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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The leading cause of mortality in industrialized societies is sudden cardiac death. Almost half a million people die each year in the United States from myocardial ischemia and infarction leading to ventricular fibrillation. These phenomena result from severe coronary artery disease due to atherosclerosis with acute mural thrombosis causing occlusion, which serves as the terminal event. Various studies have found evidence of fresh coronary artery mural thrombosis in 74 to 94 percent of patients undergoing autopsies shortly after death due to acute myocardial infarction. Not all thrombi are occlusive, but vasospasm associated with fresh injury to the diseased vessel may be sufficient with developing new thrombus to block blood flow. Because platelets are a major constituent of newly formed thrombi and contribute significantly to vaso-occlusive disease, it is important to understand basic aspects of their function. Such studies may lead to measures that prevent vascular disease and thrombosis. This chapter has described ultrastructural features of platelet-vessel wall interaction. Adhesion, spreading, secretion, and aggregate or thrombus formation have been emphasized. The findings of current studies indicate strong similarities between platelet-vessel wall interactions and the response of platelets to other surfaces. Also, platelet transformations observed during aggregate formation in suspension are identical to physical changes in thrombi on damaged vessels. The similarities are much more impressive than the differences. Therefore, the role of platelets in arterial thrombosis can be understood best as an extension of their hemostatic function. An advantage of this observation is that understanding basic mechanisms of platelet function in hemostasis can lead to solution of the problems presented by platelet involvement in thrombosis. The disadvantage is that agents used to prevent thrombosis can place the hemostatic mechanism in jeopardy. Finding the answer to this paradox will occupy our attention for years to come.
Cardiovasc Clin 1987
PMID:Platelet structural physiology: the ultrastructure of adhesion, secretion, and aggregation in arterial thrombosis. 360 10

The presence of pericardial adhesions may increase morbidity and mortality during reoperation for cardiac disease. Pericardial substitutes (patches) are commercially available, and reportedly they reduce or prevent adhesions. We implanted five (1984 to 1985) newer pericardial substitutes in dogs. A new polytetrafluoroethylene surgical membrane, two types of glutaraldehyde-stabilized bovine pericardium, formaldehyde-preserved bovine pericardium, and glutaraldehyde-stabilized equine pericardial patches were each implanted in six adult dogs (total 30 dogs) with two dogs from each of the five groups killed at 3, 9, and 18 months. At autopsy the condition of each patch was recorded photographically, and specimens were substituted for histologic examination. Adhesions and epicardial reactions were graded as none, minimal, moderate, or severe. None of the materials produced severe pericardial adhesions, and no adhesions were detected in nine dogs. Eleven dogs had no epicardial reaction and only one showed a severe reaction. Adhesions to portions of the suture line required sharp dissection in 11 dogs. If there is concern over the possibility of calcification in heterologous tissue, polytetrafluoroethylene may be chosen. Patch type did not significantly alter patch behavior.
J Thorac Cardiovasc Surg 1987 Aug
PMID:A new look at pericardial substitutes. 361 29

We examined the impact of mediastinal healing on right ventricular performance in three groups of five piglets by performing gated blood pool scans in two planes to determine right ventricular ejection fraction. Animals in Group I then had sternotomy and excision of anterior pericardium. Group II animals had a similar operation plus insertion of a silicone rubber sheet as a pericardial substitute. Group III animals (controls) had no operation. Each group was followed up for 60 days, after which gated blood pool scans were repeated in a manner identical to the initial study. Experimental animals in Groups I and II were then put to death and autopsied. Adhesion formation between the right ventricle and sternum was graded on a 0 to 3 scale. Group I animals showed a significant average decline in right ventricular ejection fraction of 19.2% (p less than 0.02). Group II animals demonstrated an average decrease in ejection fraction, although not significant, of 12.2%. Groups I and II combined showed a significant average loss in ejection fraction of 15.7% (p less than 0.01). Severity of adhesions between the right ventricle and sternum correlated well with loss of right ventricular ejection fraction (p less than 0.01). Group III controls demonstrated no significant change in ejection fraction. Mediastinal healing and fibrous attachment of the right ventricle to the sternum may play a significant role in loss of right ventricular ejection fraction after cardiac operations. Variability in loss of right ventricular ejection fraction is related to intensity of the mediastinal healing process.
J Thorac Cardiovasc Surg 1984 Apr
PMID:A cause of right ventricular dysfunction after cardiac operations. 670 74

Cytokine induction of intercellular adhesion molecule-1 (ICAM-1) in cardiac myocytes may be a critical step in inflammation associated with ischemia-reperfusion injury. We investigated the involvement of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and interleukin 8 (IL-8) on neutrophil-myocyte adhesion; These cytokines are increased in plasma of patients with acute myocardial infarction (AMI). ICAM-1 expression on cultured neonatal rat cardiac myocytes was determined through immunohistochemical and enzyme-linked immunosorbent assay (ELISA) analysis. ICAM-1 mRNA expression in myocytes was investigated by Northern blot hybridization. Rat neutrophils isolated from peripheral blood (PB) were used for adherence assay. In immunohistochemical study, cultured neonatal rat cardiac myocytes constitutively expressed ICAM-1 molecules. In ELISA analysis, ICAM-1 molecule expression on myocytes was significantly stimulated by TNF-alpha (100 U/ml), but not by IL-6 (100 U/ml) or IL-8 (100 ng/ml) dose dependently. The effect of TNF-alpha was observed as early as 6 h after stimulation. Levels of ICAM-1 mRNA were very low or almost undetectable in unstimulated myocytes, but its expression was markedly induced after exposure to TNF-alpha for 3 h. IL-6 and IL-8 showed no effect on ICAM-1 mRNA accumulation. Adhesion of rat neutrophils to myocytes was stimulated by TNF-alpha, and the effect of TNF-alpha on adherence was significantly inhibited by an anti-ICAM-1 monoclonal antibody (MoAb). These results show that TNF-alpha, but not IL-6 and IL-8, promotes neutrophil-myocyte adhesion through ICAM-1 expression, suggesting involvement of TNF-alpha in inflammation associated with ischemia-reperfusion injury.
J Cardiovasc Pharmacol 1994 Apr
PMID:Neutrophil adherence to rat cardiac myocyte by proinflammatory cytokines. 751 17

Great interest has been shown for the seeding of autologous endothelial cells on prosthetic materials. We investigated the inflammatory and immunogenic properties of xenogeneic tissue before and after seeding with cultured human great saphenous vein endothelial cells in vitro. Adhesion of monocytes to xenogeneic tissue with or without endothelium and the endothelial cell expression of E-selectin, intercellular adhesion molecule 1, vascular adhesion molecule 1, and major histocompatibility complex class II antigens were investigated 1, 3, and 7 days after seeding. Both monocyte adhesion and endothelial adhesion molecule expression were relatively high 1 day after seeding and were significantly lowered after 3 to 7 days. There was no difference between monocyte adhesion and adhesion molecule expression on viable or nonviable xenogeneic tissue. Monocyte adhesion and adhesion molecule expression increased after interleukin-1 beta or interferon-gamma stimulation of the endothelial cells. The results suggest that human endothelial cells exhibit an early proinflammatory and immunogenic activity immediately after seeding. Three and 7 days after seeding, the endothelialized surface is less adhesive for monocytes as compared with nonendothelialized tissue. These findings have implications when cultured or intraoperatively recruited endothelial cells are used clinically.
J Thorac Cardiovasc Surg 1995 Dec
PMID:Reduction of monocyte adhesion to xenogenic tissue by endothelialization: an adhesion molecule and time-dependent mechanism. 852 66

The microcirculation constitutes the functional interface between the circulating blood and the interstitial space. To gain access to sites of inflammation, leukocytes must pass the endothelial barrier. The recruitment paradigm encompasses leukocyte margination, capture, rolling, activation, firm adhesion, and transmigration. Recent experimental work has shown that E-, L- and P-selectins and alpha 4 integrins can mediate leukocyte rolling. Upon activation by chemokines, complement peptides or lipid mediators, firm adhesion is afforded by beta 1 and beta 2 integrins, InterCellular Adhesion Molecules (ICAMs) and Vascular Cell Adhesion Molecule-1 (VCAM-1). Beta 1 and beta 2 integrins as well as Platelet-Endothelial Cell Adhesion Molecule-1 (PECAM-1) have been shown to be involved in transmigration. Intravital microscopic techniques have been instrumental in applying the conceptual advances of cell and molecular biology to the in vivo situation. This review focuses on the current understanding of the leukocyte recruitment paradigm as suggested by in vivo observations and in vitro model systems. The paradigm of neutrophil recruitment is presented to serve as a model for the recruitment mechanisms of other inflammatory cells.
Cardiovasc Res 1996 Oct
PMID:Molecular mechanisms of leukocyte recruitment in the inflammatory process. 891 91

One of the major therapeutic goals of modern cardiology is to design strategies aimed at minimizing myocardial necrosis and optimizing cardiac repair following myocardial infarction. However, a sound understanding of the biology is necessary before a specific intervention is pursued on a therapeutic basis. This review summarizes our current understanding of the cellular and molecular mechanisms regulating the inflammatory response following myocardial ischemia and reperfusion. Myocardial necrosis induces complement activation and free radical generation, triggering a cytokine cascade initiated by Tumor Necrosis Factor (TNF)-alpha release. If reperfusion of the infarcted area is initiated, it is attended by an intense inflammatory reaction. Interleukin (IL)-8 synthesis and C5a activation have a crucial role in recruiting neutrophils in the ischemic and reperfused myocardium. Neutrophil infiltration is regulated through a complex sequence of molecular steps involving the selectins and the integrins, which mediate leukocyte rolling and adhesion to the endothelium. Marginated neutrophils exert potent cytotoxic effects through the release of proteolytic enzymes and the adhesion with Intercellular Adhesion Molecule (ICAM)-1 expressing cardiomyocytes. Despite this potential injury, substantial evidence suggests that reperfusion enhances cardiac repair improving patient survival; this effect may be in part related to the inflammatory response. Monocyte Chemoattractant Protein (MCP)-1 is also markedly upregulated in the infarcted myocardium inducing recruitment of mononuclear cells in the injured areas. Monocyte-derived macrophages and mast cells may produce cytokines and growth factors necessary for fibroblast proliferation and neovascularization, leading to effective repair and scar formation. At this stage expression of inhibitory cytokines such as IL-10 may have a role in suppressing the acute inflammatory response and in regulating extracellular matrix metabolism. Fibroblasts in the healing scar undergo phenotypic changes expressing smooth muscle cell markers. Our previous review in this journal focused almost exclusively on reduction of the inflammatory injury. The current update is prompted by the potential therapeutic opportunity that the open vessel offers. By promoting more effective tissue repair, it may be possible to reduce the deleterious remodeling, that is the leading cause of heart failure and death. Elucidating the complex interactions and regulatory mechanisms responsible for cardiac repair may allow us to design effective inflammation-related interventions for the treatment of myocardial infarction.
Cardiovasc Res 2002 Jan
PMID:The inflammatory response in myocardial infarction. 1174 11

An experimental study was designed to search the effectiveness of retrograde cerebral perfusion which is presently used as cerebral protection method for the surgery of arcus aorta. Twelve dogs were subjected to the study. Six of them were remained in total circulatory arrest at 20 degrees C for 60 min. Retrograde cerebral perfusion was done again at 20 degrees C for 1 h for the other six dogs. Tumor necrosis factor (TNF), P-selectin, Intracellular Adhesion Molecule (ICAM), Creatine Phosphokinase (CPK-BB) and tissue Adenosine triphosphate (ATP) levels were measured, before the cardiopulmonary bypass at 37 degrees C and during perfusion period at 5, 60 min and 4 h. Tissue ATP level for retrograde cerebral perfusion group was 3.99+/-0.7 mcmol/g tissue and 2.86+/-0.1 mcmol/g tissue for total circulatory arrest group at fourth hour (p<0.05). TNF level was significantly higher in total circulatory arrest group than retrograde cerebral perfusion group (p<0.05). The samples taken at fourth hour of reperfusion showed the TNF level was, 162.55+/-13.1 pcg/ml for total circulatory arrest group and this value was 12.5+/-3.4 pcg/ml for retrograde cerebral perfusion group.ICAM (Intracellular Adhesion Molecule) level was higher in total circulatory arrest group (18.75+/-3.6 ng/ml) when compared to retrograde cerebral perfusion group (8.75+/-1.8 ng/ml) (p<0.05). All parameters showed that retrograde cerebral perfusion preserved the brain functions better comparing with total circulatory arrest. The time necessary for aortic surgery may be provided by the retrograde cerebral perfusion technique.
Cardiovasc Surg 2002 Dec
PMID:Comparison of metabolic responses to deep hypothermic total circulatory arrest and retrograde cerebral perfusion in an experimental model. 1245 96

We studied the effect of atorvastatin on the adhesive phenotype of human endothelial cells (HUVEC) stimulated by tumor necrosis factor (TNF)-alpha. Surface expression of adhesion molecules on HUVEC was examined by flow cytometry and confocal microscopy, and adhesion of monocytes (human THP-1 cell line) was measured in vitro under flow conditions. In TNF-alpha-activated HUVEC, atorvastatin significantly enhanced surface expression of vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, E-selectin, and fractalkine, when compared with TNF-alpha stimulation alone. This enhancement was reversed by mevalonate or geranylgeranyl pyrophosphate (GGPP) and was mimicked by an inhibitor of geranylgeranylation. The enhancing effect of atorvastatin was restricted to TNF-alpha-inducible adhesion molecule and was the reflect of an increased protein synthesis (mRNA and protein) and not of a reduced shedding. Confocal microscopy examination showed that atorvastatin also altered the surface distribution of adhesion molecules. Adhesion of human THP-1 cells on TNF-alpha-activated HUVEC was significantly reduced by atorvastatin (-42% at 1 microM). Mevalonate or GGPP restored the TNF-alpha-induced adhesive potential. These results show that atorvastatin, by inhibiting prenylation of G proteins, enhances the TNF-alpha-induced expression of adhesion molecules at the endothelial cell surface and also alters their surface distribution which may account for the reduced binding of monocytes.
J Cardiovasc Pharmacol 2003 Feb
PMID:Effect of atorvastatin on adhesive phenotype of human endothelial cells activated by tumor necrosis factor alpha. 1254 94

Catheter ablation for ventricular tachycardia (VT) is becoming an essential component of the successful management of patients with structural heart disease and refractory ventricular arrhythmias. Despite detailed mapping and ablation from the endocardium, nearly a third of VT circuits remain inaccessible. Pericardial access has improved our ability to address these resistant VTs. Adhesions after cardiac surgery can impede access, necessitating a direct surgical approach to the pericardial space. Potential risks include risk of injury to an epicardial coronary artery, the phrenic nerve, subdiaphragmatic vessels, and right ventricle. We describe the indications for and approach to catheter ablation of VT for the pericardial space.
J Cardiovasc Electrophysiol 2009 Jun
PMID:Strategies for epicardial mapping and ablation of ventricular tachycardia. 1920 80


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