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)

Patients with coronary heart disease and angina pectoris were examined. The blood outflowing from the myocardium at the height of ischemia induced by atrial stimulation was found to have lower levels of fibronectin. Ten minutes after the stimulation discontinuation the concentration of fibronectin returned to baseline. A reduction in the fibronectin content during myocardial ischemia seems to be related to its consumption as a result of maintaining antithrombotic function.
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PMID:[Fibronectin level in coronary sinus blood in myocardial ischemia caused by atrial stimulation]. 652 Nov 78

A group of 17 patients with ischemic heart disease, significant left ventricular dilatation and congestive heart failure, class III NYHA (9 patients) and class IV NYHA (8 patients) was studied. The patients received angiotensin converting enzyme inhibitor--captopril 75 mg/day or perindopril 4 mg/day--added to diuretics, digitalis and nitrates. The plasmatic level of fibronectin was investigated, by radial immunodiffusion, before and one month after the beginning of the treatment with angiotensin converting enzyme (ACE) inhibitor. The plasmatic level of fibronectin is increased significantly (p < 0.001) while the cardiothoracic ratio is decreased significantly (p < 0.02) after one month of ACE inhibitors treatment. A positive correlation between the increase of the plasmatic level of fibronectin and the decrease of cardiothoracic ratio is found (r = 0.62; p < 0.01). The increased fibronectin plasmatic level can be a marker of the favorable effect of ACE inhibitor on the myocardium interstitium.
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PMID:Correlation between fibronectin and cardiothoracic ratio in heart failure treated with angiotensin converting enzyme inhibitors. 761 96

Using confocal microscopy and immunocytochemistry we have studied early changes in distribution of fibronectin (FN) in myocardial cells of rats subjected to experimental acute myocardial ischemia (AMI) by coronary ligation for several periods of 0.5 h to 6 days. In sham-operated and nonoperated rats, FN was present in the interstitium around the myocytes, and in their transverse tubules (TT). Already after 0.5 h of ischemia there was a well-defined increase of immunoreactive FN in focal areas of the interstitium of the hypoperfused portion, and distinct penetration into adjacent myocytes. The early penetration of FN into myocytes appears to follow a path through the TT, with a codistribution with actin in the I bands. This process precedes a total and diffuse infiltration of FN into the cytoplasm of disintegrating myocytes at later stages of coronary occlusion.
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PMID:Fibronectin penetration into heart myocytes subjected to experimental ischemia by coronary artery ligation. 766 Jul 55

Fibrosis makes an important contribution to the pathophysiological events leading to the development of heart failure in ischemic and hypertensive heart disease. Since cardiac fibroblasts are mainly responsible for the synthesis and deposition of the extracellular matrix, we have established a method for isolating and cultivating human cardiac fibroblasts from explanted human hearts. The cell yield was 2.14+/-0.25x10(6 )cells in five independent isolations and the cell purity was 95-97%, contaminating cells being vascular smooth muscle cells and pericytes. Cultured cells were studied with respect to growth properties, morphology and deposition of components of the extracellular matrix. Isolated cells displayed a differentiated phenotype, including the second passage in culture; they synthesised collagen I, III, IV, fibronectin, vitronectin, tenascin and chondroitin sulphate and expressed an atypical angiotensin receptor. This atypical angiotensin receptor internalised angiotensins II and III but not angiotensin IV in a time-dependent manner. Stimulation of the cells with angiotensins II and III but not with angiotensin IV resulted in a dose-dependent stimulation of DNA synthesis. Co-incubation with the subtype-specific receptor antagonists Losartan and PD 123317 did not prevent the stimulation of DNA synthesis. The further characterisation of this receptor should provide insights into the pathobiochemical events leading to heart failure in hypertension and ischemic heart disease.
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PMID:Isolation and characterisation of human cardiac fibroblasts from explanted adult hearts. 878 Dec 21

The important role of fibronectin (Fn) has been recognized in patients with ischemic heart disease. However, serial changes of Fn during both brief and prolonged ischemia-reperfusion are poorly known. Plasma Fn was measured during acute myocardial infarction (AMI) and myocardial stunning (MS), and in the absence of myocardial injury. The effects of magnesium (Mg), diltiazem, and a Mac-1 inhibitor on the level of Fn were elucidated. Forty-nine swine underwent prolonged (50 min) or brief (8 min) coronary artery occlusion followed by reperfusion, while six control animals were free of ischemia. During the AMI experiments, plasma Fn underwent a significant progressive increase. Mg or diltiazem similarly affects the plasma Fn, reducing its release during the entire reperfusion period, and did not influence the plasma Fn in the absence of myocardial injury. Contrarily, Mac-1 inhibition resulted in the Fn elevation in controls, and during the occlusion phase, with no significant effect during reperfusion. There were no changes in the plasma Fn during MS, while inhibition of Mac-1 was associated with the significant increase of Fn during ischemia-reperfusion. Ability of Mg, diltiazem, and leumedins to modulate plasma Fn level may have direct clinical implications for the use of these agents in patients with coronary artery disease.
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PMID:Plasma fibronectin during myocardial ischemia-reperfusion: effects of magnesium, diltiazem, and a novel Mac-1 inhibitor. 954 75

Fibronectin is a paradigm adhesive protein which has been implicated in the regulation of several cellular processes and cell-cell interactions. Large amounts of fibronectin have been detected in atherosclerotic plaques, while hypertension in animal models has been shown to rapidly increase fibronectin expression in arterial walls. The aim of the present study was to determine the levels of plasma fibronectin (FN) in 133 patients with ischemic heart disease and in 36 normal controls, and to investigate the possible association with blood pressure. Plasma FN levels in patients with ischemic heart disease were found to be significantly elevated (mean+/-S.D.; 46.5+/-14.2 mg/dl) compared with the control group (38.0+/-14.2 mg/dl) (P=0.002). Plasma FN concentrations were significantly different between the hypertensive group (52.9+/-14.5 mg/dl) and the normal blood pressure group (41.4+/-11.8 mg/dl) among the patients with ischemic heart disease (P<0.001). Plasma FN concentration was positively correlated with total cholesterol, triglyceride, systolic blood pressure and body mass index. In conclusion, the plasma fibronectin level may have pathogenetic implications in association with lipid components and blood pressure in patients with ischemic heart disease.
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PMID:Plasma fibronectin levels in ischemic heart disease. 1116 78

In this prospective study, we monitored two laboratory parameters, C-reactive protein (CRP) and fibronectin (FIN) levels, in 30 patients undergoing elective surgery for ischemic heart disease. These patients were divided into three groups according to the surgical procedure used: group A, approach through a median sternotomy with the use of extracorporeal circulation; group B, approach through a median sternotomy without the use of extracorporeal circulation; and group C, approach through a left anterior small thoracotomy (LAST) without the use of extracorporeal circulation. Peak CRP levels were found in all three groups on the second postoperative day, with the mean levels being statistically significantly higher in group C. This group also showed the highest mean CRP levels on the third and fourth postoperative days, with the difference being statistically nonsignificant. These findings can be explained by an enhanced production of cytokines, which in turn trigger CRP synthesis, induced by postoperative pain due to the LAST procedure. No statistically significant correlation between preoperative CRP levels and their postoperative development was found. None of the groups studied showed any statistically significant decrease in FIN plasma levels, either prior to adjustment for hemodilution or after adjustment for hematocrit and serum albumin.
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PMID:Development of C-reactive protein and fibronectin levels in coronary surgery patients: a comparison of on-pump, off-pump sternotomy and off-pump left anterior small thoracotomy groups. 1222 96

Current technologies make it possible to study thousands of genes simultaneously in the same biological sample - an approach termed gene expression profiling. Several techniques, including (i) differential display, (ii) serial analysis of gene expression (SAGE), (iii) subtractive hybridization and (iv) gene microarrays (Gene Chips), have been developed. Recently, gene profiling was applied in studying the mechanisms of ischemic injury and ischemic preconditioning. In the case of reversible ischemia caused by one or several brief transient episodes of complete coronary occlusion (as with ischemic preconditioning), or with a more prolonged but partial coronary ligation, many up-regulated genes were related to the "cell survival program". Protective genes included mitogen-activated protein kinase-activated protein kinase 3 (MAPKAPK 3), heat shock proteins 70, 27, 22, B-crystalline, vascular endothelial growth factor, inducible nitric oxide synthase and plasminogen activator inhibitors 1 and 2. With permanent coronary occlusion lasting from 24 h to several weeks, and resulting in a true myocardial infarction (MI), the list of up-regulated genes included those related to remodeling (e.g., collagens I and III, fibronectin, laminin) and apoptosis (Bax), while many down-regulated genes were related to major energy-generating pathways in the heart, namely, fatty acid metabolism. Gene expression profiling experiments have resulted in the discovery of two different genetic programs in the heart, namely, a protective program activated upon brief episodes of transient ischemia and an injury-related one activated in response to irreversible ischemic injury. Searching for factors turning on protective genes, and turning down injury-related ones, is a justifiable approach in developing new therapeutic strategies aimed to fight ischemic heart disease.
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PMID:Gene expression profiling--a new approach in the study of myocardial ischemia. 1282 86

Human Fibrin Glue (HFG) is made of two components contained in separate vials: a freeze dried concentrate of clotting proteins, mainly fibrinogen, Factor XIII and fibronectin (the sealant) and freeze dried thrombin (the catalyst). The first component is reconstituted with an aprotinin solution that inhibits tissue fibrinolysis. The second component (thrombin), available in 500 I.U. concentration, is dissolved with calcium chloride. It is so a set of substances involved in the hemostatic process and in the wound healing, conferring to the product the following important properties: hemostatic and sealing action, through the strengthening of the last step of the physiological coagulation; biostimulation, which favors the formation of new tissue matrix. The indications for the use of human fibrin sealant are numerous and present in all the surgical branches. A randomized controlled trial of 50 patients undergoing hernia repair according to Lichtenstein's technique under local anesthesia was performed. Patients had concurrent coagulopathies as a consequence of liver disease or long-term treatment with anticoagulants for ischemic heart disease or cardiac rhythm disturbances. Coagulopathies were defined according to the following criteria: prothrombin time < 10.5 seconds, activated partial thromboplastin time < 21 seconds, and fibrinogen < 230 mg/dL. Patients were randomized in a 1:1 ratio with (group A) or without (control group B) use of human fibrin glue: Postoperative hemorrhagic complications were significantly reduced in group A (4%) compared with group B (24%). This study showed that human fibrin glue is effective in preventing local hemorrhagic complications after inguinal hernia repair in patients with concurrent coagulation disorders.
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PMID:The use of human fibrin glue in the surgical operations. 1505 28

p38 mitogen-activated protein (MAP) kinase is activated during ischemic/hypoxic myocardial injury. However, the role of activated p38 MAP kinase on cardiac function after myocardial injury is not well understood. In the present study, we investigated the cardioprotective effects of p38 MAP kinase inhibition in a rat model of acute myocardial injury, induced by subcutaneous injection of isoproterenol (ISO, 20 mg/kg/d for 3 days). A synthetic p38 alpha MAP kinase inhibitor, SD-282 (40 mg/kg) or vehicle (0.25% Tween 80 in saline) was given intraperitoneally twice a day for 3 days, concomitant with ISO treatment. Cardiac function, systolic blood pressure, gene expression including collagen I and III, fibronectin and COX-2, and the myocardial injury were analyzed. Results showed that administration of SD-282 remarkably improved ISO-induced reduction of cardiac function with increases in ejection fraction (P < 0.001), cardiac output (P < 0.05), stroke volume (P < 0.001), and cardiac index (P < 0.01). SD-282 abolished ISO-induced reduction of systolic blood pressure (106.7 +/- 2.2 versus 123.1 +/- 5.3 mm Hg, P < 0.05). The ISO-induced expression of COX-2, collagen I and III, and fibronectin genes was reduced significantly (P < 0.05 in all cases) by administration of SD-282. The myocardial injury induced by ISO was significantly reduced by the treatment of SD-282 as judged by the reduction of myocardial necrosis. Data suggest that p38 alpha MAP kinase may be involved in the pathogenesis of cardiac dysfunction in ischemic myocardial injury. Inhibition of this enzyme may improve cardiac function and protect myocardium from ischemic/hypoxic injury that occurs during ischemic heart disease.
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PMID:p38 alpha mitogen-activated protein kinase inhibition improves cardiac function and reduces myocardial damage in isoproterenol-induced acute myocardial injury in rats. 1545 58


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