury, but rather the unmasking of a regulatory mechanism to protect the heart against premature or further damage. The observation that coronary occlusion causes both stunning and preconditioning by a parallel, and not by a sequential, mechanism and that a multitude of genes alter their expression in order to protect the myocyte argue for a regulatory change.
 ...
PMID:Molecular mechanisms in "stunned" myocardium. 175 39

Following acute myocardial infarction, fragments of human cardiac myosin can be detected in plasma by means of monoclonal antibodies to myosin heavy chains from the left human ventricle. The cumulative amounts of myosin released during the first 9 post-infarction days are proportional to the size of the infarct (Tao Ming et al., in the press). The purpose of our study was to evaluate the effectiveness of a fibrinolytic treatment administered in the acute phase of myocardial infarction by measuring in the plasma, the circulating fragments of human cardiac myosin. Three groups of patients with acute myocardial infarction were investigated: 13 patients (group A) received a conventional treatment; 8 patients (group B) were treated with intravenous streptokinase without success, i.e. with persistence of the coronary occlusion; 9 patients (group C) were successfully treated with intravenous streptokinase, resulting in recanalization of the coronary artery. We found that the cumulative amount of myosin released during the first 9 post-infarction days was significantly lower in patients successfully treated with streptokinase [group C: (3.8 +/- 2.3) 10(3) ng/ml/day]. There was no difference in cumulative release of myosin between control patients [group A: (7.0 +/- 3.3) 10(3) ng/ml/day] and patients with unsuccessful fibrinolytic treatment [group B: (10.0 +/- 4.1) 10(3) ng/ml/day]. These results were unrelated to the localisation of the infarct. It is concluded that measuring the cumulative amounts of myosin released is a means of evaluating the effectiveness of fibrinolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Evaluation of the efficacy of intravenous fibrinolytic treatment in the acute phase of myocardial infarction. Value of the determination of human plasma cardiac myosin]. 312 4

1. Quantitative analysis of structural proteins from a minute amount of myocardial tissue was performed from 10 mu thick cardiac tissue slices weighing 2 to 5 mg by the extraction in glycerol solution and by sodium dodecylsulfate (SDS) gel electrophoresis, and these changes were compared with the histologic alterations in the striated structure of the adjacent cardiac slices in the experimental myocardial infarction in the dog. 2. Approximately 69 micrograms of structural proteins were obtained from 1 mg of the normal heart muscle. In the central portions of the myocardial infarction, reductions in myosin heavy chain (HC), light chain (LC) 1 and alpha-actinin were observed at 12 to 24 hours after the coronary occlusion followed by the decrease in myosin LC 2 at 48 hours. Those changes became intense at 72 hours to 7 days, but restored gradually at 14 to 28 days. 3. Alterations in the striated structure of cardiac muscle fibers of the adjacent tissues slices were found simultaneously with the changes in structural proteins. At 12 to 24 hours after the coronary ligation increase in eosinophilia and overstretch of cross-striation were observed. The findings of coagulation necrosis, loss of striation, fragmentation, swelling of A-band, etc. of the infarcted fibers were markedly observed at 48 hours to 7 days, but the histologic restoration of cardiac fibers was found with the recovery of the infarcted tissue at 14 to 28 days after the coronary ligation. 4. Changes in the compositions of structural proteins corresponded well to the alterations in the striated structure in chronology and in quantity.
 ...
PMID:Regional changes in cardiac structural proteins in myocardial infarction: biochemical and histologic correlates. 723 Apr 98

A sensitive radioimmunoassay for cardiac myosin light chain II (LCII) was developed, and changes of serum LCII levels were studied in experimental myocardial infarction in dogs. This radioimmunoassay employed an antiserum which was prepared in rabbits against canine LCII. In our assay, 0.2-5.0 ng of LCII were effectively measurable. In normal dogs, LCII concentration in serum was less than 20 ng/ml. The serum LCII level began to rise within 6 hr after ligation of the left anterior descending coronary artery, reaching maximum level at 3-5 days (40-320 ng/ml). In eight out of ten cases with coronary occlusion, LCII could be detected as long as 7 days after operation. In one sham-operated dog, LCII was detected at 2 and 3 days, but its concentrations were less than 30 ng/ml. When LCII was injected intravenously, it dissipated from the blood stream within 48 hr. The time course curves of serum LCII level had two characteristics that had not been observed in serum enzyme studies: 1) LCII level rose rapidly and stayed up during a long period after coronary occlusion, and 2) changes of serum LCII levels were biphasic in six out of ten dogs with coronary occlusion. These results, and our previous studies of synthesis rate of light chains, suggest that when a coronary artery is occluded LCII may first be released from a pool of uncombined LCII in myocardial cells, and then continuously liberated from cardiac myosin molecules. This radioimmunoassay can be expected to be useful when applied to clinical use.
 ...
PMID:Radioimmunoassay of cardiac myosin light chain II in the serum following experimental myocardial infarction. 742 55

Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
 ...
PMID:Ventricular remodeling after myocardial infarction. Experimental and clinical studies. 835 28

Previous studies have shown that proinflammatory cytokines, such as tumor necrosis factor (TNF), are expressed after acute hemodynamic overloading and myocardial ischemia/infarction. To define the role of TNF in the setting of ischemia/infarction, we performed a series of acute coronary artery occlusions in mice lacking one or both TNF receptors. Left ventricular infarct size was assessed at 24 h after acute coronary occlusion by triphenyltetrazolium chloride (TTC) staining in wild-type (both TNF receptors present) and mice lacking either the type 1 (TNFR1), type 2 (TNFR2), or both TNF receptors (TNFR1/TNFR2). Left ventricular infarct size as assessed by TTC staining was significantly greater (P < 0.005) in the TNFR1/TNFR2-deficient mice (77.2% +/- 15.3%) when compared with either wild-type mice (46.8% +/- 19.4%) or TNFR1-deficient (47.9% +/- 10.6%) or TNFR2-deficient (41.6% +/- 16.5%) mice. Examination of the extent of necrosis in wild-type and TNFR1/TNFR2-deficient mice by anti-myosin Ab staining demonstrated no significant difference between groups; however, the peak frequency and extent of apoptosis were accelerated in the TNFR1/TNFR2-deficient mice when compared with the wild-type mice. The increase in apoptosis in the TNFR1/TNFR2-deficient mice did not appear to be secondary to a selective up-regulation of the Fas ligand/receptor system in these mice. These data suggest that TNF signaling gives rise to one or more cytoprotective signals that prevent and/or delay the development of cardiac myocyte apoptosis after acute ischemic injury.
 ...
PMID:Endogenous tumor necrosis factor protects the adult cardiac myocyte against ischemic-induced apoptosis in a murine model of acute myocardial infarction. 1077 46

The directed generation of cardiac myocytes from endogenous stem cells offers the potential for novel therapies for cardiovascular disease. To facilitate the development of such approaches, we sought to identify and exploit the pathways directing the generation of cardiac myocytes from adult rodent bone marrow cells (BMCs). In vitro cultures supporting the spontaneous generation of functional cardiac myocytes from murine BMCs demonstrated induced expression of platelet-derived growth factor (PDGF)-A and -B isoforms with alpha- and beta-myosin heavy chains as well as connexin43. Supplementation of PDGF-AB speeded the kinetics of myocyte development in culture by 2-fold. In a rat heart, myocardial infarction pretreatment model PDGF-AB also promoted the derivation of cardiac myocytes from BMCs, resulting in a significantly greater number of islands of cardiac myocyte bundles within the myocardial infarction scar compared with other treatment groups. However, gap junctions were detected only between the cardiac myocytes receiving BMCs alone, but not BMCs injected with PDGF-AB. Echocardiography and exercise testing revealed that the functional improvement of hearts treated with the combination of BMCs and PDGF-AB was no greater than with injections of BMCs or PDGF-AB alone. These studies demonstrated that PDGF-AB enhances the generation of BMC-derived cardiac myocytes in rodent hearts, but suggest that alterations in cellular patterning may limit the functional benefit from the combined injection of PDGF-AB and BMCs. Strategies based on the synergistic interactions of PDGF-AB and endogenous stem cells will need to maintain cellular patterning in order to promote the restoration of cardiac function after acute coronary occlusion.
 ...
PMID:Platelet-derived growth factor-AB promotes the generation of adult bone marrow-derived cardiac myocytes. 1496 8


1 2 Next >>