Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The findings after biochemical analysis of heart muscle taken at autopsy are given in this preliminary communication. Human myosin is made up of two heavy sub-units and two light sub-units: it is similar to cardiac myosin found in other mammals, but is different in certain characteristics, particularly immunological ones. Tropomyosin is made up of two different sub-units. The normal human heart contains 1 mg of collagen and 130 microgram of desoxyribonucleic acid (DNA) per 100 mg of fresh tissue. The degree of cardiac hypertrophy correlates with the increase total DNA within the heart, and with the lowering of myofibrillary Ca2+ ATPase, the concentration in the collagen remaining unchanged providing there is no ischaemic heart disease. These techniques may be used to quantify several factors, such as the degree of sclerosis or the nuclear mass in ill-understood conditions such as the primary cardiomyopathies.
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PMID:[Biochemistry of myocardium taken at autopsy. Preliminary report]. 15 17

Cardio- and hemodynamics was investigated in 69 patients with chronic coronary insufficiency without manifestations of cardiac decompensation and with symptoms of congestive incompetence of the heart by using radiocardiography and analyzing systolic phases of the left ventricle. Furthermore, fractional composition of myocardial proteins and the ATP-ase myosin activity were studied in 31 persons, who during their life-time suffered from ischemic heart disease. In patients presenting no symptoms of cardiac insufficiency significant changes in cardio- and hemodynamics along with a reduced content of the actomyosin complex proteins and their disturbed ATP-ase activity were uncovered. These changes proved more intensive in the face of manifestations indicating cardiac decompensation. Thus, a complex investigation of cardio- and hemodynamics enabled it to disclose initial disorders in the contractile activity of the myocardium in patients with chronic coronary insufficiency, when such disturbances are associated both with deranged utilization and with defective accumulation of energy in the myocardium.
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PMID:[Contractile activity of the myocardium in chronic coronary insufficiency]. 123 9

Recently we have shown that actomyosin ATPase activity decreases with age when measured under appropriate conditions (Yoshida K et al, Age 12: 97-102, 1989). Many previous studies, which examined changes in ATPase activity in myosin, actomyosin, or myofibrils under pathological states, ignored the age-related changes. In this study actomyosin was isolated from myocardia of middle-aged subjects (37-49 years old) and examined for ATPase activity under various conditions and protein composition. Proteolysis of myosin and troponin was more frequently observed in ischemic heart disease (IHD) subjects than in non-IHD subjects. The proteolysis was associated with a decrease in Ca2+ sensitivity of Mg2(+)-ATPase activity and enhanced stimulation of Ca2(+)-ATPase activity with a sulfhydryl reagent, N-ethylmaleimide. Hypertrophy appeared not to significantly affect ATPase activity.
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PMID:ATPase activity and proteolysis of human myocardial actomyosin in ischemia and hypertrophy. 182 69

The treatment with pyromecaine and pyrroxan for 5 days was found to prevent disturbances of the physicochemical properties and the composition of the components of actomyosin complex of the rat heart left ventricle caused by experimental myocardial ischemia. Pyrroxan is able to change also the gene expression thereby leading to the appearance of a new isoform of myocardial myosin reminding by its characteristics the isoform of myosin of the rapidly contracting skeletal muscles.
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PMID:[The Ca2+ reactivity and the subunit composition of myocardial actomyosin during the pyromecaine and pyrroxan treatment of experimental ischemia]. 197 Mar 9

The aim of the investigation is to study the influence of human myocardium myosin on the quantitative values of T-lymphocytes examined as active rosettes [correction of rosellae] in patients with ischemic heart disease. The study included 99 patients with ischemic heart disease, 49 of them with myocardial infarction and 50--with stenocardia. The controls were 61 clinically healthy donors. It was established that the active rosettes [correction of rosellae] in the patients with myocardial infarction were significantly less than in the controls (p less than 0.05). A significant inhibiting action of the human myocardium myosin on the active rosettes [correction of rosellae] was manifested (p less than 0.002). This action in the patients with stenocardia was less expressed (p less than 0.05). Myosin from a striated muscle did not exert an inhibiting action (p greater than 0.1). The results prove the participation of human myocardium myosin in the pathogenetic mechanism of T-lymphocytes suppression in patients with ischemic heart disease.
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PMID:[The effect of myosin from the human myocardium on quantitative T-lymphocyte values--active rosettes in patients with myocardial infarct and stenocardia]. 208 Jun 8

There is currently great interest in acute coronary reperfusion as a therapeutic modality for severe myocardial ischemia. While some studies have demonstrated a reduction in the overall extent of necrosis by early reperfusion, other studies have identified potentially deleterious effects produced by reflow. Because membrane disruption may be an important mechanism of irreversible cell injury, we measured changes in cell membrane integrity early during reperfusion using radiolabeled anticardiac myosin (Fab')2 antibody fragments in dogs. Our method involved brief periods of exposure to the (Fab')2 so that the levels of (Fab')2 binding indicated the degree of membrane disruption at discrete times during the progression of cell injury. In the first protocol (Fab')2 fragments labeled with either 125I and 131I were injected into the left circumflex coronary artery at the onset of reflow and at 45 min of reflow after a 1-h circumflex artery occlusion. Coronary sinus flow was diverted for 5 min following each injection to prevent recirculation. The (Fab')2 binding ratio (ischemic/control) increased during the first 45 min of reflow in each of eight experiments (mean increase 170%, P less than 0.01). No significant increase in (Fab')2 binding was observed in five additional experiments in which nonspecific (Fab')2 was injected. This indicates that the increase in binding seen with antimyosin-specific (Fab')2 was due to changes in specific binding rather than to alterations in (Fab')2 delivery produced by changes in blood flow distribution. The increase in membrane damage during reflow was confirmed by a second protocol in which each animal received only a single left atrial injection of (Fab')2 followed by rapid excision of the heart. The (Fab')2 binding ratio was 1.7 +/- 0.3 (SEM) in the group that received (Fab')2 at the onset of reflow and 3.7 +/- 0.6 (SEM) (P less than 0.05) in the group that received (Fab')2 after 45 min of reflow. In a third set of experiments in which hyperosmotic mannitol was infused during reflow the mean increase in (Fab')2 binding using the first protocol was only 80 +/- 40 vs. 170 +/- 30% without mannitol (P less than 0.05). Thus, membrane damage develops early during coronary reperfusion following 1 h of circumflex coronary artery occlusion, and part of this membrane damage can be prevented by altering the conditions of reflow. A method involving brief exposure of the myocardium to antimyosin (Fab')2 is promising for detecting changes in membrane integrity during evolving ischemic injury.
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PMID:Early membrane damage during coronary reperfusion in dogs. Detection by radiolabeled anticardiac myosin (Fab')2. 622 42

Ischemia is known to produce damage to subcellular organelles, such as nuclei and mitochondria, in myocardial tissue. We tested the hypothesis that during myocardial ischemia various cytoskeletal and contractile proteins also undergo changes. We induced total global ischemia by incubation in buffer of tissue samples from six human left ventricles that were obtained from heart transplant recipients. Samples were removed from the incubation medium at different time intervals and investigated by immunohistochemistry using monoclonal antibodies against myosin, actin, tropomyosin, troponin T, myomesin, desmin, tubulin, and vinculin. The degree of ischemic injury was determined by electron microscopy. Ischemic cardiomyopathic human tissue showed disturbances of the localization pattern of myosin, actin, tropomyosin, and troponin T as early as 10 minutes after the onset of ischemia; this disruption was complete at 20 minutes. Tubulin also started changing at 10 minutes, but complete disruption was only evident after 120 minutes. Desmin and myomesin showed an intermediate response; changes began at 30 to 40 minutes, and disruption was complete at 90 to 120 minutes. Vinculin was most resistant to ischemia. Ultrastructurally, the tissue showed moderate reversible ischemic injury during the entire period of 180 minutes. Measuring the exposure time in seconds allowed quantitation of the intensity of the fluorescence. We reached the following conclusions: (1) Ischemia causes damage to the contractile proteins sooner than to the cytoskeleton and subcellular organelles. (2) Diseased human hearts are extremely susceptible to the effects of ischemia. These findings are important for the situation of induced cardiac arrest in heart operations and for preservation of donor hearts for transplantation.
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PMID:Ischemia induces early changes to cytoskeletal and contractile proteins in diseased human myocardium. 760 73

An indirect ELISA method has been used to study formation of autoantibodies (AA) to myocardial myofibrillar proteins in patients with different clinical IHD forms. Purified myosin (MS), actin (AC) and tropomyosin (TM) of the intact human myocardium acted as antigens. The highest level of AA to MS and AC was found in patients with AMI (acute myocardial infarct): it exceeded twice that of the norm and 1.5 times that in patients with IAP (instable angina pectoris). Moreover the AA level in IAP patients exceeded that of normal 1.5 times. In PC (postinfactional cardiosclerosis) patients the MS AA and AC AA tend to the norm. The TM AA contents in PC patients is 1.2 times higher than that in AMI and IAP patients, not differing from the norm in all patient groups. The role of autosensibilization to contrectile proteins in progress of IHD and development of AMI is discussed.
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PMID:[Autosensitization to myofibrillar proteins of myocardium in patients with different clinical forms of ischemic heart disease]. 775 96

An experimental model of myocardial ischemia/reperfusion injury was used to assess the cardioprotective effects of SC-52608, a low molecular weight superoxide dismutase mimetic. Langendorff perfused rabbit isolated hearts were subjected to 30 min of global ischemia followed by 45 min of reperfusion. Hearts perfused in the presence of 20 microM SC-52608 exhibited a decrease in the release of creatine kinase and intracellular potassium compared to hearts receiving vehicle (control). A progressive increase in left ventricular end-diastolic pressure developed upon reperfusion in all hearts, but was significantly greater in control hearts when compared to hearts treated with SC-52608 (P < 0.05). In addition, results obtained with a radiolabeled monoclonal antibody to the intracellular protein myosin, indicate an increased degree of irreversible damage in vehicle-treated hearts. Myocardial protection was not significant in an additional group of hearts treated with 10 microM SC-52608. The hemodynamic, biochemical, morphological, as well as the antimyosin binding data, demonstrate that pretreatment with SC-52608 protects the myocardium from damage associated with global ischemia and reperfusion. The mechanism by which SC-52608 mediates the observed protective effect is most likely related to its ability to scavenge superoxide.
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PMID:Protective effects of the SOD-mimetic SC-52608 against ischemia/reperfusion damage in the rabbit isolated heart. 779 54

Myoglobin, myosin creatine kinase MM (CK-MM), creatine kinase BB(CK-BB) in cardiac muscle and H chain of myosin in atrial and ventricular muscle were studied in specimens from 8 patients who died of sudden nocturnal death syndrome (SNDS) by avidin-biotin complex (ABC) method to investigate the possible early or very early myocardial ischemia in the syndrome. Hematoxylin-eosin staining was conducted for comparison. The results showed evident loss of CK-MM, CK-BB, myoglobin and myosin from cardiac muscle cells, indicating that occurrence of SNDS is closely associated with acute myocardial ischemia.
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PMID:Changes of myocardial myoglobin, myosin and creatine kinase in cases of sudden nocturnal death syndrome. 818 70


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